Regional hemodynamic effects of changes in PaCO 2 in the vagotomized, sino-aortic de-afferented rat

Abstract

Rats were anesthetized with urethane (1.5 g/kg i.p.) paralyzed with gallamine (3 mg/kg, i.v.), artificially ventilated and the vagi, carotid sinus and aortic nerves were cut. PaCO 2 levels of 16.4 ± 0.8, 23.3 ± 1.6, 32.3 ± 1.8 and 51.9 ± 2.2 mm Hg were obtained by hyperventilation in 0%, 3%, 5% and 8% CO 2 in O 2, respectively. Radioactive microspheres labelled with 57Co or 113Sn were injected into the left ventricle and cardiac output and regional blood flows were determined by the ‘arterial reference sample’ method. Increasing PaCO 2 induced an increase in systemic arterial pressure which was predominantly due to a significant increase in total peripheral resistance, while the increase in cardiac output was much less pronounced and no changes in heart rate were observed. The effect of increasing PaCO 2 on regional vascular resistance (VR) was not uniformly distributed. CO 2 induced a dilatation in the cerebral, bronchial and hepatic artery vascular beds. Coronary VR was not affected while vasoconstriction was induced by CO 2 in the other vascular territories. This vascoconstriction was most significant in skeletal muscle, skin, pancreas, large intestine and kidneys. In most of these territories the vasoconstrictor effect of CO 2 was observed at PaCO 2 levels above 23.3 mm Hg, while between 16.4 and 23.3 mm Hg there was either no change or a decrease in VR. Propranolol and phentolamine (1 mg/kg and 10 mg/kg, i.v., respectively), which caused a 78% ± 2% adrenergic blockade, significantly reduced the CO 2 pressor and vasoconstrictor effects. Our experiments show that, after peripheral chemoreceptor denervation in the rat: (a) there is a direct relationship between PaCO 2 and VR mediated by the sympathetic nervous system over the whole range of PaCO 2 values from hypocapnia to hypercapnia, and (b) the various vascular territories contribute to a different extent to the CO 2-induced changes in total peripheral resistance.