Coronary Vascular Resistance during Hypocapnia in the Closed-Chest Dog 1

Abstract

Abstract

Coronary vascular resistance during whole-body hypocapnia was studied in anesthetized dogs in which coronary blood flow (CBF) was monitored from a catheter-tip flow meter. Intravascular placement of this flow meter did not require opening the chest and avoided possible coronary denervation. Rapid flow meter response permitted determination of coronary vascular resistance during late diastole when vascular compression during systole does not affect the calculation. With rate and depth of ventilation held constant, hypocapnia was induced by a rapid change of the ventilating gas from 95% O₂-5% CO₂ to 100% O₂. Within 30 sec of the change to 100% O₂ and prior to any change in mean arterial blood pressure (AP), late diastolic coronary vascular resistance (LDR) decreased from 2.04 ± 0.26 to 1.44 ± 0.20 mm Hg/ml/min. LDR remained below control throughout the hypocapnic period while AP decreased from 122 ± 7 to 111 ± 7 mm Hg and CBF was unchanged. β-Adrenergic blockade with propranolol eliminated the decrease in LDR seen during hypocapnia prior to block, AP was unchanged, and CBF decreased from 36 ± 8 to 27 ± 7 ml/min. The decrease in LDR during hypocapnia was reversed following combined α-and β-adrenergic blockade with propranolol plus dibenamine and LDR increased from 0.90 ± 0.14 to 2.27 ± 0.85 mm Hg/ml/min. After combined block, CBF decreased from 78 ± 8 to 53 ± 8 ml/min by 3 min of hypocapnia and AP increased from 84 ± 19 to 108 ± 16 mm Hg by the end of the hypocapnic period. The increase in heart rate observed late in the hypocapnic period persisted following β block but was eliminated following combined blockade. These data suggest that adrenergic effects during whole-body hypocapnia may initially offset a local coronary vasocontriction which is unmasked following combined α- and β-adrenergic blockade.