Effects of vasoconstrictors on intestinal vascular resistance and oxygen extraction

Abstract

To delineate the mechanism through which vasoactive compounds alter intestinal oxygen consumption and to determine the pharmacological nature of the receptors involved, we quantitated the effects of vasoconstrictors on arteriovenous oxygen difference and on vascular resistance in isolated constant-flow perfused canine small bowel. Norepinephrine (NE) and sympathetic stimulation (SS) increased vascular resistance and depressed O2 extraction. These effects were not altered by beta-blockade, but were abolished by alpha-blockade. Since capillary filtration coefficients at constant-pressure perfusion and 86Rb extraction at constant flow are reported to diminish during NE and SS, it follows that these agents reduce O2 extraction by an alpha-adrenergic closure of precapillary sphincters. Vasopressin had similar effects which were not affected by adrenergic blocking agents. Epinephrine (Epi) in high doses or after propranolol produced the same effects as NE and SS. By contrast, Epi in low doses increased O2 and 86Rb extraction. This response to low doses of Epi was not affected by phentolamine, but was reversed by propranolol. We conclude that Epi in high doses or after propranolol depresses intestinal O2 extraction by the same mechanism as NE and SS, but the mechanism through which Epi increases intestinal O2 extraction is unclear.

Norepinephrine and vital organ blood flow

“…This resulted in a significant increase in both parameters (p<0.05) become compromised. These concerns are based on studies performed with extremely high doses of NE infused directly into the renal artery [12,13], other shortterm studies based on acute invasive or indirect measurements [10,11,17,18] or studies using microsphere technology [19], which allow assessment of regional circulations only at a particular moment in time. Despite the limitations and questionable clinical relevance of such studies NE has developed a reputation as a dangerous drug [20].…”

The Gastrointestinal Circulation: Physiology and Pathophysiology

“…Catecholamines induce vasoconstriction or vasodilation depending on whether α-or β-adrenergic receptors are activated. Exogenous epinephrine at low doses induces vasodilation via β-adrenergic receptors and at high doses, vasoconstriction via α-adrenergic receptors (375,442). The α-adrenergic agonist, norepinephrine, elicits vasoconstriction; however, autoregulatory escape occurs during prolonged norepinephrine administration (103,199,375,442).…”

Effect of Acidosis and Hypoxia on Intestinal Blood Flow of Sheep Fetus

“…However, the levels of circulating catechol amines have been reported to increase abruptly during hypoxia in fetal and newborn lambs [Cohen et al, 1982]. Epinephrine and norepinephrine are known to affect mesen teric blood flow and have been implicated in the redistribution of flow within the wall of the small intestine in adult animals [Hulten et al, 1977;Shepherd et al, 1976]. In lamb fetuses norepinephrine significantly de creased blood flow to the abdominal organs, as well as to the liver and spleen [Zink and VanPetten, 1981].…”