Mechanism of Plasma Catecholamine Increases During Surgical Stress in Man

Abstract

In order to determine whether the sympathetic nervous system participates in the neuroendocrine response to surgical stress in man, plasma levels of norepinephrine (NE) and epinephrine (E) were measured by enzymatic assay in eight patients undergoing elective abdominal operations. Basal NE levels (pre-anesthesia) were comparable to those of 11 normal controls: 180 ± 20 pg/ml, X̄ ± sem (patients), vs. 180 ± 20 (controls), but basal E levels were higher: 70 ± 10 (patients) vs. 20 ± 5 (controls), P < .001. Halothane anesthesia caused no changes of plasma NE (Δ NE = +50 ± 40 pg/ml, p = NS), but suppressed plasma E (Δ E = −50 ± 10 pg/ml, P < .01). During the operation plasma catecholamines rose above anesthesia levels in all patients: Δ NE = +380 ± 60, Δ E = +250 ± 100, both P < .01. Plasma catecholamines remained elevated through 2 h after surgery: Δ NE (vs. pre-anesthesia baseline) = +290 ± 60, P < .01, Δ E = +200 ± 60, P < .05. Throughout the procedure Δ NE correlated with Δ E (r = .75, P < .001). These findings indicate that adrenergic activation does occur during surgical stress in man. This activation is not due to anesthesia, which appears to suppress E release. During these studies Δ mean arterial pressure correlated positively both with Δ NE (r = .68, P < .001) and with Δ E (r = .73, P < .001), indicating that the increases of adrenergic activity were associated with increases of mean arterial pressure and were not a response to hypotension or hypovolemia. Changes of plasma catecholamine levels were unrelated to either hypoxia or hypothermia. Thus, the increases of NE and E during surgical stress may reflect an adrenergic response to afferent pain stimuli which are not blocked by anesthesia.