Lack of Peripheral Sympathetic Control of Uterine Blood Flow during Acute Heat Stress1

Publisher Website
Google Scholar
Abstract
Peripheral α- and β-adrenergic control of uterine blood flow (UBF) during acute heat stress of the gravid ewe was investigated. An electromagnetic blood flow probe was surgically implanted around the left miduterine artery and catheters inserted in the left carotid artery and right jugular vein in ewes between d 120 and 130 of gestation. Four or more days postsurgery, ewes were fitted with instruments to measure rectal temperature (Tr), heart rate (HR), respiratory rate (RR), blood pressure (BP) and UBF. One-half hour after instrument calibration, a 15-min thermoneutral control period was initiated with carotid artery blood samples taken at 5-min intervals for pH and PCO2 determinations. Ewes were then subjected to a heat challenge that reached 40 C at 2 h. All physiological data were recorded every 5 min as 1-min mean values. In seven experiments on five ewes, an α-adrenergic blocking drug, phenoxybenzamine (PB) was infused at 1 mg/min for 15 min subsequent to maximum depression of UBF. A β-adrenergic blocking drug, propranolol (PR) was infused at .35 mg/min for 15 min in eight experiments on five ewes. Analysis of variance comparisons were made between the control period and heat stress infusion periods within the PB and PR experiments. Further comparisons were made between the start and 5, 10 or 15 min of PB or PR infusion in order to test drug effects during an acute heat stress. Rectal temperature HR, RR and arterial pH were higher (P<.05) at the start of PR and PB infusions than during the thermoneutral control period. By the start of PB and PR infusions, both PCO2 and UBF were depressed (P<.05) from their respective thermoneutral control period values. The 15-min infusions of PB or PR did not increase UBF during heat stress. The UBF of PB-treated ewes remained depressed (P<.05) at the end of infusion without a change in uterine vascular resistance (UVR). The PR blocked tachycardia (P<.05) without a depression in systemic BP. These data indicate that peripheral α- or β-adrenergic mediated vasoconstriction do not appear to be responsible for the heat stress-induced depression of UBF. Alternate mechanisms are proposed for the phenomenon. Copyright © 1984. American Society of Animal Science . Copyright 1984 by American Society of Animal Science.

This publication has 0 references indexed in Scilit: