Endogenous nitric oxide reduces microvascular permeability and tissue oedema during exercise in cat skeletal muscle

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.