We evaluated the efficacy of combined antegrade and retrograde intermittent cold cardioplegia for patients with prolonged aortic cross-clamping. Thirty patients with cross-clamping time of more than 4h were divided into three groups according to the method of cardioplegia. Antegrade crystalloid cardioplegia was performed in 9 cases, combined antegrade and retrograde crystalloid cardioplegia was performed in 5 cases, and combined antegrade and retrograde cold blood cardioplegia was performed in 16 cases. There was no statistical difference in mean aortic cross-clamping time among the three groups. The hospital mortality was 33% in the antegrade crystalloid group, 20% in the combined crystalloid group, and 0% in the combined blood group. There was a significant statistical difference in the hospital mortality between the antegrade crystalloid and combined blood group. The incidence of low cardiac output syndrome (LOS) was 67% in the antegrade crystalloid group, 20% in the combined crystalloid group, and 6% in the combined blood group. There was a significant difference in the incidence of LOS between antegrade crystalloid and combined blood groups. The recovery rate of spontaneous rhythm after the release of the cross-clamp was also significantly greater in the combined blood group than in the antegrade crystalloid group. In conclusion, combined antegrade and retrograde intermittent cold cardioplegia provides excellent myocardial protection for patients with prolonged aortic cross-clamping.

Lecithinized superoxide dismutase (L-SOD) has a higher affinity for cell membranes than recombinant human superoxide dismutase has. The purpose of this study, is to evaluate the protective effects of L-SOD against ischemia/reperfusion injury in blood-perfused isolated rat heart subjected to 30-min global normothermic ischemia. Fifteen isolated hearts were divided into three groups: group I (n=5), the untreated control group, group II (n=5) received 3, 000 units of L-SOD administered into the perfusion circuit at the beginning of reperfusion, and group III (n=5) received 3, 000 units of L-SOD administered into the perfusion circuit 10min after reperfusion. Left ventricular developed pressure, maximum positive and negative dp/dt, coronary vascular resistance and myocardial water content were assessed in each group. The percent recovery of left ventricular developed pressure in group II was significantly higher than that in group I and group III (77.4±11.1% in group II, 38.2±4.4% in group I, 40.2±4.1% in group III, p<0.01). The percent recovery of maximum positive dp/dt in group II was significantly higher than that in group I and group III (70.0±11.2% in group II, 41.8±7.8% in group I, 38.0±5.7% in group III, p<0.01). The percent recovery of maximum negative dp/dt in group II was also significantly higher than that in group I and group III (74.9±11.0% in group II, 41.3±8.0% in group I, 46.3±5.9% in group III, p<0.01).There was no significant difference of coronary vascular resistance or myocardial water content among the three groups. These results suggest that L-SOD administered at the time of reperfusion has protective effects against ischemia/reperfusion injury in the isolated rat heart.