Carl E. Jones

Coronary and cardiac responses to exercise after chronic ventricular sympathectomy

This study examined the effects of chronic surgical ventricular sympathectomy on the relationships between left ventricular mechanical performance, coronary blood flow, and exercise workload in sham-operated control dogs and dogs which had been ventricular sympathectomized 8 wk earlier. During exercise, left ventricular global contractile state was less in sympathectomized ventricles than in control ventricles, as indicated by reduced systolic pressure and maximal rate of pressure generation. Regional contractile shortening was not different. Heart rate was significantly elevated in sympathectomized ventricles. Therefore, peak systolic pressure-heart rate product and tension-time index were not different in sympathectomized ventricles compared to control ventricles. However, at each level of exercise, mean coronary flow in sympathectomized ventricles was reduced by about 50% compared to control values. The slopes of coronary flow on pressure-rate product and tension-time index were also reduced. No difference in left ventricular oxygen extraction between control and sympathectomized hearts were observed. Thus, chronic ventricular sympathectomy altered the relationships between coronary flow and oxygen consumption, on the one hand, and ventricular oxygen-dependent performance and whole-body exercise level, on the other hand.

Reduced resistances of septal artery collateral channels after cardiac sympathectomy

SummaryWe have shown that chronic cardiac sympathectomy reduces coronary collateral resistances. The present experiments in isolated dog hearts delineated the role of intramyocardial collateral channels from the septal (SEP) to the circumflex (CIRC), left anterior descending (LAD), and right (RT) coronary arteries in this phenomenon. In 11 controls and 8 2-wk sympathectomized hearts, a retrograde flow technique was used to determine collateral resistances between the epicardial arteries (CIRC, LAD, RT). Collateral resistances between the CIRC and LAD and between the LAD and RT were 42–68% less in sympathectomized hearts (P<0.05). Collateral resistances from the SEP to each epicardial artery were determined from retrograde flows simultaneously collected on each epicardial artery when the SEP was the only vessel perfused. Collateral resistances from the SEP to the CIRC and LAD were 51–59% less in the sympathectomized hearts (P<0.05). Thus, intramyocardial channels from the SEP to the left coronary arteries show reduced resistances after sympathectomy and can provide a substantial portion of the increased collateral flow to these vessels.

α1-Adrenergic Coronary Constriction during Exercise and Ischemia

This paper reviews work primarily from our laboratories, examining an alpha 1-adrenergic receptor-mediated coronary constriction during exercise and myocardial ischemia in dogs. It was demonstrated that in the quiescent conscious dog, the coronary circulation is devoid of an alpha 1-coronary constriction. Furthermore, it was shown by the intracoronary injection of selective agonists that both alpha 1- and alpha 2-receptor subtypes are present in coronary vessels. However, during exercise or ischemia only the selective alpha 1-antagonist prazosin caused an increase in coronary inflow, indicating that only alpha 1-receptors were activated. During both conditions, the increase in flow caused by alpha 1-blockade was associated with an increased contractile function in subendocardium. In experiments on anesthetized dogs, it was shown that prazosin caused an equal increase in perfusion of subepicardial and subendocardial layers during stellate ganglion stimulation. However, contractile function was increased only in subendocardium. It was proposed that only in deeper muscle layers does an alpha 1-coronary constriction impose a flow-limitation on contractile function. Finally, recent results indicate that myocardial ischemia, produced either by partial coronary stenosis or by maintenance of coronary inflow at the resting level during exercise, may initiate a vicious cycle with a further increase in alpha 1-adrenergic coronary constriction. Abolition of this positive feedback mechanism may partially explain the anti-infarction effects of chronic ventricular sympathectomy, as previously observed in our laboratories.

Thromboresistant Polymers: A New Approach

Selected antithrombotic agents were found to impart improved thromboresistance to polysilicone tubes when covalently bound to such tubes in pilot studies. Bonding was accomplished by radiation grafting of epoxypropyl acrylate monomer on the polysilicone, followed by reaction of the hydroxyl groups of the antithrombotic agents with the epoxy groups on the grafted monomer chains. The bound antithrombotic agents may act by chelating or complexing calcium ions, which are known to perform several functions in blood coagulation.