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  • 1.
    Alm, Albert
    et al.
    Uppsala University.
    Nilsson , Siv
    Linköping University, Department of Medicine and Health Sciences, Pharmacology . Linköping University, Faculty of Health Sciences.
    Uveoscleral outflow - A review2009In: EXPERIMENTAL EYE RESEARCH, ISSN 0014-4835 , Vol. 88, no 4, p. 760-768Article, review/survey (Other academic)
    Abstract [en]

    The uveoscleral outflow route was described more than 40 years ago. Part of aqueous leaves the eye through the iris root. The ciliary muscle, and there are large species differences in the fraction of aqueous outflow that leaves the eye through this route. In non-human primates 40-50% of aqueous leaves the eye by the uveoscleral route. In human eyes most data has been collected by indirect calculations, with results suggesting a similar fraction, at least in eyes from younger individuals. An age-dependent reduction in uveoscleral flow in human eyes may explain the initial difference seen between non-human primate and human eyes. Unlike trabecular outflow, intraocular pressures within the normal range have little effect on uveoscleral outflow. This may be explained by the fact that changes in intraocular pressure have little effect on the pressure gradient for flow through the ciliary muscle, which is likely to be the rate-limiting step in uveoscleral outflow. The state of the ciliary muscle is important and contraction reduces while relaxation increases uveoscleral flow. Similar effects are achieved with cholinergic agonists and antagonists. Epinephrine increases uveoscleral flow, most likely through stimulating beta(2)-adrenergic receptors. Prostaglandin F-2 alpha and prostaglandin F-2 alpha-analogues effectively reduce intraocular pressure by increasing uveoscleral flow. This is mediated by structural changes in the extracellular matrix of the ciliary muscle, and is likely to contribute to a valuable excess route for aqueous and proteins during intraocular inflammation. Whether uveoscleral flow plays a significant role in any other eye disease is not clear. Thus, 40 years later we are able to successfully increase aqueous flow through the uveoscleral route, a valuable contribution to glaucoma treatment, but we still have only a limited understanding on its physiological role.

  • 2.
    Björck, Hanna M.
    et al.
    Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Medical and Health Sciences, Physiology. Linköping University, Faculty of Health Sciences.
    Renner, Johan
    Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics. Linköping University, The Institute of Technology.
    Maleki, Shohreh
    Atherosclerosis Research Unit, Center for Molecular Medicine, Department of Medicine, Karolinska Institute, Sweden.
    Nilsson, Siv F.E.
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Kihlberg, Johan
    Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Medical and Health Sciences, Radiology. Linköping University, Faculty of Health Sciences.
    Folkersen, Lasse
    Atherosclerosis Research Unit, Center for Molecular Medicine, Department of Medicine, Karolinska Institute, Sweden.
    Karlsson, Matts
    Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics. Linköping University, The Institute of Technology.
    Ebbers, Tino
    Linköping University, Center for Medical Image Science and Visualization, CMIV. 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.
    Eriksson, Per
    Atherosclerosis Research Unit, Center for Molecular Medicine, Department of Medicine, Karolinska Institute, Sweden.
    Länne, Toste
    Linköping University, Center for Medical Image Science and Visualization, CMIV. Linköping University, Department of Medical and Health Sciences, Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Thoracic and Vascular Surgery in Östergötland.
    Characterization of Shear-Sensitive Genes in the NormalRat Aorta Identifies Hand2 as a Major Flow-ResponsiveTranscription Factor2012In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 7, no 12Article in journal (Refereed)
    Abstract [en]

    Objective: Shear forces play a key role in the maintenance of vessel wall integrity. Current understanding regarding shear-dependent gene expression is mainly based on in vitro or in vivo observations with experimentally deranged shear, hence reflecting acute molecular events in relation to flow. Our objective was to determine wall shear stress (WSS) in the rat aorta and study flow-dependent vessel wall biology under physiological conditions.

