HYPERBARIC-OXYGEN WORSENS MYOCARDIAL LOW-FLOW ISCHEMIA-REPERFUSION INJURY IN ISOLATED RAT-HEART

In these experiments rats were exposed to hyperbaric oxygen (100% oxyg en; 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 ischem ia (perfusion rate from 12 ml/min to 2 ml/min for 40 min) and reperfus ion. Hearts excised from control rats were subjected to the same proce dure of ischemia and reperfusion. The data obtained from these experim ents clearly indicate that the ischemic picture observed in control he arts is worsened in hearts obtained from hyperbaric oxygen-exposed ani mals. In fact, after ventricular standstill of the ischemic phase, the left ventricular end-diastolic pressure increased significantly and p roportionally 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 prepara tion: these alterations, well correlated to the time of hyperbaric oxy gen exposure! seem to suggest impairment of the vascular endothelium-d ependent relaxant function. Futhermore N-acetylcysteine and defibrotid e, given orally to the rats before hyperbaric oxygen exposure, prevent ed the aggravation of the ischemic damage induced in ex vivo hearts.