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Pulmonary vasodilation by inhaled nitric oxide after endothelial injury

Journal Article · · Journal of Applied Physiology (1985); (United States)
OSTI ID:6899841
;  [1]
  1. Yale Univ. School of Medicine, New Haven, CT (United States)
Inhaled nitric oxide gas (NO) has recently been shown to reverse experimentally induced pulmonary vasoconstriction. To examine the effect of free radical injury and methylene blue exposure on inhaled NO-induced pulmonary vasodilation the authors studied ventilated rabbit lungs perfused with Krebs solution containing 3% dextran and indomethacin. When NO gas (120 ppm) was added to the inhaled mixture for 3 min, the elevated pulmonary arterial perfusion pressure (Ppa) induced by the thromboxane analogue U-46619 was significantly reduced [8 [+-] 2 (SE) mmHg]. Acetylcholine similarly reduced Ppa (9 [+-] 1 mmHg). After free radical injury and methylene blue exposure, inhaled NO again produced significant vasodilation (5 [+-] 1 and 9 [+-] 2 mmHg, respectively), but acetylcholine resulted in an increase in Ppa ([minus]9 [+-] 3 and [minus]4 [+-] 1 mmHg, respectively). These data demonstrate that pulmonary vasodilation produced by inhaled NO is unaffected by free radical injury or methylene blue in the intact lung despite concomitant reversal of acetylcholine-induced vasodilation. 21 refs., 4 figs.
OSTI ID:
6899841
Journal Information:
Journal of Applied Physiology (1985); (United States), Journal Name: Journal of Applied Physiology (1985); (United States) Vol. 73:5; ISSN JAPHEV; ISSN 8750-7587
Country of Publication:
United States
Language:
English

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