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Liss, Per
Publications (10 of 10) Show all publications
Eckerbom, P., Hansell, P., Bjerner, T., Palm, F., Weis, J. & Liss, P. (2013). Intravoxel Incoherent Motion MR Imaging of the Kidney: Pilot Study. Advances in Experimental Medicine and Biology, 765, 55-58
Open this publication in new window or tab >>Intravoxel Incoherent Motion MR Imaging of the Kidney: Pilot Study
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2013 (English)In: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, Vol. 765, p. 55-58Article in journal (Refereed) Published
Abstract [en]

MR examinations (Achieva 3 T, Philips, Best, The Netherlands) were performed at five different occasions in a healthy volunteer (male 60 years) and in one renal cancer patient (male 78 years) with normal renal function (creatinine 88 μmol/L). Intravoxel incoherent motion (IVIM) coefficients D + D* were measured using respiratory-triggered diffusion-weighted spin-echo echo-planar imaging. Perfusion data of the patient were acquired using a saturation-recovery gradient-echo sequence and with the bolus of Gd-BOPTA (Multihance). D + D* were computed by monoexponential fitting of MR signal intensity attenuation versus b for b = 0, 50, 100, 150 s/mm2. Perfusion parameters were evaluated with “NordicICE” software. The map of D + D* was compared qualitatively with the perfusion map computed from the Gd scan. D + D* values of the cortex and medulla were in the range 2.3–2.7 and 1.1–1.6 × 10-3 mm2/s, respectively. In conclusion, in this pilot study a good qualitative relation between IVIM variables D + D* and renal perfusion has been found.

National Category
Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:liu:diva-99618 (URN)10.1007/978-1-4614-4989-8_8 (DOI)22879014 (PubMedID)
Available from: 2012-10-09 Created: 2013-10-18 Last updated: 2017-12-06
Edlund, J., Fasching, A., Liss, P., Hansell, P. & Palm, F. (2010). The roles of NADPH-oxidase and nNOS for the increased oxidative stress and the oxygen consumption in the diabetic kidney. Diabetes/Metabolism Research Reviews, 26(5), 349-356
Open this publication in new window or tab >>The roles of NADPH-oxidase and nNOS for the increased oxidative stress and the oxygen consumption in the diabetic kidney
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2010 (English)In: Diabetes/Metabolism Research Reviews, ISSN 1520-7552, E-ISSN 1520-7560, Vol. 26, no 5, p. 349-356Article in journal (Refereed) Published
Abstract [en]

Background

Sustained hyperglycaemia induces increased renal oxygen consumption resulting in reduced oxygen availability in the diabetic kidney. We investigated the roles of the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase and the neuronal nitric oxide synthase (nNOS) for the increased oxygen consumption in streptozotocin-diabetic rats.

Methods

Oxygen consumption was measured in isolated proximal tubular cells (PTC) from streptozotocin-induced diabetic rats (n = 7-9 per group) with and without chronic treatment with apocynin, a NADPH-oxidase inhibitor, or S-methyl-L-thiocitrulline (SMTC), a selective nNOS inhibitor, or a combination of the two and the results were compared to normoglycaemic controls (n = 10). Oxidative stress was estimated from thiobarbituric acid reactive substances and protein expression measured by Western blot.

Results

Proximal tubular cells from untreated diabetic rats had increased oxygen consumption compared to controls (40.6 +/- 7.9 versus 10.9 +/- 2.0 nmol/mg protein/min). All treatments reduced the diabetes-induced increase in oxygen consumption (apocynin 10.5 +/- 1.7, SMTC 19.7 +/- 3.0 and apocynin +/- SMTC 21.6 +/- 3.6 nmol/mg protein/min). Neither apocynin nor SMTC had any effect on the oxygen consumption in cells pre-incubated with ouabain, an inhibitor of active electrolyte transport. Oxidative stress was elevated in the diabetic kidney and inhibited by all treatments. The increased oxygen consumption by diabetic proximal tubular cells correlated with increased protein expressions of p47phox and nNOS and the treatments prevented these increases.

