THERMAL PANTING AND THE INITIATION OF RESPIRATORY ALKALOSIS

Abstract

Forty-five dogs were exposed to nine different environmental conditions (five dogs per condition) consisting of three ambient temperatures (100 °F, 110 °F, and 120 °F) and relative humidities (30%, 60%, and 90%). After an initial control period of 30 minutes (ambient 21–24 °C) the animals were exposed to one of the experimental conditions for [Formula: see text] hours or until rectal temperature reached 42.0 °C. Under combined conditions of high temperature and humidity the non-biothermally involved consequences of panting became evidenced by an increase in blood pH, a decrease in blood CO2 (as a result of the thermally forced hyperventilation), and an increase in blood O2. The more severe the heat load (combined temperature and humidity) the greater was the rate of elevation of rectal temperature over control levels. It was evident that both relative humidity and ambient temperature were drives for increasing respiratory rate. It was also evident that increased humidity as well as increased temperature facilitated the rate of change of rectal temperature, blood pH, and blood CO2 and O2 concentrations. It appears possible that only under heat loads in which rectal temperature can be maintained at control levels by panting can the shift in acid–base balance be avoided.