α-Adrenergic control of intestinal circulation in heat-stressed baboons

The mechanisms involved in producing intestinal vasoconstriction during a hyperthermia-producing environmental heat stress are unknown. Five conscious baboons (Papio anubis), each with chronically implanted catheters and a flow probe around the superior mesenteric artery, were subjected to environmental heating (T(a) 40-45°C) to raise their arterial blood temperature (Tbl) 2.0-2.5°C to approximately 39.5°C. Accompanying the gradual rise in Tbl was a fall in mean superior mesenteric artery blood flow (MSMF) and a progressive rise in superior mesenteric vascular resistance (SMR). At peak Tbl, MSMF had fallen 28.8 ± 0.6% (mean ± SE) and SMR had risen 50.2 ± 4.2%. To determine the involvement of the sympathetic nervous system in producing this intestinal vasoconstriction, the baboon was subjected to environmental heating after induction of α-adrenergic receptor blockade by phenoxybenzamine or phentolamine. In this state, the rise in Tbl was accompanied by no change in MSMF and a slight, but not statistically significant, rise (7.8 ± 3.8%) in SMR. Since α-receptor blockade nearly completely abolishes intestinal vasoconstriction during heat stress, this intestinal vasoconstriction must be mediated primarily by elevated sympathetic outflow.