Conclusions

Diabetes induces oxidative stress, which increases oxygen consumption in proximal tubular cells. Inhibition of either NADPH-oxidase or nNOS prevented the increased oxygen consumption. The effect of blocking both these enzymes was less than additive suggesting overlapping pathways which warrant further studies.

Keywords
NADPH-oxidase, neuronal nitric oxide synthase, diabetes mellitus, oxygen consumption, oxidative stress
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99322 (URN)10.1002/dmrr.1099 (DOI)000280033900004 ()20583310 (PubMedID)
Available from: 2010-12-09 Created: 2013-10-15 Last updated: 2017-12-06
Liss, P., Hansell, P., Carlsson, P.-O., Fasching, A. & Palm, F. (2009). Iodinated contrast media decrease renomedullary blood flow. A possible cause of contrast media-induced nephropathy. Advances in Experimental Medicine and Biology, 645, 213-218
Open this publication in new window or tab >>Iodinated contrast media decrease renomedullary blood flow. A possible cause of contrast media-induced nephropathy
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2009 (English)In: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, Vol. 645, p. 213-218Article in journal (Refereed) Published
Abstract [en]

The renal medulla has been implicated as a key target for contrast media-induced nephropathy (CIN). Although the effects of contrast media (CM) on whole kidney blood flow are well characterized, the effect of CM on renal medullary blood flow has been controversial. It has been reported that an extremely high dose of a high osmolar CM (iothalamate; 2900 mg I/kg bw) injected rapidly increased the renal outer medullary blood flow (OMBF). However, more clinical relevant doses consistently result in a sustained decrease in medullary blood flow. Furthermore, simultaneous measurements using both laser-Doppler flowmetry and hydrogen washout yield similar results of a decrease in OMBF after CM administration. CM induced a transient 28% decrease in the laser-Doppler signal from the outer medulla, while the hydrogen washout rate in the same region was reduced by approximately 50%. Furthermore, CM administration consistently results in decreased medullary oxygen tension (PO2). The renal medulla works already during normal physiological conditions at the verge of hypoxia, and the majority of the studies published so far are in agreement with the hypothesis that CIN may have its origin in a further reduction in blood flow and/or oxygen availability of this region of the kidney.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99315 (URN)19227474 (PubMedID)
Available from: 2009-02-24 Created: 2013-10-15 Last updated: 2017-12-06
Edlund, J., Hansell, P., Fasching, A., Liss, P., Weis, J., Glickson, J. D. & Palm, F. (2009). Reduced oxygenation in diabetic rat kidneys measured by T2* weighted magnetic resonance micro-imaging. Advances in Experimental Medicine and Biology, 645, 199-204
Open this publication in new window or tab >>Reduced oxygenation in diabetic rat kidneys measured by T2* weighted magnetic resonance micro-imaging
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2009 (English)In: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, Vol. 645, p. 199-204Article in journal (Refereed) Published
Abstract [en]

