The Effect of Acetylcholine on Regional Myocardial O2 Consumption and Coronary Blood Flow in the Rabbit Heart
The effect of acetylcholine on the regional coronary perfusion and O2 consumption was determined in anesthetized open chest rabbits in order to compare its direct vasodilatory effects with the metabolic vasoconstriction it induces. Experiments were conducted in seven untreated controls and seven rabbits which were infused with acetylcholine (1 μg/kg/min). Myocardial blood flow was determined before and during acetylcholine infusion using radioactive microspheres. Regional arterial and venous O2 saturation was analyzed microspectrophotometrically. Acetylcholine reduced heart rate by 30% and significantly depressed the arterial systolic and diastolic blood pressure. The mean O2 consumption was significantly reduced with acetylcholine from 9.6±2.0 to 6.1±3.6 ml O2/min/100 g. Coronary blood flow decreased uniformly across the left ventricular wall by about 50% and resistance to flow increased by 42% despite potential direct cholinergic vasodilation. O2 extraction was not affected during acetylcholine infusion. It is concluded that the acetylcholine infusion directly decreased myocardial O2 consumption which in turn lowered the coronary blood flow and increased the resistance. The decreased flow was related to a reduced metabolic demand rather than a direct result of lowered aortic blood pressure. Unaffected myocardial O2 extraction also suggests that blood flow and metabolism were matched. This indicates that direct cholinergic vasodilation of the coronary vasculature does not allow a greater reduction in metabolism than flow in the anesthetized open chest rabbit heart during acetylcholine infusion.
KeywordsCatheter Ischemia Respiration Acetylcholine Purine
Unable to display preview. Download preview PDF.
- 8.A. M. Brown, Motor innervation of the coronary arteries of the cat, J. Phvsiol (London) 198:311–328 (1968).Google Scholar
- 14.J. Kedem, et al., An experimental approach for evaluation of the O2 balance in local myocardial regions in vivo. Quart. J. Exp. Physiol. 66:501–514 (1981).Google Scholar