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Ann Thorac Surg 1982;33:55-63
© 1982 The Society of Thoracic Surgeons

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Articles

Cold Blood–Diltiazem Cardioplegia

From the Department of Surgery, St. Louis University, St. Louis, MO.

^* Address reprint requests to Dr. Barner, 1325 S Grand Blvd, St. Louis, MO 63104.

The calcium channel blocker, diltiazem, has been studied in the same model used for evaluation of cold blood–potassium cardioplegia. Six dogs (Group 1) had one hour of myocardial ischemia with topical ice (myocardial temperature, 7° ± 2°C) after coronary perfusion with 200 ml of cold blood (5° ± 1°C) containing diltiazem, 400 µg per kilogram of body weight. Seven dogs (Group 2) had two hours of ischemia after perfusion with 200 ml of cold blood containing 200 µg/kg and reperfusion every 30 minutes with 100 ml of cold blood and diltiazem, 100 µg/kg. Baseline studies were repeated after rewarming and 40 minutes of reperfusion. No inotropic agents or calcium were used.

Heart rate, peak systolic pressure, velocity of the contractile element, peak + rate of rise of left ventricular pressure (dP/dt), peak – dP/dt, dP/dt over common peak isovolumic pressure, left ventricular compliance and stiffness, and heart water were unchanged in Group 1. In Group 2, heart rate slowed (p < 0.025) and compliance decreased (p < 0.02). In both groups, coronary vascular resistance declined (p < 0.001) and recovery of adenosine triphosphate (p < 0.001), adenosine diphosphate (p < 0.025), and the adenosine pool (p < 0.001) was impaired. Ultrastructure was well preserved, but myofibrillar lesions were noted in Group 2.

Diltiazem cardioplegia was associated with good functional recovery, but there was impairment of high-energy phosphate metabolism.

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