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  • 1. Carlhall, C.
    et al.
    Wigström, Lars
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Clinical Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Heiberg, Einar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Clinical Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Karlsson, Matts
    Linköping University, The Institute of Technology. Linköping University, Department of Biomedical Engineering, Biomedical Modelling and Simulation .
    Bolger, A.F.
    Department of Medicine, Division of Cardiology, University of California, San Francisco, CA, United States.
    Nylander, Eva
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Clinical Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Reply [2]2006In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 291, no 5Other (Other academic)
    Abstract [en]

    [No abstract available]

  • 2.
    Carlhäll, Carljohan
    et al.
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences.
    Kindberg, Katarina
    Linköping University, Department of Biomedical Engineering. Linköping University, The Institute of Technology.
    Wigström, Lars
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences.
    Daughters, G. T.
    Linköping University, Faculty of Health Sciences.
    Millers, D. C.
    Linköping University, Faculty of Health Sciences.
    Karlsson, Matts
    Linköping University, Department of Biomedical Engineering. Linköping University, The Institute of Technology.
    Ingels Jr, N. B.
    Linköping University, Faculty of Health Sciences.
    Contribution of mitral annular dynamics to LV diastolic filling with alteration in preload and inotropic state2007In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 293, no 3, p. G1473-H1479Article in journal (Refereed)
    Abstract [en]

    Mitral annular (MA) excursion during diastole encompasses a volume that is part of total left ventricular (LV) filling volume (LVFV). Altered excursion or area variation of the MA due to changes in preload or inotropic state could affect LV filling. We hypothesized that changes in LV preload and inotropic state would not alter the contribution of MA dynamics to LVFV. Six sheep underwent marker implantation in the LV wall and around the MA. After 7–10 days, biplane fluoroscopy was used to obtain three-dimensional marker dynamics from sedated, closed-chest animals during control conditions, inotropic augmentation with calcium (Ca), preload reduction with nitroprusside (N), and vena caval occlusion (VCO). The contribution of MA dynamics to total LVFV was assessed using volume estimates based on multiple tetrahedra defined by the three-dimensional marker positions. Neither the absolute nor the relative contribution of MA dynamics to LVFV changed with Ca or N, although MA area decreased (Ca, P < 0.01; and N, P < 0.05) and excursion increased (Ca, P < 0.01). During VCO, the absolute contribution of MA dynamics to LVFV decreased (P < 0.001), based on a reduction in both area (P < 0.001) and excursion (P < 0.01), but the relative contribution to LVFV increased from 18 ± 4 to 45 ± 13% (P < 0.001). Thus MA dynamics contribute substantially to LV diastolic filling. Although MA excursion and mean area change with moderate preload reduction and inotropic augmentation, the contribution of MA dynamics to total LVFV is constant with sizeable magnitude. With marked preload reduction (VCO), the contribution of MA dynamics to LVFV becomes even more important.

  • 3.
    Carlhäll, Carljohan
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Wigström, Lars
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Heiberg, Einar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Karlsson, M.
    Östergötlands Läns Landsting, Centre for Medical Imaging, Department of Biomedical Engineering in Östergötland. Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Bolger, A. F.
    Department of Medicine, Division of Cardiology, University of California, San Francisco, California, USA.
    Nylander, E.
    Linköping University, Department of Medicine and Care. Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Reply to article: Misinterpretation About the Contribution of the Left Ventricular Long-Axis Shortening to the Stroke Volume2006In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 291, no 5, p. 2551-2552Article in journal (Other academic)
    Abstract [en]

       

  • 4.
    Carlhäll, Carljohan
    et al.
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Department of Medicine and Care, Center for Medical Image Science and Visualization. Linköping University, Faculty of Health Sciences.
    Wigström, Lars
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Department of Medicine and Care, Center for Medical Image Science and Visualization. Linköping University, Faculty of Health Sciences.
    Heiberg, Einar
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Department of Medicine and Care, Center for Medical Image Science and Visualization. Linköping University, Faculty of Health Sciences.
    Karlsson, Matts
    Linköping University, Department of Biomedical Engineering. Linköping University, Department of Medicine and Care, Center for Medical Image Science and Visualization. Linköping University, Faculty of Health Sciences.
    Bolger, A. F.
    Department of Medicine/Cardiology, University of California, San Francisco, California.
    Nylander, Eva
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Department of Medicine and Care, Center for Medical Image Science and Visualization. Linköping University, Faculty of Health Sciences.
    Contribution of mitral annular excursion and shape dynamics to total left ventricular volume change2004In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 287, no 4, p. H1836-H1841Article in journal (Refereed)
    Abstract [en]

