Abstract

Myocardial contusion is frequently suspected after blunt chest trauma, but the exact mechanisms of resulting cardiac dysfunction and the time course for enzymatic alterations have not yet been fully understood. Therefore, we investigated pathophysiological aspects of myocardial contusion in a controlled animal model. Male Wistar rat hearts were studied in an isolated perfusion model and were divided into two groups: control (n = 4) and heart contusion (n = 6) groups. The cardiac contusion was produced by a single blow with a weighted pendulum (m = 44 g, height = 20 cm). Functional implications of the contusion were examined in an "isolated perfused heart" model. Troponin 1 concentrations were determined in the perfusate. Cardiac contusion resulted in an increase of coronary perfusion pressure (CPP) of 9 mmHg (P < 0.05, 20 min postcontusion versus baseline and control), followed by a significant increase of left ventricular end-diastolic pressure (LVEDP) of 6 mmHg (P < 0.05, 20 min postcontusion versus baseline and control). Heart contusion was followed by an early increase of troponin 1 (+0.82 ng/mL). The troponin 1 concentration decreased again and, after 20 min, baseline levels were reached. The control group showed no such changes. In this model, high troponin 1 levels after cardiac contusion suggest direct damage to the myocardium. First functional response was shown by the alteration of the coronary perfusion, followed by impaired diastolic function, which persisted even after lowering of the troponin 1 levels.

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