Effect of hypertonic mannitol on microvascular function in hypoxic and reoxygenated rat myocardium

The left ventricular resting tension, myocardial perfusability and creatine phosphokinase (CK) release were studied in isolated rat hearts during hypoxia and reoxygenation. The infusion fluid was either isotonic (290 mOsmol·litre−1) or made hypertonic (420 mOsmol·litre−1) by addition of mannitol. The left ventricular tension was measured by an intraventricular balloon connected to a pressure recorder. The myocardial perfusability was tested by infusing fluorescein into the cannulated aortic root and the proportion perfused with fluorescein in horizontal myocardial section was measured by a planimeter. The reoxygenation was carried out for 10 min after 30 and 60 min of hypoxia. The left ventricular resting tension increased to a maximum (myocardial contracture) in 13 min during isotonic hypoxic perfusion and in 9 min in the hypertonic group. The CK release was very significantly lower in the hypertonic hearts (6.4 mIU·cm−3) than in the isotonic hearts (71.3 mIU·cm−3) during 60 min of hypoxia. The CK release was markedly increased during reoxygenation especially after 60 min of hypoxia (“oxygen paradox”) in both isotonic (700 mIU·cm−3) and hypertonic groups (513 mIU·cm−3). The perfusability by fluorescein was 100, 87, 70 and 65% at 0, 15, 30 and 60 min of hypoxia in the isotonic and 100, 70 and 68 and 61% in the hypertonic hearts, respectively. The injury induced by reoxygenation did not further restrict the perfusability. The results show that the myocardial perfusability decreases during the first 15 min of hypoxia in which time the myocardial contracture is completed. The intramyocardial tension generated by the contracture seems to be the main determinant of the impaired perfusability, and hypertonic mannitol does not prevent the deterioration of microvascular function in the hypoxic myocardium in isolated rat heart.