Vascular capacitance responses to hypercapnia of the vascularly isolated head

Abstract

Hypercapnic stimulation of the brain may account for some of the decrease in vascular capacitance (venoconstriction) seen with whole-body hypercapnia. Six mongrel dogs were anesthetized with alpha-chloralose and paralyzed with pancuronium bromide. The vagi were cut and the carotid bodies and sinuses were denervated. The head circulation was isolated and perfused with normoxic [arterial partial pressure of O2 (Pao2) = 112 mmHg], normocapnic (PaCO2 = 40 mmHg) blood, or one of three levels of normoxic, hypercapnic (PaCO2 = 56, 68, or 84 mmHg) blood. A membrane oxygenator was used to change gas tensions in the perfusate blood. The systemic circulation received normoxic, normocapnic blood (Pao2 = 107 mmHg; PaCO2 = 32 mmHg). Systemic arterial pressure increased from 111 to 134 mmHg, and heart rate decreased from 174 to 150 beats/min with a head blood PaCO2 of 84 mmHg. Central blood volume was not affected by head hypercapnia. Cardiac output significantly decreased only with a head blood PaCO2 of 84 mmHg. Mean circulatory filling pressure increased by 0.014 mmHg/1 mmHg increase in head PaCO2. The sensitivity of the total peripheral resistance to cephalic blood hypercapnia was 0.88%/mmHg, whereas that for the mean circulatory filling pressure was only 0.19%/mmHg. We conclude that stimulation of the brain, via perfusion of the head with hypercapnic blood, causes a small but significant increase in mean circulatory filling pressure, due to systemic venoconstriction.

Partial Liquid Ventilation Ventilates Better than Gas Ventilation

“…Increased mean airway pressures and hypercapnia both contribute to these hemodynamic changes. Acute increases in Pa CO 2 increase vascular filling by constricting capacitance vessels (33,34), reducing left ventricular contractility and improving left heart ejection by reducing arteriolar tone and afterload (35). However, severe respiratory acidosis may have blunted myocardial and vascular responsiveness to catecholamines and therefore may have resulted in the compromised hemodynamics during GV.…”

Permissive hypercapnia. How permissive should we be?

“…IncreasedPC0 2 elicits constriction of the vascular capacitance system and tends to increase ventricular filling and cardiac output (53)(54)(55). Also, hypercapnia improves left ventricular ejectionby reducing arteriolartone and thus decreasing afterload.…”

The effect of hypercapnia on the sensitivity to flicker defined stimuli

“…It is also well established that mild hypercapnia increases peripheral perfusion and tissue PO 2 as a result of central chemoreceptor response which in turn increases the cardiac output26 and/or by locally mediating peripheral vasodilation, which in turn overcomes sympathetic vasoconstriction 27. Consequently, an increase in blood CO 2 levels has been known to trigger the dissociation of oxyhaemoglobin and thus increase haemoglobin O 2 loading (Bohr effect), which can potentially contribute to changes in ocular blood flow and ultimately visual function.…”