The effect of verapamil on ischaemic contracture, reperfusion injury after global ischaemia, and calcium paradox was studied in isolated rat heart. The development of ischaemic contracture was measured by a balloon catheter inserted into the left ventricle, filled with water, and connected to a pressure recorder. Myocardial perfusability was tested by infusing sodium fluorescein solution into the cannulated aortic root. Creatine kinase (CK) activity and protein leakage from myocardium into the effluent were measured during reperfusion (30 min) after ischaemia (50 min) and during calcium repletion (30 min) after calcium depletion (5 min). Ischaemic contracture developed later in the verapamil-treated group (31.7 +/- 0.7 min) than in the control group (23.6 +/- 2.2 min). There was less CK (29.16 +/- 3.26 U/g) and protein leakage (4.81 +/- 0.41 mg/g) in the verapamil-treated group than in the control group (38.81 +/- 3.30 U/g and 6.14 +/- 0.49 mg/g, respectively) during reperfusion. Verapamil had no effect on the myocardial perfusability or on the strength of the ischaemic contracture. Verapamil did not reduce the CK or protein leakage in calcium paradox. It was concluded that verapamil has some protective effect against cell injury on myocardium during post-ischaemic reperfusion but none in calcium paradox.
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