Effect of elevations of coronary artery partial pressure of carbon dioxide (Pco2) on coronary blood flow

Abstract

This study was designed to examine the effect of increases in the partial pressure of carbon dioxide (PCO2) in coronary artery blood on coronary blood flow, coronary reactive hyperemia and the coronary response to intracoronary adenosine administration. The left anterior descending coronary artery was cannulated and perfused over a wide range of perfusion pressure (P) and flow (F) with blood equilibrated with 0 to 40% carbon dioxide in 16 open chest dogs. Increases in coronary artery PCO2 from 20 +/- 2 to 93 +/- 8 to 211 +/- 22 mm Hg (mean +/- SEM) increased the coronary flow from 28 +/- 3 to 68 +/- 16 to 87 +/- 22 ml/min, respectively, at a perfusion pressure of 60 mm Hg and from 49 +/- 6 to 139 +/- 30 to 206 +/- 48 ml/min, respectively, at a perfusion pressure of 100 mm Hg. Coronary reactive hyperemia following a 30 second coronary perfusion line occlusion and the response to an intracoronary bolus of adenosine (60 micrograms) were prominent at a low PCO2 but absent at a high PCO2. Beta-adrenergic blockade did not abolish the increase in coronary flow that occurred at increased PCO2. Thus, progressive elevations of regional coronary PCO2 produced substantial increases in coronary blood flow and maximal or near maximal coronary vasodilation.

Heart and brain circulation and CO2 in healthy men

“…1965, van den Bos et al. 1979), whereas other studies showed that hypercapnea could increase myocardial blood flow (Case & Greenberg 1976, Powers et al. 1986).…”

“…Use of beta‐blockers to exclude an influence of increase in cardiac workload for the myocardial blood flow measurement during hypercapnea (van den Bos et al. 1979, Powers et al. 1986) would also be helpful to understand myocardial blood flow responsiveness to hypercapnea.…”

“…To resolve such issues, much stronger hypercapneic stress tests at different hypercapnic levels for increasing arterial carbon dioxide tension are required to clarify whether hypercapnea directly increases myocardial blood flow independent of an increase in cardiac workload. Use of beta-blockers to exclude an influence of increase in cardiac workload for the myocardial blood flow measurement during hypercapnea (van den Bos et al 1979, Powers et al 1986 would also be helpful to understand myocardial blood flow responsiveness to hypercapnea. For future studies, it would be of interest to test the effect of normalization with both cardiac workload and arterial carbon dioxide tension changes on myocardial blood flow.…”

Myocardial oxygenation is maintained during hypoxia when combined with apnea - a cardiovascular MR study

“…In this study, we did not measure venous blood gases from the coronary sinus. Other studies have shown that during hypercapnia saturation of the blood in the coronary sinus increased demonstrating a decrease in myocar-dial oxygen extraction (Wexels et al 1985;Powers et al 1986). Flow measurements are challenging to obtain in an MRI environment, therefore we lack the data to augment this study.…”

Cerebral and myocardial blood flow responses to hypercapnia and hypoxia in humans

“…In dogs, MBF increases, ϳ1-4%/Torr increase in Pa CO 2 (4,31,53) and ϳ28% when Pa O 2 is decreased from ϳ100 to 40 Torr (63). In sheep, MBF increases ϳ90% with a similar decrease in Pa O 2 (41).…”