Influence of the ischemic coronary bed on collateral blood flow.

The purpose of this study was to determine the influence of the resistance of the terminal vascular bed of an occluded coronary artery on collateral blood flow and collateral resistance. In 6 anesthetized dogs, left anterior descending coronary artery (LAD) was ligated, cannulated, and the terminal vascular bed was occluded by latex microspheres (diameter: 25 mu). Retrograde flow was measured using a new technique, which allowed control of outflow pressure of retrograde flow (PRF) at the LAD cannula.

The dependence of coronary collateral blood flow on regional vascular resistances. Pharmacological studies with glyceryl trinitrate, adenosine and verapamil.

A method was applied in anesthetized dogs enabling the measurement of regional resistances up to and behind the start of collaterals and the collateral resistance. The studies show that peripheral coronary pressure, i.e.

On the range of alpha-adrenergic regulation of coronary vascular resistance.

In order to obtain an estimate of the range of alpha-adrenergic resistance regulation in the coronary vascular system, the following studies were performed: in 15 anesthetized dogs the circumflex coronary artery was cannulated and perfused with above-normal constant pressure to that coronary venous oxygen tension never fell below 40 mmHg. Thus, it was possible to eliminate the influence of the metabolic factor regulating coronary resistance. Furthermore, 15 isolated isovolumetrically working guinea-pig hearts were perfused according to the Langendorff method.

Pharmacological alterations of coronary collateral circulation; implication to the steal-phenomenon.

Measurements of resistances were performed on different parts of coronary vessels, including spontaneous collaterals in anesthetized dogs, following ligation and embolization of the descending branch of the left coronary artery. The normal situation was compared with the state of maximal pharmacological dilatation. The pharmacological dilatation decreased the collateral resistance by 24% in spite of the fact that the collaterals supplied an infarcted area in this case; the precollateral resistance, which chiefly consists of large vessels was also diminished.