    The mitral annulus (MA) has a complex shape and motion, and its excursion has been correlated to left ventricular (LV) function. During the cardiac cycle the annulus’ excursion encompasses a volume that is part of the total LV volume change during both filling and emptying. Our objective was to evaluate the contribution of MA excursion and shape variation to total LV volume change. Nine healthy subjects aged 56 ± 11 (means ± SD) years underwent transesophageal echocardiography (TEE). The MA was outlined in all time frames, and a four-dimensional (4-D) Fourier series was fitted to the MA coordinates (3-D+time) and divided into segments. The annular excursion volume (AEV) was calculated based on the temporally integrated product of the segments’ area and their incremental excursion. The 3-D LV volumes were calculated by tracing the endocardial border in six coaxial planes. The AEV (10 ± 2 ml) represented 19 ± 3% of the total LV stroke volume (52 ± 12 ml). The AEV correlated strongly with LV stroke volume (r = 0.73; P < 0.05). Peak MA area occurred during middiastole, and 91 ± 7% of reduction in area from peak to minimum occurred before the onset of LV systole. The excursion of the MA accounts for an important portion of the total LV filling and emptying in humans. These data suggest an atriogenic influence on MA physiology and also a sphincter-like action of the MA that may facilitate ventricular filling and aid competent valve closure. This 4-D TEE method is the first to allow noninvasive measurement of AEV and may be used to investigate the impact of physiological and pathological conditions on this important aspect of LV performance.

  • 5.
    Dahlfors, Gunilla
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Chen, Yun
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Wasteson, Maria
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Arnqvist, Hans J.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    PDGF-BB-induced DNA synthesis is delayed by angiotensin II in vascular smooth muscle cells1998In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 274, no 5, p. H1742-H1748Article in journal (Refereed)
    Abstract [en]

    The interaction of ANG II with platelet-derived growth factor (PDGF)-BB-induced DNA synthesis was studied in cultured rat aortic smooth muscle cells. PDGF-BB-induced DNA synthesis was delayed (∼6–8 h) by ANG II as shown by a time-course experiment. Losartan, an AT1-receptor antagonist, blocked the transient inhibitory effect of ANG II, whereas the AT2-receptor antagonist PD-123319 had no effect. Autocrine- or paracrine-acting transforming growth factor-β1 (TGF-β1), believed to be a mediator of ANG II-induced inhibitory effects, was not responsible for the delay of PDGF-BB-induced DNA synthesis, because a potent TGF-β1 neutralizing antibody could not reverse this effect of ANG II, nor was the delay of the PDGF-BB effect caused by inhibition of PDGF-β-receptor phosphorylation as shown by Western blot analysis of immunoprecipitated PDGF-β receptor. In conclusion, our results show that ANG II can exert a transient inhibitory effect on PDGF-BB-induced proliferation via the AT1 receptor.

  • 6.
    Fernlund, Eva
    et al.
    Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Paediatrics in Linköping. Lund University, Sweden.
    Schlegel, Todd T.
    Karolinska Institute, Sweden; Karolinska University Hospital, Sweden.
    Platonov, Pyotr G.
    Lund University, Sweden.
    Carlson, Jonas
    Lund University, Sweden.
    Carlsson, Marcus
    Lund University, Sweden.
    Liuba, Petru
    Lund University, Sweden.
    Peripheral microvascular function is altered in young individuals at risk for hypertrophic cardiomyopathy and correlates with myocardial diastolic function2015In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 308, no 11, p. H1351-H1358Article in journal (Refereed)
    Abstract [en]

