Soza M, Karpati G, Carpenter S, Prescott S
Acta Neuropathol. 1986;71(1-2):70-5. doi: 10.1007/BF00687964.
Vascular perfusion of rat hind limbs with a Ca2+-free physiological solution containing ethylenediaminetetraacetate, when followed by a physiological solution with normal concentration of Ca2+, caused a marked rise of creatine kinase (CK) in the venous effluent. When calcium channel blockers were present in the perfusing solutions, no rise of CK occurred. On histological sampling of perfused muscles, CK rise was roughly correlated with muscle fiber damage of the appropriate muscles. Removal of calcium from the plasmalemma of muscle fibers appears to prevent closure of calcium channels, making the muscle fibers susceptible to a deleterious influx of extracellular calcium. This influx can be prevented by the presence of calcium channel blockers in the perfusates.
用含乙二胺四乙酸的无钙生理溶液灌注大鼠后肢，随后再用钙浓度正常的生理溶液灌注，会导致静脉流出液中肌酸激酶（CK）显著升高。当灌注溶液中存在钙通道阻滞剂时，CK不会升高。对灌注肌肉进行组织学取样时，CK升高大致与相应肌肉的肌纤维损伤相关。从肌纤维质膜去除钙似乎会阻止钙通道关闭，使肌纤维易受细胞外钙有害内流的影响。灌注液中存在钙通道阻滞剂可防止这种内流。
