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      Endogenous Nitric Oxide Reduces Microvascular Permeability and Tissue Oedema during Exercise in Cat Skeletal Muscle

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          Based on a proposed increase in the release of the vasodilators nitric oxide (NO) and prostacyclin during exercise, and the fact that these substances have vascular permeability-reducing properties, this study was designed to evaluate (1) possible effects of exercise on hydraulic permeability, (2) whether permeability and muscle swelling are reduced by an increased release of NO and prostacyclin during exercise and (3) whether NO and prostacyclin are involved in exercise hyperaemia. The study was performed on an autoperfused cat calf muscle preparation with ligated lymph vessels, and exercise was induced by somatomotor nerve stimulation. Change in microvascular hydraulic permeability was estimated by a capillary filtration coefficient (CFC) technique. We found that the marked muscle volume increase after the start of the exercise gradually decreased, reaching an isovolumetric state within 25 min where CFC had decreased by about 25% (p < 0.05). CFC recovered completely after exercise was stopped. The decrease in CFC was abolished during blockade of endogenous NO by the NO synthase inhibitor L-NAME, but was preserved during blockade of endogenous prostacyclin by tranylcypromine. The muscle volume increase during exercise was about 60% greater with L-NAME than during vehicle or tranylcypromine (p < 0.01). Neither L-NAME nor tranylcypromine had any effect on exercise hyperaemia. We conclude that microvascular hydraulic permeability is reduced during exercise, that this effect reduces exercise-induced muscle swelling, and that the effects are mediated via release of NO. NO and prostacyclin are not involved in exercise hyperaemia.

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          Most cited references 6

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          Nitric oxide as a signaling molecule in the vascular system: an overview.

          In retrospect, basic research in the fields of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) during the past two decades appears to have followed a logical course, beginning with the findings that NO and cGMP are vascular smooth muscle relaxants, that nitroglycerin relaxes smooth muscle by metabolism to NO, progressing to the discovery that mammalian cells synthesize NO, and finally the revelation that NO is a neurotransmitter mediating vasodilation in specialized vascular beds. A great deal of basic and clinical research on the physiologic and pathophysiologic roles of NO in cardiovascular function has been conducted since the discovery that endothelium-derived relaxing factor (EDRF) is NO. The new knowledge on NO should enable investigators in this field to develop novel and more effective therapeutic strategies for the prevention, diagnosis, and treatment of numerous cardiovascular disorders. The goal of this review was to highlight the early research that led to our current understanding of the pathophysiologic role of NO in cardiovascular medicine. Furthermore, we discussed the possible mechanism of some drugs interfering with NO signaling cascade.
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            Arterial walls are protected against deposition of platelet thrombi by a substance (prostaglandin X) which they make from prostaglandin endoperoxides.

            Prostaglandin (PG) endoperoxides (PGG2 and PGH2) contract arterial smooth muscle and cause platelet aggregation. Microsomes from pig aorta, pig mesenteric arteries, rabbit aorta and rat stomach fundus enzymically transform PG endoperoxides to an unstable product (PGX) which relaxes arterial strips and prevents platelet aggregation. Microsomes from rat stomach corpus, rat liver, rabbit lungs, rabbit spleen, rabbit brain, rabbit kidney medulla, ram seminal vesicles as well as particulate fractions of rat skin homogenates transform PG endoperoxides to PGE- and PGF- rather than to PGX-like activity. PGX differs from the products of enzymic transformation of prostaglandin endoperoxides so far identified, including PGE2, F2alpha, D2, thromboxane A2 and their metabolites. PGX is less active in contracting rat fundic strip, chick rectum, guinea pig ileum and guinea pig trachea than are PGG2 and PGH2. PGX does not contract the rat colon. PGX is unstable in aqueous solution and its antiaggregating activity disappears within 0.25 min on boiling or within 10 min at 37degrees C. As an inhibitor of human platelet aggregation induced in vitro by arachidonic acid PGX was 30 times more potent than PGE1. The enzymic formation of PGX is inhibited by 15-hydroperoxy arachidonic acid (IC50 = 0.48 mug/ml), by spontaneously oxidised arachidonic acid (IC 50 less than 100 mug/ml) and by tranylcypromine (IC50 = 160 mug/ml). We conclude that a balance between formation by arterial walls of PGX which prevents platelet aggregation and release by blood platelets of prostaglandin endoperoxides which induce aggregation is of the utmost importance for the control of thrombus formation in vessels.
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              A comparison between “red” and “white” muscle with respect to blood supply, capillary surface area and oxygen uptake during rest and exercise


                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                December 2003
                29 January 2004
                : 40
                : 6
                : 538-546
                Departments of aPhysiology, bAnaesthesia and Intensive Care and cMedicine, University of Lund and University Hospital of Lund, Lund, Sweden
                75677 J Vasc Res 2003;40:538–546
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 3, Tables: 1, References: 47, Pages: 9
                Research Paper


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