    Hypertrophic cardiomyopathy (HCM) is a major cause of sudden cardiac death in the young. Based on previous reports of functional abnormalities in not only coronary but also peripheral vessels in adults with HCM, we aimed to assess both peripheral vascular and myocardial diastolic function in young individuals with an early stage of HCM and in individuals at risk for HCM. Children, adolescents, and young adults (mean age: 12 yr) with a family history of HCM who either had (HCM group; n = 36) or did not have (HCM-risk group; n = 30) echocardiography-documented left ventricular (LV) hypertrophy as well as healthy matched controls (n = 85) and healthy young athletes (n = 12) were included in the study. All underwent assessment with 12-lead electrocardiography, two-dimensional echocardiography, tissue Doppler imaging and laser Doppler with transdermal iontophoresis of ACh and sodium nitroprusside. LV thickness and mass were increased in HCM and athlete groups compared with control and HCM-risk groups. The mitral E-to-e ratio, measured via tissue Doppler, was increased in HCM (P less than 0.0001) and HCM-risk (P less than 0.01) groups compared with control and athlete groups, as were microvascular responses to ACh (HCM group: P less than 0.045 and HCM- risk group: P less than 0.02). Responses to ACh correlated with the E-to-e ratio (r = 0.5, P = 0.001). Microvascular responses to sodium nitroprusside were similar in all groups (P = 0.2). HCM-causing mutations or its familial history are associated with changes in cardiac diastolic function and peripheral microvascular function even before the onset of myocardial hypertrophy. Tissue Doppler can be used to differentiate HCM from physiological LV hypertrophy in young athletes.

  • 7.
    Fredriksson, Alexandru G
    et al.
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization, CMIV.
    Zajac, Jakub
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization, CMIV.
    Eriksson, Jonatan
    Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Medical and Health Sciences, Physiology.
    Dyverfeldt, Petter
    Linköping University, Department of Medical and Health Sciences, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Clinical Physiology UHL. Linköping University, Center for Medical Image Science and Visualization, CMIV.
    Bolger, Ann F
    University of California San Francisco.
    Ebbers, Tino
    Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Clinical Physiology UHL. Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Medical and Health Sciences, Physiology. Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics.
    Carlhäll, Carljohan
    Linköping University, Department of Medical and Health Sciences, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Clinical Physiology UHL. Linköping University, Center for Medical Image Science and Visualization, CMIV.
    4-D blood flow in the human right ventricle2011In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 301, no 6, p. H2344-H2350Article in journal (Refereed)
    Abstract [en]

    Right ventricular (RV) function is a powerful prognostic indicator in many forms of heart disease, but its assessment remains challenging and inexact. RV dysfunction may alter the normal patterns of RV blood flow, but those patterns have been incompletely characterized. We hypothesized that, based on anatomic differences, the proportions and energetics of RV flow components would differ from those identified in the left ventricle (LV) and that the portion of the RV inflow passing directly to outflow (Direct Flow) would be prepared for effective systolic ejection as a result of preserved kinetic energy (KE) compared with other RV flow components. Three-dimensional, time-resolved phase-contrast velocity, and balanced steady-state free-precession morphological data were acquired in 10 healthy subjects using MRI. A previously validated method was used to separate the RV and LV end-diastolic volumes into four flow components and measure their volume and KE over the cardiac cycle. The RV Direct Flow: 1) followed a smoothly curving route that did not extend into the apical region of the ventricle; 2) had a larger volume and possessed a larger presystolic KE (0.4 +/- 0.3 mJ) than the other flow components (P andlt; 0.001 and P andlt; 0.01, respectively); and 3) represented a larger part of the end-diastolic blood volume compared with the LV Direct Flow (P andlt; 0.01). These findings suggest that diastolic flow patterns distinct to the normal RV create favorable conditions for ensuing systolic ejection of the Direct Flow component. These flow-specific aspects of RV diastolic-systolic coupling provide novel perspectives on RV physiology and may add to the understanding of RV pathophysiology.

  • 8.
    Itoh, Akinobu
    et al.
    Stanford University.
    Stephens, Elizabeth H
    Rice University.
    Ennis, Daniel B
    University of Calif Los Angeles.
    Carlhäll, Carljohan
    Linköping University, Department of Medical and Health Sciences, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Clinical Physiology UHL.
    Bothe, Wolfgang
    Stanford University.
    Nguyen, Tom C
    Stanford University.
    Swanson, Julia C
    Stanford University.
    Miller, D Craig
    Stanford University.
    Ingels, Nei lB
    Palo Alto Medical Fdn.
    Contribution of myocardium overlying the anterolateral papillary muscle to left ventricular deformation2012In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 302, no 1, p. H180-H187Article in journal (Refereed)
    Abstract [en]