By applying invasive techniques for direct measurements of oxygen tension, we have reported decreased kidney oxygenation in experimental diabetes in rats. However, the non-invasive MRI technique utilizing the BOLD effect provides several advantages with the possibility to perform repetitive measurements in the same animals and in human subjects. In this study, we applied a modified single gradient echo micro-imaging sequence to detect the BOLD effect in kidneys of diabetic rats and compared the results to normoglycemic controls. All measurements were performed on inactin-anaesthetized adult male Wistar Furth rats. Diabetes was induced by streptozotocin (45 mg/kg) 14 days prior to MRI-analysis. Sixteen T2*-weighted image records (B0=1.5 T) were performed using radiofrequency spoiled gradient echo sequence with 2.6 ms step increments of TE (TE1=12 ms), while TR (75 ms) and bandwidth per pixel (71.4 Hz) were kept constant. T2* maps were computed by mono-exponential fitting of the pixel intensities. Relaxation rates R2* (1/T2*) in cortex and outer stripe of the outer medulla were similar in both groups (cortex for controls 22.3 +/- 0.4 vs. diabetics 23.1 +/- 1.8 Hz and outer stripe of outer medulla for controls 24.9 +/- 0.4 vs. diabetics 26.4 +/- 1.8 Hz; n=4 in both groups), whereas R2* was increased in the inner stripe of the outer medulla in diabetic rats (diabetics 26.1 +/- 2.4 vs. controls 18.8 +/- 1.4 Hz; n=4, P<0.05). This study demonstrates that experimental diabetes in rats induces decreased oxygenation of the renal outer medulla. Furthermore, the proposed T2*-weighted MR micro-imaging technique is suitable for detection of regional changes in kidney oxygenation in experimental animal models.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99314 (URN)19227472 (PubMedID)
Available from: 2009-02-24 Created: 2013-10-15 Last updated: 2017-12-06
Palm, F., Friederich, M., Carlsson, P.-O., Hansell, P., Teerlink, T. & Liss, P. (2008). Reduced nitric oxide in diabetic kidneys due to increased hepatic arginine metabolism: implications for renomedullary oxygen availability. American Journal of Physiology - Renal Physiology, 294(1), F30-7
Open this publication in new window or tab >>Reduced nitric oxide in diabetic kidneys due to increased hepatic arginine metabolism: implications for renomedullary oxygen availability
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2008 (English)In: American Journal of Physiology - Renal Physiology, ISSN 0363-6127, E-ISSN 1522-1466, Vol. 294, no 1, p. F30-7Article in journal (Refereed) Published
Abstract [en]

Nitric oxide (NO) is a potent regulator of both vascular tone and oxygen utilization. Diabetes is commonly associated with both NO deficiency and reduced renomedullary oxygen availability. Arginine availability as regulator of NO production has gained growing interest. We hypothesized that arginine limitation causes diabetes-induced renomedullary NO deficiency, which directly influences renomedullary oxygen tension (P(o2)). Medullary NO, P(o2), and blood flow were measured in control and streptozotocin-induced diabetic rats, which were treated or not treated with alpha-tocopherol, and administered l-arginine followed by N(omega)-nitro-l-arginine methyl ester. Major components of arginine metabolism were also investigated. Diabetic rats had reduced renomedullary NO levels compared with controls. Arginine selectively increased NO levels in diabetic rats and totally restored NO levels in alpha-tocopherol-treated animals. Tocopherol prevented the reduction in medullary P(o2) in the diabetic animals. Although blood flow increased equally in all groups, arginine increased P(o2) exclusively in the diabetic groups. Diabetes decreased plasma arginine and asymmetric dimethylarginine concentrations, but increased hepatic CAT-2A and plasma ornithine independently of alpha-tocopherol treatment. In conclusion, diabetic rats had reduced renomedullary NO due to decreased plasma arginine following increased hepatic arginine uptake and degradation. This was unrelated to oxidative stress. The diabetes-induced reduction in renomedullary P(o2) was restored by either acute arginine administration, which also restored NO levels, or long-term antioxidant treatment. Arginine increased medullary NO and P(o2) independently of altered hemodynamics in the diabetic groups. This reveals a direct regulatory function of NO for renomedullary P(o2) especially during situations of elevated oxidative stress.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99305 (URN)10.1152/ajprenal.00166.2007 (DOI)17942569 (PubMedID)
Available from: 2009-06-03 Created: 2013-10-15 Last updated: 2017-12-06
Friederich, M., Olerud, J., Fasching, A., Liss, P., Hansell, P. & Palm, F. (2008). Uncoupling protein-2 in diabetic kidneys: increased protein expression correlates to increased non-transport related oxygen consumption. Advances in Experimental Medicine and Biology, 614, 37-43
Open this publication in new window or tab >>Uncoupling protein-2 in diabetic kidneys: increased protein expression correlates to increased non-transport related oxygen consumption
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2008 (English)In: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, Vol. 614, p. 37-43Article in journal (Refereed) Published
Abstract [en]

