Blood pH and $$P_{aCO_2 } $$ as chemical factors in myocardial blood flow control

Abstract

The effect of metabolic and hypercapnic acidosis on myocardial blood flow was studied during intravenous infusions of hydrochloric acid solutions (n = 12) and during passive ventilation with 5% CO2 (n = 5) in anaesthetized, closed chest dogs. Below a pH of 7.2 metabolic acidosis at normal arterial CO2-tensions caused an increase of coronary blood flow and a decrease of coronary vascular resistance associated with a narrowed myocardial arteriovenous O2-difference, indicating vasodilation at unchanged myocardial oxygen consumption. In propranolol-pretreated dogs myocardial blood flow and coronary oxygen AV difference remained unaffected, suggesting that the coronary dilatory effect of metabolic acidemia involves beta adrenergic stimulation. Coronary vasodilation induced by increasing arterial pCO2 was found to the significantly greater as compared with the dilatory effect of metabolic acidosis at the same blood pH level. Blocking of beta receptors did not reduce the coronary response to increased arterial CO2-tensions. It is concluded that the coronary vasodilation observed during hypercapnic acidosis is neither mediated by a beta adrenergic stimulation nor dependent of the concomitant change in blood pH. The possible sites of the coronary dilatory actions of increased arterial CO2-tensions are discussed.

Deletion of proton-sensing receptor GPR4 associates with lower blood pressure and lower binding of angiotensin II receptor in SFO

“…Severe metabolic acidosis, as in life-threatening conditions such as diabetic ketoacidosis or hypoxic lactic acidosis, elicits vasodilation by affecting vascular smooth muscle directly (14,26). In contrast, mild subclinical acidosis associates with higher BP and incident hypertension over time (12,30).…”

Current views on mechanisms of vasodilation in response to ischemia and hypoxia

“…19 The claim has also been put forward that coronary dilation produced by systemic hypercapnia seems to be due to carbon dioxide per se rather than to changes in extracellular pH. 73 Although a concomitant rise of CO~ in reactive hyperemia has to be considered, note that carbon dioxide is a far less potent coronary vasodilator than mere hypoxia is. For instance, coronary sinus PCO2 had to be increased roughly twice as much as coronary sinus PCO~ was decreased in order to produce a comparable coronary vasodilation under constant-flow conditions.…”