    Itoh A, Stephens EH, Ennis DB, Carlhall CJ, Bothe W, Nguyen TC, Swanson JC, Miller DC, Ingels NB Jr. Contribution of myocardium overlying the anterolateral papillary muscle to left ventricular deformation. Am J Physiol Heart Circ Physiol 302: H180-H187, 2012. First published October 28, 2011; doi:10.1152/ajpheart.00687.2011.-Previous studies of transmural left ventricular (LV) strains suggested that the myocardium overlying the papillary muscle displays decreased deformation relative to the anterior LV free wall or significant regional heterogeneity. These comparisons, however, were made using different hearts. We sought to extend these studies by examining three equatorial LV regions in the same heart during the same heartbeat. Therefore, deformation was analyzed from transmural beadsets placed in the equatorial LV myocardium overlying the anterolateral papillary muscle (PAP), as well as adjacent equatorial LV regions located more anteriorly (ANT) and laterally (LAT). We found that the magnitudes of LAT normal longitudinal and radial strains, as well as major principal strains, were less than ANT, while those of PAP were intermediate. Subepicardial and midwall myofiber angles of LAT, PAP, and ANT were not significantly different, but PAP subendocardial myofiber angles were significantly higher (more longitudinal as opposed to circumferential orientation). Subepicardial and midwall myofiber strains of ANT, PAP, and LAT were not significantly different, but PAP subendocardial myofiber strains were less. Transmural gradients in circumferential and radial normal strains, and major principal strains, were observed in each region. The two main findings of this study were as follows: 1) PAP strains are largely consistent with adjacent LV equatorial free wall regions, and 2) there is a gradient of strains across the anterolateral equatorial left ventricle despite similarities in myofiber angles and strains. These findings point to graduated equatorial LV heterogeneity and suggest that regional differences in myofiber coupling may constitute the basis for such heterogeneity.

  • 9.
    Krishnamurthy, G.
    et al.
    Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States, Department of Mechanical Engineering, Stanford University, Stanford, CA, United States.
    Ennis, D.B.
    Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States.
    Itoh, A.
    Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States.
    Bothe, W.
    Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States.
    Swanson, J.C.
    Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States.
    Karlsson, Matts
    Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics . Linköping University, The Institute of Technology.
    Kuh, E.
    Department of Mechanical Engineering, Stanford University, Stanford, CA, United States.
    Miller, D.C.
    Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States.
    Ingels, Jr. N.B.
    Ingels Jr., N.B., Department of Cardiothoracic Surgery, Stanford University, Stanford, CA, United States, Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, Palo Alto, CA, United States, Laboratory of Cardiovascular Physiology and Biophysics, Research Institute, Palo Alto Medical Foundation, 795 El Camino Real, Palo Alto, CA 94301-2302, United States.
    Material properties of the ovine mitral valve anterior leaflet in vivo from inverse finite element analysis2008In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 295, no 3Article in journal (Refereed)
    Abstract [en]

    We measured leaflet displacements and used inverse finite-element analysis to define, for the first time, the material properties of mitral valve (MV) leaflets in vivo. Sixteen miniature radiopaque markers were sewn to the MV annulus, 16 to the anterior MV leaflet, and 1 on each papillary muscle tip in 17 sheep. Four-dimensional coordinates were obtained from biplane videofluoroscopic marker images (60 frames/s) during three complete cardiac cycles. A finite-element model of the anterior MV leaflet was developed using marker coordinates at the end of isovolumic relaxation (IVR, when the pressure difference across the valve is ~0), as the minimum stress reference state. Leaflet displacements were simulated during IVR using measured left ventricular and atrial pressures. The leaflet shear modulus (Gcirc-rad) and elastic moduli in both the commisure-commisure (Ecirc) and radial (Erad) directions were obtained using the method of feasible directions to minimize the difference between simulated and measured displacements. Group mean (±SD) values (17 animals, 3 heartbeats each, i.e., 51 cardiac cycles) were as follows: Gcirc-rad = 121 ± 22 N/mm2, Ecirc = 43 ± 18 N/mm2, and Erad = 11 ± 3 N/mm2 (Ecirc > E rad, P < 0.01). These values, much greater than those previously reported from in vitro studies, may result from activated neurally controlled contractile tissue within the leaflet that is inactive in excised tissues. This could have important implications, not only to our understanding of mitral valve physiology in the beating heart but for providing additional information to aid the development of more durable tissue-engineered bioprosthetic valves. Copyright © 2008 the American Physiological Society.

