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Objective: The aim was to determine whether cocaine has a direct effect on the myocardium which is independent of coronary vasospasm. Methods: Cocaine was introduced into the perfusate of the isolated rabbit ventricular septal preparation in the concentration range 10−5 to 10−3 M while holding coronary flow of oxygenated Krebs solution constant at 3.0 ml·min−1 by a perfusion pump. The septa were obtained from white male New Zealand rabbits and were paced at 48 beats·min−1. Mechanical and enzymatic measurements were performed. Results: Developed tension (T), maximum contraction velocity (+dT/dt), and maximum relaxation velocity (-dT/ dt) were all depressed to approximately the same degree at each different cocaine concentration and averaged 4, 48, and 95% at 10−5 10−4, and 10−3 M cocaine respectively, with an ED50=9 × 10−5 M. Relaxation time (tR/T) was prolonged, but the ED50 was greater (by 1.5 times) than for the other mechanical parameters. Simultaneously, an increase in excitation threshold dysrhythmia developed which resulted in 17, 50, and 90 beats missed per 100 stimulations at 10−5, 10−4 and 10−3 M cocaine respectively. Resting tension (RT) was not altered. Coronary flow rate was not reduced in presence of cocaine because of the constant delivery pump. T, +dT/dt, -dT/dt and modulation of the excitation threshold completely recovered after washout of cocaine. Conclusions: Cocaine has acute direct, though reversible, depressant effects on the myocardium, including depression of function and modulation of excitation threshold, which are independent of its effect on coronary flow.Cardiovascular Research 1993;27:269-273 [ABSTRACT FROM PUBLISHER]

It has proved difficult to record satisfactorily echocardiograms during patient motion. This report describes the design and preliminary results obtained with an echo harness with which the transducer can be held stationary or moved rapidly and predictably by remote control. With this apparatus, recordings can be made during tilting, drug intervention, and during bicycle and treadmill exercise. [ABSTRACT FROM PUBLISHER]

Beta-adrenergic blockade with propranolol caused mild impairment in cardiovascular adaptation to volume (blood infusion) and pressure (angiotensin infusion) challenges in the dog. The impairment was manifested by smaller increases in stroke volume and cardiac output. The altered response to angiotensin infusion was completely attributable to β-adrenergic blockade. The possible role of a non-specific effect of propranolol on cardiovascular adjustment to volume stress was also discussed. [ABSTRACT FROM PUBLISHER]