模拟失重大鼠心肌收缩性能降低的过程及其可逆性

Time course of cardiac contractility depression in simulated weightlessness rats and its reversibility

采用Krebs－Henseleit溶液灌流离体乳头肌标本，观察尾部悬吊大鼠心肌收缩性能降低的过程及其可逆性。发现尾部悬吊1周后，大鼠心肌收缩性能呈增高趋势，2周后趋于降低，4周（SUS－4）后显著降低。SUS－4组：等长收编张力（DT）降低了29．2％±0．32％（P＜0．01），达到张力峰值的时间（TPT）延长了10．4％±1．7％（P＜0．05），舒张一半所需的时间（T1／2R）呈缩短趋势。又观察了悬吊4周后所致心肌收缩性能降低在解除悬吊后2周内的可逆程度。结果表明，解除悬吊后1周，没有迹象显示心肌收缩性能已恢复：DT值降低了24．0％±0．96％（P＜0．01），TPT没有明显变化，T1／2R缩短了13．3％±1．5％（P＜0．05）。而当解除悬吊2周后，乳头肌的收缩性能已基本恢复。提示悬吊4周后所引起的心肌收缩性能降低可能是失重情况下对低动力状况的一种代偿反应，并且这种由于失重所导致的心肌收缩性能降低是可逆转的，但需要相当长的一段时间恢复。

The time course of cardiac contractility depression in tail-suspended rats and its reversibility were observed using the isolated papillary muscle preparation perfused with Krebs-Henseleitsolution. It was found that cardiac contractility of the rats showed an increasing a tendency of increaseafter 1 week of tail suspension, a tendency of decrease after 2 weeks, and a significant decrease following 4 weeks (SUS-4). In SUS-4 group,developed tension (DT) decreased by 29- 2% fO. 32 %, time topeak tension (TPT) prolonged by 10. 4% ±1. 7% (P＜0. 05 ), and time to half relaxation (T1/2R)showed a tendency of shortening. The reversibility of depressed cardiaccontractility after 4 weeks of tailsuspension was observed for 2 weeks. After removal of tail suspension for 1 week,the cardiac contractility function did notshow marked recovery with DT decreased by 24. 0% ± 1. 96% (P＜0. 01), TPTessentially unchanged, and T1/2R shortened by 13- 3% ± 1. 5 % (P＜0. 05) ； while after removal of tailsuspension for 2 weeks, the cardiac contractility of papillary muscles was essentially recovered. It is suggested that the depressed contractility of papillary muscles in SUS-4 group may be a compensative response to hypo-dynamic state during weightlessness, and the depressed cardiac contractility caused byweightlessness may be reversible,but the recovery takes a relatively long period.