Diabetic patients have an elevated risk to develop renal dysfunction and it has been postulated that altered energy metabolism is involved. We have previously shown that diabetic rats have markedly decreased oxygen availability in the kidney, resulting from increased oxygen consumption. A substantial part of the increased oxygen consumption is unrelated to tubular transport, suggesting decreased mitochondrial efficiency. In this study, we investigated the protein expression of mitochondrial uncoupling protein (UCP)-2 in kidney tissue from control and streptozotocin (STZ)-induced diabetic rats. Protein levels of UCP-2 were measured in adult male control and STZ-diabetic Wistar Furth as well as Sprague Dawley rats in both the kidney cortex and medulla by Western blot technique. Two weeks of hyperglycemia resulted in increased protein levels of UCP-2 in kidneys from both Wistar Furth and Sprague Dawley rats. Both cortical and medullary UCP-2 levels were elevated 2-3 fold above control levels. We conclude that sustained STZ-induced hyperglycemia increases the kidney levels of mitochondrial UCP-2, which could explain the previously reported increase in non-transport related oxygen consumption in diabetic kidneys. The elevated UCP-2 levels may represent an effort to reduce the increased production of superoxide radicals which is evident during diabetes.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99306 (URN)18290312 (PubMedID)
Available from: 2009-06-03 Created: 2013-10-15 Last updated: 2017-12-06
Palm, F., Carlsson, P.-O., Fasching, A., Hansell, P. & Liss, P. (2006). Diabetes-induced decrease in renal oxygen tension: effects of an altered metabolism. Advances in Experimental Medicine and Biology, 578, 161-166
Open this publication in new window or tab >>Diabetes-induced decrease in renal oxygen tension: effects of an altered metabolism
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2006 (English)In: Advances in Experimental Medicine and Biology, ISSN 0065-2598, E-ISSN 2214-8019, Vol. 578, p. 161-166Article in journal (Refereed) Published
Abstract [en]

During conditions with experimental diabetes mellitus, it is evident that several alterations in renal oxygen metabolism occur, including increased mitochondrial respiration and increased lactate accumulation in the renal tissue. Consequently, these alterations will contribute to decrease the interstitial pO2, preferentially in the renal medulla of animals with sustained long-term hyperglycemia.

Keywords
Animals, Diabetes Mellitus; Experimental/metabolism/physiopathology, Diabetic Nephropathies/*metabolism/*physiopathology, Humans, Kidney/*metabolism/physiology, Oxygen Consumption/physiology
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99289 (URN)16927687 (PubMedID)
Available from: 2008-01-21 Created: 2013-10-15 Last updated: 2017-12-06
Liss, P., Aukland, K., Carlsson, P.-O., Palm, F. & Hansell, P. (2005). Influence of iothalamate on renal medullary perfusion and oxygenation in the rat.. Acta Radiologica, 46(8), 823-9
Open this publication in new window or tab >>Influence of iothalamate on renal medullary perfusion and oxygenation in the rat.
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2005 (English)In: Acta Radiologica, ISSN 0284-1851, E-ISSN 1600-0455, Vol. 46, no 8, p. 823-9Article in journal (Other academic) Published
Keywords
Animals, Blood Pressure/drug effects/physiology, Contrast Media/administration & dosage/*pharmacology, Injections; Intravenous, Iothalamic Acid/administration & dosage/*pharmacology, Kidney Medulla/*drug effects/metabolism/physiopathology, Laser-Doppler Flowmetry, Male, Oxygen Consumption/*drug effects, Rats, Rats; Sprague-Dawley, Renal Circulation/*drug effects/physiology
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99285 (URN)16392607 (PubMedID)
Available from: 2007-11-06 Created: 2013-10-15 Last updated: 2017-12-06
Palm, F., Buerk, D. G., Carlsson, P.-O., Hansell, P. & Liss, P. (2005). Reduced nitric oxide concentration in the renal cortex of streptozotocin-induced diabetic rats: effects on renal oxygenation and microcirculation. Diabetes, 54(11), 3282-7
Open this publication in new window or tab >>Reduced nitric oxide concentration in the renal cortex of streptozotocin-induced diabetic rats: effects on renal oxygenation and microcirculation
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2005 (English)In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 54, no 11, p. 3282-7Article in journal (Refereed) Published
Abstract [en]