  • 10.
    Lindenberger, Marcus
    et al.
    Linköping University, Department of Medicine and Health Sciences, Physiology . Linköping University, Faculty of Health Sciences.
    Olsen, H.
    Helsingborg Hospital.
    Länne, Toste
    Linköping University, Department of Medicine and Health Sciences, Physiology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Lower capacitance response and capillary fluid absorption in women to defend central blood volume in response to acute hypovolemic circulatory stress2008In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 295, p. H867-H873Article in journal (Refereed)
    Abstract [en]

    Acute hemorrhage is a leading cause of death in trauma, and women are more susceptible to hypovolemic circulatory stress than men. The mechanisms underlying the susceptibility are not clear, however. The aim of the present study was to examine the compensatory mechanisms to defend central blood volume during experimental hypovolemia in women and men. Twenty-two women (23.1 ± 0.4 yr) and 16 men (23.2 ± 0.5 yr) were included. A lower body negative pressure (LBNP) of 11–44 mmHg induced experimental hypovolemic circulatory stress. The volumetric technique was used to assess the capacitance response (redistribution of peripheral venous blood to the central circulation) as well as to assess net capillary fluid transfer from tissue to blood in the arm. Plasma norepinephrine (NE) and forearm blood flow were measured before and during hypovolemia, and forearm vascular resistance (FVR) was calculated. LBNP created comparable hypovolemia in women and men. FVR increased less in women during hypovolemic stress, and no association between plasma NE and FVR was seen in women (R2 = 0.01, not significant), in contrast to men (R2 = 0.59, P < 0.05). Women demonstrated a good initial capacitance response, but this was not maintained with time, in contrast to men [e.g., decreased by 24 ± 4% (women) vs. 4 ± 5% (men), LBNP of 44 mmHg, P < 0.01], and net capillary fluid absorption from tissue to blood was lower in women (0.086 ± 0.007 vs. 0.115 ± 0.011 ml·100 ml–1·min–1, P < 0.05). In conclusion, women showed impaired vasoconstriction, reduced capacitance response with time, and reduced capillary fluid absorption during acute hypovolemic circulatory stress, indicating less efficiency to defend central blood volume than men.

  • 11.
    Lindenberger, Marcus
    et al.
    Linköping University, Department of Medicine and Health Sciences, Physiology . Linköping University, Faculty of Health Sciences.
    Toste, Länne
    Linköping University, Department of Medicine and Health Sciences, Physiology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Decreased capillary filtration but maintained venous compliance in the lower limb of aging women2007In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 293, p. H3568-H3574Article in journal (Refereed)
    Abstract [en]

    There are sex-related differences in venous compliance and capillary filtration in the lower limbs, which to some extent can explain the susceptibility to orthostatic intolerance in young women. With age, venous compliance and capacitance are reduced in men. This study was designed to evaluate age-related changes in venous compliance and capillary filtration in the lower limbs of healthy women. Included in this study were 22 young and 12 elderly women (23.1 ± 0.4 and 66.4 ± 1.4 yr). Lower body negative pressure (LBNP) of 11, 22, and 44 mmHg created defined transmural pressure gradients in the lower limbs. A plethysmographic technique was used on the calf to assess venous capacitance and net capillary filtration. Venous compliance was calculated with the aid of a quadratic regression equation. No age-related differences in venous compliance and capacitance were found. Net capillary filtration and capillary filtration coefficient (CFC) were lower in elderly women at a LBNP of 11 and 22 mmHg (0.0032 vs. 0.0044 and 0.0030 vs. 0.0041 ml·100 ml–1·min–1·mmHg–1, P < 0.001). At higher transmural pressure (LBNP, 44 mmHg), CFC increased by 1/3 (0.010 ml·100 ml–1·min–1·mmHg–1) in the elderly (P < 0.001) but remained unchanged in the young women. In conclusion, no age-related decrease in venous compliance and capacitance was seen in women. However, a decreased CFC was found with age, implying reduced capillary function. Increasing transmural pressure increased CFC in the elderly women, indicating an increased capillary susceptibility to transmural pressure load in dependent regions. These findings differ from earlier studies on age-related effects in men, indicating sex-specific vascular aging both in the venous section and microcirculation.