    Methods and Results: Animal-specific aortic WSS magnitude and vector direction were estimated using computational fluid dynamic simulation based on aortic geometry and flow information acquired by MRI. Two distinct flow pattern regions were identified in the normal rat aorta; the distal part of the inner curvature being exposed to low WSS and a non-uniform vector direction, and a region along the outer curvature being subjected to markedly higher levels of WSS and a uniform vector direction. Microarray analysis revealed a strong differential expression between the flow regions, particularly associated with transcriptional regulation. In particular, several genes related to Ca2+-signalling, inflammation, proliferation and oxidative stress were among the most highly differentially expressed.

    Conclusions: Microarray analysis validated the CFD-defined WSS regions in the rat aorta, and several novel flow-dependent genes were identified. The importance of these genes in relation to atherosusceptibility needs further investigation.

  • 3.
    Nilsson, Siv
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Neuropeptides in theautonomic nervous systeminfluencing uveal blood flowand aqueous humour dynamics2009In: Neuropeptides in the Eye, Kerala, India: Research Signpost , 2009, p. 147-167Chapter in book (Other academic)
    Abstract [en]

    The uveal blood vessels, especially those of the choroid, have a rich innervation from the autonomic nervous system. The superior cervical ganglion is the source of the sympathetic nerve fibres, and the facial nerve, with a synapse in the pterygopalatine ganglion, is the major parasympathetic supply in mammals. Neuropeptide YNPY) is the most abundant peptide in the sympathetic nerve fibres, whereas (vasoactive intestinal polypeptide (VIP) is the main peptide in the parasympathetic nerve fibres. Pituitary adenylate cyclase activating polypeptide (PACAP-27 and PACAP-38) and peptide histidine isoleucine (PHI/PHM) are also present in the parasympathetic fibres.

    NPY is a potent vasoconstrictor in the rabbit uvea, but has only minor effect on uveal blood flow in the cat. These observations agree well with the effects of sympathetic nerve stimulation, which in cats causes an uveal vasoconstriction that is completely abolished by α-adrenoreceptor blockade. In rabbits, the uveal vasoconstriction is resistant to α-adrenoreceptor blockade at high frequencies. The contribution of different neurotransmitters to the uveal vasodilatation caused by facial nerve stimulation seems to differ as well. In cats, the effect is almost abolished by muscarinic blockade combined with inhibition of nitric oxide synthase (NOS), indicating that nitric oxide and acetylcholine are the major transmitters. NO-inhibition and muscarinic blockade have only minor effects on the parasympathetic vasodilatation in the rabbit, however, suggesting that a peptide(s) can be the main mediator(s). In agreement with this, VIP, PHI and PACAP-27 and PACAP-38 are potent vasodilators in the rabbit choroid, but have no effect on uveal blood flows in the cat. The potency of PACAP-27 and PACAP-38 is about 100 times higher than that of VIP and PHI, indicating that selective PAC1 receptors may be involved. In humans, PACAP has been shown to increase blood flow velocity in the ophthalmic artery, indicating choroidal vasodilatation.

    Receptors for VIP/PACAP are present on the ciliary epithelium from several species, and VIP and PACAP-27 stimulates aqueous humour flow in monkeys.

    The significance of the various neuropeptides for the regulation ocular blood flow seems to vary considerably between species and the effects of neuropeptides on ocular circulation in humans is largely unknown.

  • 4.
    Nilsson, Siv
    et al.
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Alm, Albert
    Division of Ophthalmology, Department of Neurosciences, University Hospital, University of Uppsala.
    Determination of Ocular Blood Flows with the Microsphere Method2012In: Ocular Blood Flow / [ed] Leopold Schmetterer, Jeffrey Kiel, Berlin Heidelberg: Springer-Verlag , 2012, p. 25-47Chapter in book (Refereed)
    Abstract [en]

