Myocardial Bed Research Articles

The effects of dipyridamole on the myocardial vasodilator actions of noradrenaline, isoprenaline and adenosine.

1. In anaesthetized cats, intravenous adenosine infusions decreased resistance to blood flow in the myocardial vascular bed. This effect of adenosine was augmented during the 60 min following the intravenous injection of dipyridamole (1 mg/kg).2. In different experiments, intravenous infusions of noradrenaline caused either a slight increase or a slight decrease in myocardial vascular resistance. The dilator component of the action of noradrenaline was not augmented by dipyridamole.3. Isoprenaline infusions decreased the resistance of the myocardial bed. This effect was unaltered after dipyridamole.4. These results do not support the hypothesis that part of the effect of catecholamines on myocardial vascular resistance involves the release of adenosine from hypoxic myocardial cells.

A COMPARISON OF THE EFFECTS OF THE PLASMA KININS, BRADYKININ AND KALLIDIN, ON MYOCARDIAL BLOOD FLOW AND METABOLISM.

Using a heated thermocouple technique it was shown that the plasma kinins, kallidin (lys-bradykinin) and bradykinin, increased myocardial blood flow, when given either by single injection or by continuous slow infusion, in the rabbit, cat, dog, monkey and chimpanzee. In every experiment systemic arterial blood pressure and myocardial vascular resistance fell by an amount related to the log of the dose of the kinin administered. These effects were seen with quite small doses of bradykinin and kallidin and demonstrate that the myocardial vascular bed is very sensitive to these plasma kinins. In larger doses, bradykinin increased "corrected temperature" -the myocardial temperature change corrected for alterations in blood flow and with heat losses controlled. This response represents a stimulation of metabolic heat production which was not observed with kallidin.

Effect of Cardiac Contraction on Coronary Blood Flow

In the experimental animal the basic and controversial problem was studied of the influence of cardiac contraction on coronary blood flow. Normally beating hearts were perfused at a constant pressure, and coronary inflow and outflow were determined. In order to assess the role of systole, prolonged periods of ventricular asystole and fibrillation were induced and observations were made of the changes in coronary flow. With the cessation of cardiac contraction blood flow in the coronary arteries and coronary sinus rose appreciably. The results of these studies support the concept that contraction of the heart muscle, by compression of the myocardial vascular bed, behaves as a throttling mechanism and impedes coronary flow. The method employed permits a separation and quantitation of the effects on coronary flow resulting from cardiac contraction and the vasomotor state of the coronary vessels.

VENTRICULAR FIBRILLATION OF LONG DURATION ABOLISHED BY ELECTRIC SHOCK

Ventricular fibrillation occurs as the terminal arrhythmia in approximately 50 per cent of patients. 1 If ventricular fibrillation develops in hearts that are relatively normal, especially during operations, defibrillation may be life saving. During the period before regular rhythm is restored the heart must be exposed and rhythmically massaged in the interval. This method of cardiac resuscitation has been developed in the laboratory by Hooker, 2 Wiggers, 3 and Beck, 4 and applied to patients by the latter. The method consists of the injection of 5 cc. of 2 per cent procaine hydrochloride into the right side of the heart followed by a brief period of cardiac massage to distribute the drug throughout the myocardial bed. The heart is then placed between two large electrodes and ordinary 110 volt alternating current with 1.5 amperes is momentarily impressed through the heart between the electrodes. Usually a series of such shocks is