Regional venous outflow, blood volume, and sympathetic nerve activity during hypercapnia and hypoxic hypercapnia

Abstract

We examined the changes in systemic blood volume and regional venous outflow from the splanchnic, coronary, and other remaining vascular beds in response to acute hypercapnia or hypoxic hypercapnia in dogs, using cardiopulmonary bypass and a reservoir. Hypercapnia (PCO2 = 105 mmHg) (1 mmHg = 133 Pa) and hypoxic hypercapnia (PO2 = 23 mmHg, PCO2 = 99 mmHg) caused marked decreases in systemic blood volume of 14 +/- 3 and 16 +/- 3 mL/kg in spleen-intact dogs, and 3 +/- 2 and 10 +/- 2 mL/kg in splenectomized dogs, respectively. Splanchnic venous outflow increased by 12% at 3.5 min hypercapnia, whereas it decreased by 60% at 3.5 min hypoxic hypercapnia. Coronary venous outflow increased by 85 and 400% at 3.5 min hypercapnia and hypoxic hypercapnia, respectively. Sympathetic efferent nerve activity revealed a significant augmentation during hypoxic hypercapnia and a relatively smaller increase (30% of the response to hypoxic hypercapnia) during hypercapnia. Carotid and aortic chemoreceptor and baroreceptor denervation attenuated significantly the response of systemic blood volume to hypercapnia and hypoxic hypercapnia. The regional venous outflow responses to hypercapnia were not altered after chemodenervation, but those to hypoxic hypercapnia were significantly attenuated after chemodenervation. These results suggest that acute hypercapnia and hypoxic hypercapnia caused a marked decrease in vascular capacitance owing primarily to an increase in sympathetic efferent nerve activity via chemoreceptor stimulation. They also indicate that blood flow to the splanchnic vascular bed during hypercapnia increased (even though the cardiac output was constant), whereas it increased to the extrasplanchnic and coronary vascular beds during hypoxic hypercapnia.

Changes in Partial Pressure of Arterial Carbon Dioxide Induces Redistribution of Oral Tissue Blood Flow in the Rabbit

“…Hypercapnia increases sympathetic nervous activities which are followed by an increase in cardiac output and peripheral vasodilatation (25)(26)(27)(28). Increases in CBF in both groups were proportional to those in ETCO 2 in the present study.…”

Pet CO2 inversely affects MSNA response to orthostatic stress

“…First, elevated Pa CO 2 may exert direct vasconstrictor effects (10). In addition, central chemoreceptor activation may increase venous return (6,11,23). If so, then hypercapnia may support cardiac output (Q) and blood pressure maintenance during head-up tile (HUT) so that requirements for a sympathetically mediated vasoconstriction are diminished.…”

“…Receptors in the cardiac chambers, aorta, and carotid bodies respond to changes in the heart wall or vascular stretch leading to increases in sympathetic outflow during reductions in venous return or pulse pressure (13,16). Changes in arterial CO 2 pressure (Pa CO 2 ) also influence autonomic outflow primarily through receptors located on the ventral medullary surface (11,32). The afferent neural projections from these receptors converge on the nucleus tractus solitaris of the rostral ventrolateral medulla (see Ref.…”

Tissue Blood Flow During Remifentanil Infusion With Carbon Dioxide Loading

“…Hypercapnia activates the sympathetic nervous system and increases tissue blood flow. [12][13][14] Meanwhile, other studies have reported that skeletal muscle blood flow decreased during hypercapnia 15 or that tissue blood flow in the liver and kidneys increased while muscular blood flow decreased. 16 In the present study, similar results were observed during hypercapnia.…”