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. perfusion pressure of the collaterals, can change when the ratio of pre- and post-collateral resistance alters. Drugs can influence collateral blood flow not only by directly effecting the collaterals but also by altering collateral perfusion pressure. Glyceryl trinitrate given in minor doses improved collateral blood flow by directly dilating the collaterals and also by increasing collateral perfusion pressure. Higher doses did not improve collateral flow due to a decrease of collateral perfusion pressure. A steal-phenomenon occurred in some cases. Adenosine and verapamil had no direct influence on the collateral resistance. Verapamil given in small doses increased perfusion pressure slightly but not enough to improve collateral blood flow. High doses of verapamil, like low doses of adenosine, had no significant influence on collateral perfusion pressure and collateral blood flow. Adenosine given in high dosage led to a diminution of collateral flow by decreasing collateral perfusion pressure, i.e. a steal-phenomenon.

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Summ,~5 rAfter embolising the terminal bed of a coronary artery, a peripheral coronary pressure Ppc and the total collateral blood flow can be measured. Assuming that Ppc represents the pressure at the branching off of collaterals, the resistances of the following sections of the coronary vascular bed can be determined: the resistance of the precollateral arteries (R1), the resistance of the vessels behind the start of collaterals (R2), and the collateral resistance (R3).The present study demonstrates that this simple 3-resistances model can be derived from an anatomically more adequate model which consists of a network of

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