Acute myocardial infarction is often produced experimentally in anesthetized dogs to study hemodynamic responses. The anesthetic agents employed often alter hemodynamics, and interpretation of results is therefore more difficult. In the present study acute coronary occlusion was produced by the mercury embolization technique in 5 dogs anesthetized with pentobarbital, 30 mg/kg, (group I) and in 10 awake trained dogs sedated with morphine, 1 mg/kg (group II). Control heart rate averaged 161.0 in group I and 67.0 in group II (p <0.001) and control mean arterial pressure was 155 mm Hg in group I vs 102 in group II (p <0.001). Control cardiac output was similar in the 2 groups, but stroke volume was significantly lower and systemic vascular resistance significantly higher at control in group I dogs. After embolization, heart rate fell to 142.0 (p <0.01) in group I, and rose to 104.2 (p <0.01) in group II. Mean arterial pressure also fell to 112 mm Hg (p <0.02) in group I while it rose to 124 mm Hg (p <0.001) in group II. Cardiac output fell significantly in both groups, but was higher in group II dogs after embolization (96.2 vs 47.8 ml/kg/min, p <0.02). Left ventricular end-diastolic pressure increased significantly in both groups after embolization. Thus the marked fall in heart rate, blood pressure, and cardiac output in anesthetized dogs characterized a shock state and contrasted with the rise in heart rate and blood pressure and modestly reduced cardiac output in awake animals. The hemodynamic changes in awake animals more closely resemble those of left ventricular failure seen in clinical acute myocardial infarction. Awake animals should be used whenever possible in experimental myocardial infarction.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Dec 1 1977|