Verapamil has been shown to depress the contractility of ischemic myocardium. The present study was designed to determine whether that effect is due to an increase in ischemic injury caused by the drug or whether it might reflect a protective effect. A critical partial occlusion was effected on the left anterior descending coronary artery of 16 open chest foxhounds. A fiberoptic pH probe was implanted in the subendocardium of the ischemic zone, and coronary blood flow was reduced by 79% from a control value of 38 ± 4 ml/min and held constant. Mean coronary perfusion pressure was decreased 48% from its control value of 90 ± 6 mm Hg and remained constant. Eight animals were treated with intravenous verapamil, beginning 20 to 30 minutes after the onset of ischemia, in incremental doses (5, 10 and 20 μg/kg per min) and eight were treated with placebo. The pH of the ischemic zone increased after institution of treatment in the verapamil group (+0.04 ± 0.05 pH unit) whereas it decreased in the placebo group (- 0.06 ± 0.4 pH unit) during the first dose (p <0.05). Although the difference in pH between the two groups was marked at all doses (p <0.03) compared with control partial occlusion, verapamil caused no significant change in heart rate (+ 0.1 ± 1 beat/min in the verapamil group versus + 0.6 ± 4.5 beats/min in the placebo group), mean arterial pressure (- 7.5 ± 4 versus - 4.3 ± 3 mm Hg, respectively) or cardiac output (- 0.2 ± 0.07 versus - 0.02 ± 0.04 liters/min, respectively) comparing control with the first or the second dose of verapamil. The third dose of verapamil caused large decreases in heart rate (29%) and mean arterial pressure (23%) and caused conduction block in most animals. Improvement of myocardial acidosis after 20 to 30 minutes of ischemia as a result of verapamil infusion confirms that verapamil exerts a beneficial effect on ischemic myocardium in this experimental model.
|Number of pages||8|
|Journal||Journal of the American College of Cardiology|
|Publication status||Published - 1985|
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