Ruigrok T J, Boink A B, Slade A, Zimmerman A N, Meijler F L, Nayler W G
Am J Pathol. 1980 Mar;98(3):769-90.
Reperfusion of isolated rat hearts with calcium-containing medium after a short period of calcium-free perfusion results in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether the slow-channel calcium-antagonist drug verapamil protects calcium-deprived rat heart muscle against the consequences of readmitting calcium. Cell damage was quantitated in terms of creatine kinase (CK) release, depletion of endogenous creatine phosphate (CP) and adenosine triphosphate (ATP) stores, development of contracture as measured by longitudinal shortening of the left ventricle, and ultrastructural damage. Verapamil (1 mg/l) did not reduce the initial rate of CK release during reperfusion with calcium but reduced the initial rate at which myocardial CP and ATP stores were depleted and decreased the shortening of the longitudinal axis of the left ventricle. After 30 seconds of reperfusion the mean sarcomere length was significantly greater in the verapamil-treated hearts. These results can be interpreted to mean that inhibition of calcium inflex via the slow channels does not protect heart muscle against the deleterious effects of readmitting calcium after a period of calcium-free perfusion.
在短时间无钙灌注后，用含钙培养基对离体大鼠心脏进行再灌注会导致不可逆的细胞损伤（钙反常）。进行实验以确定慢通道钙拮抗剂药物维拉帕米是否能保护缺钙的大鼠心肌免受重新引入钙的后果影响。通过肌酸激酶（CK）释放、内源性肌酸磷酸（CP）和三磷酸腺苷（ATP）储备的消耗、通过左心室纵向缩短测量的挛缩发展以及超微结构损伤来定量细胞损伤。维拉帕米（1毫克/升）在钙再灌注期间并未降低CK释放的初始速率，但降低了心肌CP和ATP储备消耗的初始速率，并减少了左心室纵轴的缩短。再灌注30秒后，维拉帕米处理的心脏中平均肌节长度明显更长。这些结果可以解释为，通过慢通道抑制钙内流并不能保护心肌免受无钙灌注一段时间后重新引入钙的有害影响。
