Reversal of Depressed Miduterine Arterial Flow during Hyperthermia-Induced Respiratory Alkalosis

Abstract

The influence of ambient and arterial PCO₂ on miduterine arterial flow of pregnant sheep acutely exposed to hot environments was investigated. Five mixed-breed ewes between 120 and 130 days of gestation were subjected to hot environments (increasing from thermoneutral 23 to 40°C), and arterial blood pH, PCO₂, and PO₂ were determined at 5-min intervals. Respiratory rate, heart rate, rectal temperature, blood pressure, and miduterine arterial flow were continuously monitored prior to and during elevation of ambient air temperature. When miduterine arterial flow had decreased to 50% of thermoneutral control levels, ambient air CO₂ was increased to 2.5%. Elevated ambient inspired CO₂ caused a reversal in arterial pH and PCO₂ to near thermoneutral levels. Miduterine arterial flow increased to 77% of the control levels following the elevated ambient PCO₂ period. Respiratory rate also decreased when ambient CO₂ was increased but remained 136% greater than the thermoneutral control level. All other parameters remained near their heat stress (40 °C) level during the elevation of ambient CO₂. These data indicate that heat-stress-induced depression of miduterine arterial flow is vasoactively regulated, and cause-effect related to both arterial pH and PCO₂, and thermoregulatory Shunting of blood to heat-dissipating surfaces.