Effects of hypercapnia and hypoxia on the cardiovascular system: vascular capacitance and aortic chemoreceptors

Abstract

Aortic chemoreceptor influences on vascular capacitance after changes in blood carbon dioxide and oxygen were studied in mongrel dogs anesthetized with methoxyflurane and nitrous oxide. The mean circulatory filling pressure (Pmcf), measured during transient cardiac fibrillation, provided a measure of capacitance vessel tone. Hypercapnia, hypoxia, and hypoxic hypercapnia significantly increased most variables, except that hypercapnia caused the total peripheral resistance (TPR) to decrease. Hypocapnia caused a significant decrease in mean systemic (Psa) and pulmonary (Ppa) arterial blood pressures, cardiac output (CO), and central blood volume and an increase in TPR and heart rate. The changes in Pmcf on changing blood gas tensions could be described by the equation delta Pmcf = -1.60 + 0.036 (arterial PCO2) + 50.8/arterial PO2. Thus a 10 mmHg increase in arterial PCO2 caused a 0.36 mmHg increase in Pmcf with receptors intact. Cold block (2 degrees C) of the cervical vagosympathetic trunks did not significantly influence the measured variables at control. During severe hypercapnia, vagal cooling caused a small but significant decrease in Pmcf, Psa, Ppa, and CO but not TPR. During hypoxia, vagal cooling caused the Pmcf, Psa, and TPR to decrease. We conclude that although hypercapnia or hypoxia acts reflexly to increase the capacitance vessel tone (an increase in Pmcf), the aortic and cardiopulmonary chemoreceptors with afferents in the vagi have only a small influence on the capacitance system, accounting for only approximately 25% of the total body response.

Cardiovascular changes during acute episodic repetitive hypoxic and hypercapnic breathing in rats

“…In another study, PELLETIER [12] showed, in dogs, that the pressor response to the stimulation of carotid chemoreceptors with hypoxic blood is augmented by hypercapnic acidosis. On the other hand, increasing Pa,CO 2 by 1.4 kPa in anaesthetised dogs increased arterial pressure only by about 5 mmHg [13] when blood pressure increased more than 20 mmHg during the obstructive period in sleep apnoea [1]. These results [3,5,7] conflict with previous data [1,[8][9][10] and our finding showing the predominant role of hypoxaemia over hypercapnia in acute changes in SBP, DBP and HR.…”

Hemodynamic Effect of Different Doses of Fluids for a Fluid Challenge: A Quasi-Randomized Controlled Study

“…The ΔPmsf depends on the change of stressed volume and the capacitance of the vascular system 13 , which in turns depends on several factors such as the sympathetic tone, hypercapnea, hypoxia and aortic and cardiopulmonary chemoreceptors 14 . The Pmsf values reported in this study are similar to previous studies in similar populations 6,7,11 , and the baseline values are very similar in the four groups, which reassure that the haemodynamic effect of the intravascular volume was fairly similar on the four groups.…”

The Response of Retrobulbar Vasculature to Hypercapnia in Primary Open-Angle Glaucoma and Ocular Hypertension

“…Hypercapnia has been found to cause the following cardiovascular changes including: venoconstriction, increased mean circulatory filling pressure, increased systemic arterial pressure, increased pulmonary arterial pressure, decreased total peripheral resistance and increased cardiac output. The vascular response to hypercapnia appears to be mediated via carotid chemoreceptors, receptors in the head and aortic chemoreceptors [7] . The normal response of the cerebral vasculature to hypercapnia is vasodilatation.…”