Why the study?
Does inhaled nitric oxide reduce pulmonary arterial perfusion pressure in ventilated rabbit lungs after free radical injury and methylene blue exposure?
Does inhaled nitric oxide reduce pulmonary arterial perfusion pressure in ventilated rabbit lungs after free radical injury and methylene blue exposure?
Inhaled nitric oxide maintains its pulmonary vasodilatory effects even after free radical injury or methylene blue exposure in an intact rabbit lung model, unlike acetylcholine.
Inhaled NO may bypass endothelial injury in ventilated lungs; extends mechanistic insights but leaves open translation to human pulmonary hypertension.
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 we 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 (-9 +/- 3 and -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.
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Rimar et al. (1992) studied this question.
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