  • 12.
    Mandinov, L.
    et al.
    Maine Medical Center, Scarborough, Maine, USA.
    L. Moodie, K.
    Dartmouth-Hitchcock Medical Center, Hanover, NH, USA.
    Mandinova, A.
    Maine Medical Center, Scarborough, Maine, USA.
    Zhuang, Z.
    Dartmouth-Hitchcock Medical Center, Hanover, NH, USA.
    Redican, F.
    Dartmouth-Hitchcock Medical Center, Hanover, NH, USA.
    Baklanov, D.
    Dartmouth-Hitchcock Medical Center, Hanover, NH, USA.
    Lindner, V.
    Maine Medical Center, Scarborough, Maine, USA.
    Maciag, T.
    Maine Medical Center, Scarborough, Maine, USA.
    Simons, M.
    Dartmouth-Hitchcock Medical Center, Hanover, NH, USA.
    de Muinck, Ebo D.
    Maine Medical Center, Scarborough, Maine, USA.
    Inhibition of in-stent restenosis by oral copper chelation in porcine coronary arteries2006In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 291, no 6, p. H2692-H2697Article in journal (Refereed)
    Abstract [en]

    Stress-induced release of IL-1 alpha and fibroblast growth factor-1 is dependent on intracellular copper and is a major driver of neointimal hyperplasia. Therefore, we assessed the effect of tetrathiomolybdate (TTM), a clinically proven copper chelator, on in-stent restenosis. Nine pigs were treated with TTM (5 mg/kg po) twice daily for 2 wk before stent implantation and for 4 wk thereafter, and nine pigs served as controls. In-stent restenosis was assessed by quantitative coronary angiography (QCA), intravascular ultrasound (IVUS), and histomorphometry. Serum ceruloplasmin activity was used as a surrogate marker of copper bioavailability. In TTM-treated animals, ceruloplasmin dropped 70 +/- 10% below baseline levels. Baseline characteristics were comparable in TTM-treated and control animals. At 4-wk follow-up, all parameters relevant to in-stent restenosis were significantly reduced in TTM-treated animals: minimal lumen diameter by QCA was 2.03 +/- 0.57 and 1.47 +/- 0.45 mm in TTM-treated and control animals, respectively (P less than 0.05), percent stenosis diameter was 39% less in TTM-treated animals (27.1 +/- 16.6% vs. 44.5 +/- 16.1%, P less than 0.05), minimal lumen area by IVUS was 60% larger in TTM-treated animals (4.27 +/- 1.56 vs. 2.67 +/- 1.19 mm(2), P less than 0.05), and neointimal volume by histomorphometry was 37% less in TTM-treated animals (34.9 +/- 11.5 vs. 55.2 +/- 19.6 mm(3), P less than 0.05). We conclude that systemic copper chelation with a clinically approved chelator significantly inhibits in-stent restenosis.

  • 13.
    Olsen, Henrik
    et al.
    Endokrin klin Malmö.
    Vernersson, Einar
    Anestesi klin Malmö.
    Länne, Toste
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Vascular surgery.
    Cardiovascular response to acute hypovolemia in relation to age. Implications for orthostasis and hemorrhage2000In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 278, p. 222-232Article in journal (Refereed)
  • 14.
    Palm, Fredrik
    et al.
    Uppsala universitet, Institutionen för medicinsk cellbiologi.
    Onozato, Maristela L
    Luo, Zaiming
    Wilcox, Christopher S
    Dimethylarginine dimethylaminohydrolase (DDAH): Expression, regulation and function in the cardiovascular and renal systems2007In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 293, no 6, p. H3227-H3245Article in journal (Refereed)
    Abstract [en]

