Watts J A, Koch C D, LaNoue K F
Am J Physiol. 1980 Jun;238(6):H909-16. doi: 10.1152/ajpheart.1980.238.6.H909.
Isolated rat hearts reperfused after 25 min of ischemia have 23% of control mechanical function, 65% of control nucleotides, 52% of control ATP, and 75% of control creatine phosphate, whereas cellular calcium is increased 2.3-fold. Initiating reperfusion with verapamil or low Ca2+-containing buffer did not alter these tissue parameters or improve function over hearts reperfused with control buffer only. Also, when verapamil was present before and during ischemia, improvement in cardiac function resulted, and the adenine nucleotides, tissue ATP, and creatine phosphate concentrations were increased while cellular Ca2+ was reduced compared with the other reperfused ischemic hearts. Verapamil apparently improves recovery of function by decreasing energy demand during ischemia rather than by blocking Ca2+ influx during reprefusion. The respiration of isolated mitochondria and homogenates from reperfused ischemic hearts and homogenates of ischemic hearts was decreased by 20-30%, possibly due to sarcolemmal damage, although the respiration of isolated cells from ischemic hearts was normal. Cells isolated from ischemic hearts may represent a selected population lacking sarcolemmal damage.
缺血25分钟后再灌注的离体大鼠心脏，其机械功能为对照的23%，核苷酸含量为对照的65%，ATP含量为对照的52%，磷酸肌酸含量为对照的75%，而细胞内钙增加了2.3倍。用维拉帕米或含低钙缓冲液启动再灌注，与仅用对照缓冲液再灌注的心脏相比，并未改变这些组织参数或改善功能。此外，当在缺血前及缺血期间使用维拉帕米时，心脏功能得到改善，腺嘌呤核苷酸、组织ATP和磷酸肌酸浓度增加，而与其他再灌注的缺血心脏相比，细胞内钙减少。维拉帕米显然是通过在缺血期间降低能量需求而非在再灌注期间阻断钙内流来改善功能恢复的。再灌注的缺血心脏的离体线粒体和匀浆以及缺血心脏匀浆的呼吸作用降低了20%-30%，这可能是由于肌膜损伤所致，尽管缺血心脏的分离细胞呼吸正常。从缺血心脏分离的细胞可能代表了一群未受肌膜损伤的细胞。
