The Response of Canine Coronary Vascular Resistance to Local Alterations in Coronary Arterial Pco,

The effect of hypercapnia on coronary vascular resistance (CVR) was studied in seven open-chest dogs. Coronary blood flow was supplied to the cannulated left main coronary artery from the femoral artery by a precision pump. Coronary arterial Pco, was locally controlled with a small membrane oxygenator in the coronary perfusion circuit. Each Pco, change was made at a constant coronary flow, and CVR was calculated from the ratio of perfusion pressure to flow. Coronary sinus (CS) Pco , and Po, were recorded continuously from blood withdrawn through a CS catheter. Normocapnia (Pco, =• 423 ± 2.8 mm Hg) was obtained with a membrane oxygenator gas composition of 95% O,-5% CO,, and hypocapnia was produced with 100% O,-0% CO,. In addition to physiologically normal coronary flow (determined by a CS Po, of 20-30 mm Hg) relatively high and low flow states were studied. At a normal control CS P o , , a decrease in coronary arterial Pco , from 423 ± 2.8 to 23.8 ± 1.3 mm Hg caused CVR to increase by 84.2%, from 1.27 ± 0.06 to 2.30 ± 0.04 units. Since pH was inversely related to Pco , , the effect on CVR may have been mediated through a pH change. CS Pco, decreased from 65.2 ± 1.9 to 39.4 ± 1J mm Hg. Myocardial oxygen consumption was unchanged. Increases in CVR of 74.5, 119.5, and 69.3% occurred during hypocapnia in three additional experiments in which control arterial Po, was maintained at 52-90 mm Hg. When CS Po , was greater than 30 mm Hg, the normocapnic CVR was high, and was only minimally increased by hypocapnia. When coronary flow was reduced to an ischemic level there was little response in CVR to hypocapnia. Thus the level of arterial Pco, can have an important effect on CVR independent of changes in O2 consumption. Myocardial Pco, , derived from metabolically produced CO, and contributed to by arterial CO,, may be a major factor in normal control of coronary flow.