1. Hypoxic pulmonary vasoconstriction (HPV) plays an important role as a physical regulator in matching pulmonary perfusion to ventilation preventing systemic hypoxemia. But its precise mechanisrn is unkown.
The aim of the present study is to investigate the cellular mechanisms and potential mediators involved in hypoxic constriction of porcine pulmonary arteries.
2. Pulmonary arteries (internal diameter 2-3mm) were isolated from porcine lungs, and loaded with fura-2/AM, a Ca
2+. indicator dye、 These artery rings were suspended in an organ chamber flooded with physiological salt solution on a microscope stage of a Ca
2+ imaging spectrofluorimetric system. The light emission ratio of fura-2 for measurement of changes in intracellular calciurn levels ([Ca
2+]
i) and the isometric tension of the ring were measured simultaneously. Hypoxia was induced by flooding the reserved chamber with 95%N
2 and 5%CO
2 gas mixture.
3. Hypoxic constriction and increases in [Ca
2+]
i were observed in the endothelium-intact rings under precontraction with 10
-6M noradrenaline. In contrast, there were no hypoxic changes under precontraction with 90mM KC1.
4. In the endothelium-denuded rings which were not relaxed with acetylcholine, hypoxia caused no changes in constriction and [Ca
2+]
i
5. Hypoxic vasoconstriction of endothelium-intact rings was abolished by L-NAME, an inhibitor of nitric oxide synthetase.
6. These results suggest that hypoxic constriction of isolated pulmonary artery of porcine lungs is induced partially by inhibition of the release of nitric oxide from the endotheliurn.
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