The effect of hepatic and mesenteric arterial denervation on the hepatic haemodynamic response to hypercapnia and hypoxia was studied in 13 pentobarbitone anaesthetized greyhounds. Electromagnetic flowmeters were used to measure blood flow in the hepatic artery (HA) and portal vein (PV).
Hypercapnia of 100 mm HgPaCO2 increased PV blood flow and decreased HA blood flow, with opposite changes in mesenteric and HA vascular resistances. All parameters tended to return slightly towards baseline with extended periods of hypercapnia. HA denervation eliminated the changes in HA flow and resistance, while mesenteric arterial denervation appeared to prevent the secondary changes in PV blood flow and mesenteric vascular resistance. It is concluded that the sympathetic nervous system is responsible for the HA vasoconstriction observed during hypercapnia and that it exerts a delayed slight inhibitory influence on a predominantly direct vasodilatory effect of carbon dioxide on the mesenteric vasculature.
Hypoxia of 40 mm HgPaCO2 produced sustained increases in HA and mesenteric vascular resistances and a small increase in PV blood flow, together with a pronounced increase in systemic arterial blood pressure. HA denervation eliminated the HA resistance increase and caused the HA blood flow to increase during hypoxia. Mesenteric arterial denervation prevented the increases in mesenteric resistance, PV flow and arterial blood pressure from being sustained throughout the hypoxic period. It is concluded that hypoxia produces a sympathetically mediated mild vasoconstriction of both the HA and mesenteric vascular systems.