Ruigrok T J, Kirkels J H
Department of Cardiology, University Hospital, Utrecht, The Netherlands.
Cardioscience. 1990 Sep;1(3):213-6.
Successive perfusion of a heart with a Ca(2+)-free and Ca(2+)-containing solution results in irreversible myocardial cell damage: the calcium paradox. Experiments were undertaken to assess whether pretreatment of rats with the new calcium antagonist anipamil (5 mg/kg body weight, twice daily for 5 days) protects the isolated heart against a submaximal calcium paradox. A submaximal calcium paradox was induced by successive perfusion with a Ca(2+)-free solution and a solution containing 0.1 mM Ca2+. Hearts from rats pre-treated with anipamil did not show a negative inotropic effect during control perfusion. During reperfusion in the presence of 0.1 Ca2+, after 10 minutes of Ca(2+)-free perfusion, creatine kinase release in hearts from treated rats was significantly less than in hearts from untreated rats (p less than 0.001). It is suggested that anipamil makes the sarcolemma less sensitive to conformational changes upon Ca2+ repletion.
钙反常。进行实验以评估用新型钙拮抗剂阿尼帕米（5毫克/千克体重，每日两次，共5天）对大鼠进行预处理是否能保护离体心脏免受次最大程度的钙反常影响。通过用无钙溶液和含0.1毫摩尔钙离子的溶液连续灌注诱导次最大程度的钙反常。用阿尼帕米预处理的大鼠心脏在对照灌注期间未显示负性肌力作用。在无钙灌注10分钟后，在存在0.1毫摩尔钙离子的再灌注过程中，处理过的大鼠心脏中肌酸激酶的释放明显少于未处理大鼠的心脏（p小于0.001）。提示阿尼帕米使肌膜在钙离子再充盈时对构象变化的敏感性降低。