Nitric oxide (NO) regulates vascular tone and mitochondrial respiration. We investigated the hypothesis that there is reduced NO concentration in the renal cortex of diabetic rats that mediates reduced renal cortical blood perfusion and oxygen tension (P O2). Streptozotocin-induced diabetic and control rats were injected with l-arginine followed by Nomega-nitro-L-arginine-metyl-ester (L-NAME). NO and P O2 were measured using microsensors, and local blood flow was recorded by laser-Doppler flowmetry. Plasma arginine and asymmetric dimethylarginine (ADMA) were analyzed by high-performance liquid chromatography. L-Arginine increased cortical NO concentrations more in diabetic animals, whereas changes in blood flow were similar. Cortical P O2 was unaffected by L-arginine in both groups. L-NAME decreased NO in control animals by 87 +/- 15 nmol/l compared with 45 +/- 7 nmol/l in diabetic animals. L-NAME decreased blood perfusion more in diabetic animals, but it only affected P O2 in control animals. Plasma arginine was significantly lower in diabetic animals (79.7 +/- 6.7 vs. 127.9 +/- 3.9 mmol/l), whereas ADMA was unchanged. A larger increase in renal cortical NO concentration after l-arginine injection, a smaller decrease in NO after L-NAME, and reduced plasma arginine suggest substrate limitation for NO formation in the renal cortex of diabetic animals. This demonstrates a new mechanism for diabetes-induced alteration in renal oxygen metabolism and local blood flow regulation.

Keywords
Animals, Arginine/analogs, derivatives/pharmacology, Diabetes Mellitus, Experimental/*metabolism, Kidney Cortex/blood supply/drug effects/*metabolism, Male, Microcirculation, NG-Nitroarginine Methyl Ester/pharmacology, Nitric Oxide/*metabolism, Oxidative Stress, Oxygen/*metabolism, Rats, Rats; Inbred WF, Renal Circulation, Research Support; N.I.H, Extramural, Research Support
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99287 (URN)16249456 (PubMedID)
Available from: 2006-12-11 Created: 2013-10-15 Last updated: 2017-12-06
Palm, F., Bergqvist, D., Carlsson, P.-O., Hellberg, O., Nyman, R., Hansell, P. & Liss, P. (2005). The effects of carbon dioxide versus ioxaglate in the rat kidney.. Journal of Vascular and Interventional Radiology, 16(2 Pt 1), 269-74
Open this publication in new window or tab >>The effects of carbon dioxide versus ioxaglate in the rat kidney.
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2005 (English)In: Journal of Vascular and Interventional Radiology, ISSN 1051-0443, E-ISSN 1535-7732, Vol. 16, no 2 Pt 1, p. 269-74Article in journal (Refereed) Published
Keywords
Animals, Blood Pressure/drug effects, Carbon Dioxide/*pharmacology, Comparative Study, Contrast Media/*pharmacology, Glomerular Filtration Rate/drug effects, Injections; Intra-Arterial, Ioxaglic Acid/*pharmacology, Isotonic Solutions, Kidney/*drug effects, Kidney Cortex/drug effects, Kidney Medulla/drug effects, Laser-Doppler Flowmetry, Male, Oxygen/blood, Rats, Rats; Sprague-Dawley, Renal Circulation/drug effects, Research Support; Non-U.S. Gov't
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-99286 (URN)15713929 (PubMedID)
Available from: 2006-12-11 Created: 2013-10-15 Last updated: 2017-12-06
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