    Adequate blood supply to the eye is an important prerequisite for normal visual function. Over the past 40 years our knowledge of ocular blood flow regulation has improved significantly. This lavishly illustrated textbook provides a comprehensive overview of the current knowledge of ocular blood flow by:Evaluating the wide array of methods for measuring ocular blood flow Offering the reader an evidence-based summary on the physiological and pharmacological properties of ocular blood flow regulation Demonstrating the ocular blood flow abnormalities in different vascular diseases.This reader-friendly and well-structured book will enhance the understanding of all who are interested in learning more about ocular blood flow in health and disease

  • 5.
    Nilsson, Siv
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Pharmacology.
    Drecoll, E
    Lütjen-Drecoll, E
    Toris, C
    Krauss, A
    Kharlamb, A
    Nieves, A
    Guerra, T
    Woodward, D
    The prostanoid EP2 receptor agonist butaprost increases uveoscleral outflow in the cynomolgus monkey2006In: Investigative Ophthalmology and Visual Science, ISSN 0146-0404, E-ISSN 1552-5783, Vol. 47, no 9, p. 4042-4049Article in journal (Refereed)
    Abstract [en]

    PURPOSE. To investigate the ocular hypotensive effect of the prostanoid EP2 receptor agonist butaprost and to establish its mechanism of action. METHODS. All experiments were performed in cynomolgus monkeys after topical application of butaprost (0.1%). The effects of butaprost on aqueous humor flow were determined by fluorophotometry. Total outflow facility was measured by the two-level, constant-pressure perfusion method, and uveoscleral outflow was determined by perfusion of FITC-labeled dextran through the anterior chamber. Effects on ocular morphology were studied after tissue fixation with transcardial perfusion by paraformaldehyde and immersion fixation of the globe, in animals subjected to long-term treatment with butaprost. Conscious ocular normotensive monkeys and monkeys with unilateral ocular hypertension were used for intraocular pressure (IOP) studies. RESULTS. Butaprost had no significant effect on aqueous humor flow or total outflow facility in ocular normotensive monkeys. Uveoscleral outflow was significantly higher in the butaprost treated eyes than in vehicle treated eyes, 1.03 ± 0.20 vs. 0.53 ± 0.18 μL · min-1. After a 1-year treatment with butaprost, the morphology of the ciliary muscle was changed, showing increased spaces between ciliary muscle bundles and the apparent formation of new outflow channels. In many instances, changes were observed in the trabecular meshwork as well. Butaprost, in a single 0.1% dose, decreased IOP significantly in ocular normotensive monkeys and reduced IOP in laser-induced glaucomatous monkey eyes to the same level as that in the ocular normotensive contralateral eyes. CONCLUSIONS. The prostanoid EP2 receptor agonist butaprost appears to lower IOP by increasing uveoscleral outflow, according to both physiological and morphologic findings. Although the prostanoid EP2 receptor is structurally and functionally distinct from the FP receptor, the effects of EP2 and FP receptor stimulation on aqueous humor outflow are similar. Copyright © Association for Research in Vision and Ophthalmology.

  • 6.
    Nilsson, Siv
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Pharmacology.
    Geng, Lijung
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Pharmacology.
    Persson, Karin
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Pharmacology.
    Angiotensin (1-7) inhibits DNA synthesis in vascular smooth muscle cells (VSMC) from porcine ciliary arteries2005In: Invest Ophtalmology Vis Sci IOVS, ARVO Association for Resarch in Vision and Ophtalmology,2005, 2005Conference paper (Other academic)
  • 7.
    Woodward, David F
    et al.
    Linköping University, Faculty of Health Sciences.
    Krauss, Achim H-P
    Linköping University, Faculty of Health Sciences.
    Nilsson, Siv
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Bimatoprost effects on aqueous humor dynamics in monkeys2010In: Journal of ophthalmology, ISSN 2090-0058, Vol. 2010, p. 926192-Article in journal (Refereed)
    Abstract [en]

