Wagner S, Wu S T, Parmley W W, Wikman-Coffelt J
Department of Medicine, University of California, San Francisco.
Cell Calcium. 1990 Jun-Jul;11(6):431-44. doi: 10.1016/0143-4160(90)90056-z.
Intracellular calcium transients were studied prior, during and after 30 min of global ischemia in control and aortic constricted rat hearts, with and without acute treatment with verapamil. Calcium transients [Ca2+]i continued to occur in verapamil treated animals for 18-20 min following the onset of global ischemia, whereas untreated hearts demonstrated calcium transients for only 3-8 min following global ischemia. Following the onset of global ischemia calcium transients continued to occur even though there was no measurable developed pressure. When calcium transients occurred for shorter periods of time during global ischemia the rise in diastolic calcium was greater and recovery was less. Addition of bradykinin to the perfusate showed that an increase in diastolic [Ca2+]i was related to a decrease in amplitude of developed [Ca2+]i transients and a decrease in developed pressure, but not to a change in coronary flow.
在对照大鼠心脏和主动脉缩窄大鼠心脏中,在全心缺血30分钟之前、期间和之后,对有无维拉帕米急性治疗的情况下细胞内钙瞬变进行了研究。在全心缺血开始后,维拉帕米治疗的动物中钙瞬变[Ca2+]i持续出现18 - 20分钟,而未治疗的心脏在全心缺血后仅出现3 - 8分钟的钙瞬变。在全心缺血开始后,即使没有可测量的收缩压,钙瞬变仍继续出现。当全心缺血期间钙瞬变出现的时间较短时,舒张期钙的升高更大且恢复更少。向灌注液中添加缓激肽表明,舒张期[Ca2+]i的增加与收缩期[Ca2+]i瞬变幅度的降低和收缩压的降低有关,但与冠状动脉血流的变化无关。