Graded experimental myocardial contusion: impact on cardiac rhythm, coronary artery flow, ventricular function, and myocardial oxygen consumption.

Current management of myocardial contusion is based on experience with ischemic heart disease, but the mechanism responsible for cardiac dysfunction may be quite different. The purpose of this study was to characterize the pathophysiology of myocardial contusion in a controlled animal model. Sprague-Dawley rat hearts were prepared on a standard Langendorff apparatus, and myocardial function (DP, + dP/dT, - dP/dT) measured via a left ventricular balloon. Bipolar atrial and ventricular leads were placed to define conduction changes. Coronary sinus effluent was sampled for pO2, pH, creatine phosphokinase (CPK), and lactic dehydrogenase (LDH). The hearts were freeze-clamped to measure phosphocreatine (PC) and adenosine triphosphate (ATP). Myocardial contusion was produced by a single blow with a weighted pendulum. Hearts were divided into control (n = 5), moderate impact--Group I (n = 5), and major impact--Group II (n = 5). Group I sustained a 25% decrease in function after an impact of 78 +/- 5 mJoules/gm, and Group II a 50% deficit after 87 +/- 7 mJoules/gm. Impact resulted in complete electrical arrest, followed by sequential ventricular, atrial, and AV nodal recovery; recovery time correlated directly with degree of injury. Coronary flow at 2 min postinjury was decreased (p less than 0.05) in Group I (12.8 +/- 0.8 ml/min) and Group II (11.5 +/- 1.3) compared to control (17.2 +/- 0.5), and returned to baseline levels at 20 min. LDH and CPK levels were twice as high in Group II as in Group I. The PC/ATP ratio in Group II increased from 1.63 at baseline to 2.54 (p less than 0.05) at 25 min, confirming ischemic reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)