Original Article

Effects of Imidazole Buffered Cardioplegia on Isolated Guinea Pig Hearts

Circulation Technology Division School of Allied Medical Professions The Ohio State University

Abstract

The imidazole moiety of histidine is responsible for the alpha-stat theory of intracellular pH regulation, which conserves the function of essential enzymes at different temperatures. This study tests the hypothesis that the addition of imidazole to cardioplegia enhances myocardial protection.

Eighteen isolated guinea pig hearts were randomly divided into 3 groups and perfused with Krebs-Henseleit solution at 35°C using the Langendorff technique. Perfusion was discontinued after 25 minutes, and each group was arrested by the infusion of cold (4-6°C) oxygenated cardioplegic solution at 2.8 mL/min/ g. Group 1 acted as a control, while Groups 2 and 3 were infused with a cardioplegic solution containing 15 mmol/L and 30 mmol/L imidazole respectively. After 30 minutes of hypothermic (< 16°C) ischemia, perfusion was resumed for 15 minutes. Hemodynamic measurements and analysis of perfusate and effluent were made prior to arrest and after 15 minutes of reperfusion. Post-ischemic lactate levels were linearly related to cardioplegia pH (r = 0.7148) and non-bicarbonate buffer capacity (r = 0.8006). Cardiac edema was lower in Group 3 (P < 0.05). Persistent arrhythmic activity was exhibited by 83% of Group 1 throughout reperfusion, compared to 33% and 14% of Groups 2 and 3 respectively. These results suggest that the addition of imidazole enhanced anaerobic metabolism during ischemia, facilitating the preservation of membrane integrity and function.