Abstract
In these experiments rats were exposed to hyperbaric oxygen (100% oxygen; 2.5 atmospheres absolute pressure) for 1, 3 or 6 h. At the end of these periods the hearts were removed and subjected to low flow ischemia (perfusion rate from 12 ml/min to 2 ml/min for 40 min) and reperfusion. Hearts excised from control rats were subjected to the same procedure of ischemia and reperfusion. The data obtained from these experiments clearly indicate that the ischemic picture observed in control hearts is worsened in hearts obtained from hyperbaric oxygen-exposed animals. In fact, after ventricular standstill of the ischemic phase, the left ventricular end-diastolic pressure increased significantly and proportionally according to the time of hyperbaric oxygen exposure. The vasopressor activity of angiotensin II on coronary perfusion pressure was significantly changed, as compared to that in the control preparation: these alterations, well correlated to the time of hyperbaric oxygen exposure, seem to suggest impairment of the vascular endothelium-dependent relaxant function. Futhermore N-acetylcysteine and defibrotide, given orally to the rats before hyperbaric oxygen exposure, prevented the aggravation of the ischemic damage induced in ex vivo hearts.
Published Version
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