Coronary collateral reserve during exercise induced ischemia in swine.

We determined coronary collateral vasodilator reserve during exercise-induced ischemia in 17 mini-swine. We induced coronary collateral development in the left circumflex bed by placing an ameroid occluder on that artery. Four weeks later we studied the animals at rest and during exercise (EX) eliciting heart rates (HR) of 240 and 265 beats/min. We measured myocardial blood flow with microspheres and myocardial function by wall thickness sonomicrometry gauges. At matched exercise HRs we treated the animals with nifedipine (10 micrograms/kg IV) (EXN 10), nifedipine (100 micrograms/kg IV), (EXN 100), and adenosine infusion (1.2 mg/min/kg) EXAD. EXN 10 did not significantly alter hemodynamics compared to EX but EXN 100 and EXAD both decreased blood pressure significantly (p less than 0.05). Ischemic endocardial/nonischemic endocardial flow ratios and collateral resistance served as indices of vasodilator reserve. In the ischemic zone exercise reduced vasodilator reserve to 24 +/- 3% in the endocardium and 64 +/- 7% in the epicardium. Neither EXN 10 nor EXAD improved exercise-induced ischemia measured either as flow or function. However EXN 100 improved function during exercise-induced ischemia without improving coronary collateral flow. We conclude there is no additional coronary flow reserve during exercise-induced ischemia in the collateral dependent bed of the pig a few days after occlusion that can be recruited. Large doses of nifedipine improve function by direct action on the myocardium or by reducing afterload. The lack of development and deep myocardial distribution of the coronary collateral vessels in the pig may be an important factor of why these nifedipine responses differ from those reported in species which have primarily large epicardial coronary collaterals.