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In humans, coronary blood flow is tightly regulated by microvessels within the myocardium to match myocardial energy demand. However, evidence regarding inherent sensitivity of the microvessels to changes in arterial partial pressure of carbon dioxide and oxygen is conflicting because of the accompanied changes in myocardial energy requirements. This study aimed to investigate the changes in coronary blood velocity while manipulating partial pressures of end-tidal CO2 (Petco2) and O2 (Peto2). It was hypothesized that an increase in Petco2 (hypercapnia) or decrease in Peto2 (hypoxia) would result in a significant increase in mean blood velocity in the left anterior descending artery (LADVmean) due to an increase in both blood gases and energy demand associated with the concomitant cardiovascular response. Cardiac energy demand was assessed through noninvasive measurement of the total left ventricular mechanical energy. Healthy subjects (n = 13) underwent a euoxic CO2 test (Petco2 = -8, -4, 0, +4, and +8 mmHg from baseline) and an isocapnic hypoxia test (Peto2 = 64, 52, and 45 mmHg). LADVmean was assessed using transthoracic Doppler echocardiography. Hypercapnia evoked a 34.6 ± 8.5% (mean ± SE; P &lt; 0.01) increase in mean LADVmean, whereas hypoxia increased LADVmean by 51.4 ± 8.8% (P &lt; 0.05). Multiple stepwise regressions revealed that both mechanical energy and changes in arterial blood gases are important contributors to the observed changes in LADVmean (P &lt; 0.01). In summary, regulation of the coronary vasculature in humans is mediated by metabolic changes within the heart and an inherent sensitivity to arterial blood gases.

The effects of graded changes in oxygen and carbon dioxide tension on coronary blood velocity independent of myocardial energy demand