    The effects of bimatoprost on aqueous humor dynamics were quantified in monkey eyes. Uveoscleral outflow was measured by the anterior chamber perfusion method, using FITC-dextran. Total outflow facility was determined by the two-level constant pressure method. Aqueous flow was measured with a scanning ocular fluorophotometer. Uveoscleral outflow was 0.96 +/- 0.19 muL min(-1) in vehicle-treated eyes and 1.37 +/- 0.27 muL min(-1) (n = 6; P < .05) in eyes that received bimatoprost 0.01% b.i.d. x 5 days. Bimatoprost had no effect on total outflow facility, which was 0.42 +/- 0.05 muL min(-1) at baseline and 0.42 +/- 0.04 muL min(-1) after bimatoprost treatment. Bimatoprost had no significant effect on aqueous humor flow. This study demonstrates that bimatoprost increases uveoscleral outflow but not total outflow facility or aqueous humor flow, indicating that it lowers intraocular pressure in ocular normotensive monkeys by a mechanism that exclusively involves uveoscleral outflow.

  • 8.
    Woodward, David F
    et al.
    Allergan Pharmaceutical Inc.
    Nilsson, Siv
    Linköping University, Department of Medicine and Health Sciences, Pharmacology . Linköping University, Faculty of Health Sciences.
    Toris, Carol B
    University of Nebraska.
    Kharlamb, Alexander B
    Allergan Pharmaceutical Inc.
    Nieves, Amelia L
    Allergan Pharmaceutical Inc.
    Krauss, Achim H-P
    Allergan Pharmaceutical Inc.
    Prostanoid EP4 Receptor Stimulation Produces Ocular Hypotension by a Mechanism That Does Not Appear to Involve Uveoscleral Outflow2009In: INVESTIGATIVE OPHTHALMOLOGY and VISUAL SCIENCE, ISSN 0146-0404, Vol. 50, no 7, p. 3320-3328Article in journal (Refereed)
    Abstract [en]

    PURPOSE. As part of a systematic elucidation of the pharmacology of prostaglandins (PG) effects on intraocular pressure in the monkey, the prototypical selective prostanoid EP4 receptor agonist (3,7-dithia PGE(1)) was examined. It was found to be highly efficacious in nonhuman primates, and its mechanism of ocular hypotensive activity was investigated. METHODS. Intraocular pressure (IOP) was measured by pneumatonometry in conscious monkeys restrained in custom-designed chairs. All other animal experiments were performed in animals sedated with ketamine or anesthetized with ketamine/diazepam and given drug or vehicle for various lengths of time. Aqueous flow was determined by fluorophotometry. Total outflow facility was measured by the two-level, constant-pressure method and by 2-minute tonography in both normotensive and hypertensive monkey eyes. Uveoscleral outflow was measured by perfusing the anterior chamber with FITC-labeled dextran for 30 minutes at a fixed IOP of approximately 15 mm Hg. Isometric responses to drugs were measured in longitudinal and radial preparations of monkey and human isolated ciliary smooth muscle specimens. RESULTS. The selective EP4 receptor agonist 3,7-dithia PGE(1) and an isopropyl ester prodrug thereof reduced IOP in monkeys. A single dose of 3,7-dithia PGE(1) isopropyl ester, at a 0.01% or 0.1% dose, decreased IOP in the glaucomatous monkey in the range of 40% to 50%. Studies on total outflow facility by the two-level, constant-pressure perfusion method and tonography indicated that EP4 receptor stimulation facilitated aqueous humor outflow facility. No effect on aqueous flow was apparent. In contrast to all PGs and prostamides studied to date, 3,7-dithia PGE(1) exerted no effect on uveoscleral outflow measured directly. Moreover, it did not relax longitudinal or radial preparations of isolated human or monkey ciliary muscles. CONCLUSIONS. The EP4 receptor agonist 3,7-dithia PGE(1) is a highly efficacious IOP-lowering drug in monkeys. It has no effect on uveoscleral outflow but does increase total outflow facility, which accounts for a substantial proportion of the ocular hypotensive activity.

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