The effect of propranolol on cerebral oxygen consumption and blood flow in the rat: measurements during normocapnia and hypercapnia

The cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO,) in the rat during normocapnia and hypercapnia were investigated by means of the intraarterial ¹³³Xenon injection technique; measurements were performed during normocapnia and hypercapnia and the effect of propranolol upon CBF and CMRO₂ was studied. The CBF technique applied to rat yield reliable results even in high flow situations. A steady state period of only 10–15 s is all that is necessary to obtain the initial slope of the ¹³³Xenon clearance curve from which CBF is calculated and measurements may be repeated within minutes. Hypercapnia caused an increase in CMRO₂ of 35% which confirms the findings of other investigators. The beta-adrenergic receptor blocker propranolol (2 rag per kg i.v.) prevented this increase and could eliminate an increase in CMRO₂ already induced; this indicates that CO₂ affects adrenergic mechanisms. Although propranolol eliminated the CMRO₂ response to hypercapnia, it only reduced the CBF response; this dissociation of CBF and CMRO₂ response occurred probably because the beta-receptor blockage only eliminated a CBF increase mediated through an increased CMRO₂ (cellular response) whereas a direct CO₂ effect upon the arterioles (vascular response) persisted.