PROTECTIVE EFFECTS OF OXYGENATED ST-THOMAS-HOSPITAL CARDIOPLEGIC SOLUTION DURING ISCHEMIC CARDIAC-ARREST - IMPROVED FUNCTION, METABOLISM AND ULTRASTRUCTURE

The isolated working rat heart model was use to define the cardioprote ctive effects (function, metabolic and ultrastructure) of the oxygenat ed St. Thomas' Hospital No. 2 cardioplegic solution (STH) during lengt hy, hypothermic ischaemia (20 degrees C, 4 hours and 5 hours). Hearts (n = 9 for each group) were arrested with and exposed to multidose rei nfusion (2 min every 40 min interval) throughout the ischaemic period with the cold (4 degrees C) STH or oxygenated(95% O-2:5% CO2) STH. Oxy genated STH significantly (p < 0.01) improved the postischaemic recove ry of cardiac output from 49.5 +/- 11.1% to 96.8 +/- 1.5% (in 4 hours) and from 20.3 +/- 7.2% to 72.2 +/- 5% (in 5 hours). Other indices of functional recovery showed similar improved performance with the signi ficant decrease in time from the onset of reperfusion to the return of regular sinus rhythm (57 +/- 8 v 495 +/- 150 s). The efflux of lactat e during 5 hr ischaemic arrest was decreased (20.62 +/- 1.3 v 26.18 +/ - 1.73 mu mol/heart for oxygenated STH and STH, respectively, p < 0.05 ) and the progressive increase in the coronary vascular resistance was abolished in the oxygenated STH treated hearts. These improvements we re associated with the reduction in the decline of the myocardial aden osine triphosphate (14.49 +/- 2 v 3.3 +/- 0.19 mu mol/g dry wt), creat ine phosphate (24.61 +/- 3.47 v 7.48 +/- 1.34 mu mol/g dry wt) and gua nosine triphosphate (1.69 +/- 0.2 v 0.84 +/- 0.08 mu mol/g dry wt) dur ing ischaemia, total resynthesis after reperfusion (ATP: 103% v 36%, C P: 105% v 69% and GTP: 203% v 61% of control) and the total absence of myocardial cells and microvasculature injuries in ischaemic (non-repe rfused) hearts. These results confirm that the provision of additional oxygen to the St. Thomas' Hospital solution (with 95% O-2:5% CO2) can meet the metabolic demand of the ischaemic myocardium and thus increa se the safe duration of cardiac arrest.