    Asymmetric (NG,NG)-dimethylarginine (ADMA) inhibits nitric oxide(NO) synthases (NOS). ADMA is a risk factor for endothelialdysfunction, cardiovascular mortality, and progression of chronickidney disease. Two isoforms of dimethylarginine dimethylaminohydrolase(DDAH) metabolize ADMA. DDAH-1 is the predominant isoform inthe proximal tubules of the kidney and in the liver. These organsextract ADMA from the circulation. DDAH-2 is the predominantisoform in the vasculature, where it is found in endothelialcells adjacent to the cell membrane and in intracellular vesiclesand in vascular smooth muscle cells among the myofibrils andthe nuclear envelope. In vivo gene silencing of DDAH-1 in therat and DDAH +/– mice both have increased circulatingADMA, whereas gene silencing of DDAH-2 reduces vascular NO generationand endothelium-derived relaxation factor responses. DDAH-2also is expressed in the kidney in the macula densa and distalnephron. Angiotensin type 1 receptor activation in kidneys reducesthe expression of DDAH-1 but increases the expression of DDAH-2.This rapidly evolving evidence of isoform-specific distributionand regulation of DDAH expression in the kidney and blood vesselsprovides potential mechanisms for nephron site-specific regulationof NO production. In this review, the recent advances in theregulation and function of DDAH enzymes, their roles in theregulation of NO generation, and their possible contributionto endothelial dysfunction in patients with cardiovascular andkidney diseases are discussed.

  • 15. Sundblad, P
    et al.
    Wranne, Bengt
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Clinical Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Influence of posture on left ventricular long- and short-axis shortening2002In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 283, no 4, p. H1302-H1306Article in journal (Refereed)
    Abstract [en]

    End-diastolic volume and left ventricular stroke volume are increased in the supine compared with upright position, but the contribution of long-axis (LAS) and short-axis shortening (SAS) to these changes with change in posture has not been established. We examined long- and short-axis motion and dimensions with echocardiography in 10 healthy subjects in the upright and supine position. Long-axis length at end diastole was almost identical, whereas the diastolic short-axis diameter was increased in the supine position. At end systole, there was a decreased long- axis length and increased short-axis length in the supine vs. upright position. Both LAS and SAS were enhanced in supine vs. upright positions [LAS: 9.3 +/- 2.2 vs. 15.1 +/- 3.1 mm (P < 0.001), SAS: 12.7 +/- 3.2 vs. 16.3 +/- 2.8 mm (P < 0.001)], presumably via Starling mechanisms. LAS increased more in the lateral part of the mitral annulus than in the septal part [7.7 +/- 2.6 vs. 4.0 +/- 2.8 mm (P < 0.006)], which implies that the more spherical form, in the supine position, induces more stretch at the lateral free wall than in the ventricular septum. These findings support the notion that Starling mechanisms affect systolic LAS.

  • 16.
    Thore, Carl-Johan
    et al.
    Linköping University, Department of Management and Engineering, Mechanics . Linköping University, The Institute of Technology.
    Stålhand, Jonas
    Linköping University, Department of Management and Engineering, Mechanics . Linköping University, The Institute of Technology.
    Karlsson, Matts
    Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics . Linköping University, The Institute of Technology.
    Toward a noninvasive subject-specific estimation of abdominal aortic pressure2008In: American Journal of Physiology. Heart and Circulatory Physiology, ISSN 0363-6135, E-ISSN 1522-1539, Vol. 295, no 3Article in journal (Refereed)
    Abstract [en]

    A method for estimation of central arterial pressure based on linear one-dimensional wave propagation theory is presented in this paper. The equations are applied to a distributed model of the arterial tree, truncated by three-element windkessels. To reflect individual differences in the properties of the arterial trees, we pose a minimization problem from which individual parameters are identified. The idea is to take a measured waveform in a peripheral artery and use it as input to the model. The model subsequently predicts the corresponding waveform in another peripheral artery in which a measurement has also been made, and the arterial tree model is then calibrated in such a way that the computed waveform matches its measured counterpart. For the purpose of validation, invasively recorded abdominal aortic, brachial, and femoral pressures in nine healthy subjects are used. The results show that the proposed method estimates the abdominal aortic pressure wave with good accuracy. The root mean square error (RMSE) of the estimated waveforms was 1.61 ± 0.73 mmHg, whereas the errors in systolic and pulse pressure were 2.32 ± 1.74 and 3.73 ± 2.04 mmHg, respectively. These results are compared with another recently proposed method based on a signal processing technique, and it is shown that our method yields a significantly (P < 0.01) lower RMSE. With more extensive validation, the method may eventually be used in clinical practice to provide detailed, almost individual, specific information as a valuable basis for decision making. Copyright © 2008 the American Physiological Society.

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