Diastolic coronary resistance in the isolated rabbit heart during and after ischaemia: contribution of extravascular forces

Coronary blood flow is influenced by contraction of the myocardium. The contribution of extravascular forces to coronary resistance during and after a period of low pressure perfusion or hypoxia and after a period of global ischaemia was studied in experiments on rabbit hearts perfused by the Langendorff method. End diastolic flow, perfusion pressure, developed tension, and resting tension were measured. Under control conditions the relation between end diastolic flow and perfusion pressure was almost linear (r>0.92). There was an initial fall in coronary resistance on initiation of hypoxia or low pressure perfusion, but subsequently coronary resistance increased concomitantly with the rise in resting tension. After 60 min total global ischaemia and 30 min reperfusion coronary resistance increased by 410(99)% and resting tension by 382(92)%. Increasing the potassium concentration of the perfusate to 19.2 mmol·litre−1 under control conditions caused the coronary resistance to increase by 336(74)%, whereas resting tension was unchanged. The increase in resistance with potassium could be reduced but not abolished by adenosine (1.87 × 10−5 mol·litre−1), indicating that the effect was largely attributable to vasoconstriction. Increased stimulation frequency (30 Hz) raised coronary resistance by 37(10)% and resting tension by 303(53)%. Perfusion with carbonyl cyanide p-trifluoromethoxyphenylhydrazone (1 × 10−6 mol·litre−1) increased coronary resistance by 169(27)% and resting tension by 782(11)6% and relaxed isolated epicardial coronary arteries. The effects of carbonyl cyanide p-trifluoromethoxyphenylhydrazone and increased stimulation frequency on coronary resistance were due to myocardial contracture. Myocardial contracture can increase coronary resistance and contributes to the increase in resistance seen during hypoxia or low pressure perfusion. But on reperfusion after global ischaemia the major cause of the increase in coronary resistance is increased obstruction in the vascular bed; extravascular factors have only a minor effect.