Circulatory response to hypoxia in unanesthetized dogs with and without cardiac denervation

Abstract

The generally held view that acute hypoxia stimulates the cardiovascular system was reinvestigated in ten normal, trained, unanesthetized dogs and in six dogs which had previously been subjected to total cardiac denervation. In the normal dogs, no significant or consistent changes were noted in cardiac output, stroke volume index, or in systemic arterial pressure 5 and 15 min after the onset of 8% O2 inhalation. Heart rate, however, rose significantly. The dogs which had been subjected to cardiac denervation responded with small elevations of cardiac output and heart rate during the late hypoxic period. Thus, these findings are contrary to the classical concept that hypoxia elevates the cardiac output. Moreover, despite the absence of both the sympathetic and parasympathetic innervations of the heart, subjecting the denervated animals to severe hypoxia revealed that they were at no apparent hemodynamic disadvantage in comparison to the intact animals.

Studies on the regulation of myocardial blood flow in man II. Effects of acute arterial hypoxia

“…5). Increase in heart rate and cardiac output as well as alterations of arterial and pulmonary artery pressures are in accordance with findings reported in the literature (10,12,21,37,42,45,48,49,68). Undulating variations in arterial blood pressure were seen during the hypoxic tolerance test and the period of adaptation to hypoxia prior to the beginning of flow measurements.…”

“…This reaction appears to be independent from cardiac nerves. This conclusion may be drawn from very similar flow changes in the trained and untrained subjects as well as from observations in the intact or denervated canine heart (21,26,65). It is further supported by findings obtained from isolated coronary arteries (20).…”

“…These potentially deleterious reactions are considered to be modulated by cardiac nerves. It has been suggested that parasympathetic activity is reduced during mild or moderate hypoxia (21,35,45,48,50,52,75). It is overruled by central vagal stimulation during severe hypoxia (4).…”

“…However, significant changes (p<0.005) were noted when myocardial oxygen consumption was calculated per stroke. It decreased from 125 ± 30 (140 ±21) .u1/lOOg to 93 ± 10 (115 ± 37) and further to 87 ± 19 (96 ±21) .u1/lOOg.The increased flow rate slightly overcompensated for the decrease in arterial oxygen content. This is why arterial oxygen supply improved (p<0.05) from 12.73 ± 3.12 (15.86 ± 3.49) ml/min' 100g to 13.30 ± 3.04 (16.47 ± 4.12) and to 14.86 ± 2.00(16.82 ± 3.18) ml/min·100g.…”

Hypertension following denervation of aortic baroreceptors in unanesthetized dogs.

“…45, No. 1, JULY 1979 baroreceptor sites undisturbed, produces no significant change in mean arterial pressure in the dog (Glick et aL, 1964;Gregg et al, 1972;Noble et al, 1972). In anesthetized dogs, block or section of the vagus after section of the cervical aortic nerves and denervation of the carotid sinus baroreceptors (or with carotid pressure held constant) produces a rise in arterial pressure (Mancia et aL, 1975;Shepherd, 1974).…”