Epidural Morphine Decreases Postoperative Hypertension by Attenuating Sympathetic Nervous System Hyperactivity

Abstract

Twenty-four adults who were undergoing operations on the abdominal aorta were enrolled in a randomized, double-blind, placebo-controlled study in which epidural morphine sulfate (6 mg) was employed to attenuate the sympathoadrenal response to surgery to evaluate the possible contribution of sympathetic nervous system hyperactivity to postoperative hypertension. Patients who received epidural morphine required less parenteral morphine in the 24 hours following surgery, had lower analogue pain scores, and had markedly lower plasma norepinephrine levels when compared with patients in the control group who received an identical volume of saline in the epidural space. Epidural morphine had no effect on plasma epinephrine or arginine vasopressin levels. Fewer patients in the morphine group (4 of 12 vs 9 of 12 patients in the saline group) required treatment for hypertension (mean arterial blood pressure, greater than or equal to 110 mm Hg) in the 24 hours following surgery. In addition, patients in the morphine group had lower blood pressures in the 24 hours following surgery. These data suggest that sympathetic nervous system activity and not adrenal epinephrine or pituitary secretion of arginine vasopressin is responsible for the development of hypertension following aortic surgery. Furthermore, epidural narcotics appear to provide a means of attenuating this response.

Effect of Clonidine on the Circulation and Vasoactive Hormones After Aortic Surgery

“…Given the limitations of plasma noradrenaline as an index of overall sympathetic activity, this observation suggests marked attenuation of hyperactivity. These findings are similar to diose obtained after extradural morphine [18], except for the reduction of the vasopressin response seen in the present study.…”

“…Changes in concentrations of vasoactive hormones and cardiovascular variables in this study were similar to those reported during recovery from coronary [2,4,15,16] or aortic [17,18] surgery. As cardiac filling and systemic pressures and arterial blood-gas tensions were greater than baseline values or within the normal range, the surge in vasoactive hormones was not primarily a consequence of activation of baroreceptor (except immediately after administration of nifedipine) or chemoreceptor reflexes.…”

Role of Central and Mixed Venous Oxygen Saturation Measurement in Perioperative Care

“…[57][58][59][60][61] Opiates may similarly reduce perioperative VO 2 . [62][63][64][65] Neuraxial blockade has both sympatheticolytic and analgesic effects, 66,67 but we are unaware of reports specifically describing effects on VO 2 .…”

Thoracic Epidural Anesthesia and Analgesia (TEA) in Patients with Rib Fractures

“…The stress reaction is checked by stress hormones like epinephrine, norepinephrine, cortisol, and rennin, and by mediators of inflammation such as cytokines and lipid mediators in blood or other body fluids. The level of norepinephrine (noradrenalin) in the blood within 24 hours can increase up to 3 times [7]. In the past, it was understood that myocardial infarction could occur within 72 hours postoperatively.…”