Opiate modulation of thermoregulation in adult Pekin ducks

Lightly restrained, adult Pekin ducks (2-3 kg) were given a subcutaneous (sc) injection of either sterile saline or morphine sulphate (10 or 30 mg/kg), followed 90 min later by a sc injection of naloxone hydrochloride (10 mg/kg). Core (cloacal TC) and surface (web TW) temperatures were continuously monitored along with heart (fH) and respiratory rates (fresp). In a related study, another group of Pekin ducks was placed in an open respirometer chamber so that oxygen consumption (VO2) could be determined following administration of sterile saline or morphine. Morphine sulphate (10 and 30 mg/kg) caused a hyperthermic core temperature response which persisted over the 90-min test period. This hyperthermia was due to an initial but transient vasoconstriction of the peripheral vasculature, as inferred from the sudden drop in foot web temperature. It was also found that morphine rapidly enhanced VO2 of the ducks, which remained elevated throughout the entire 90-min postmorphine injection period. TWS began to increase as peak TCS were reached (congruent to 30 min postinjection), and were above control levels until the end of the morphine period. fH was elevated following morphine administration but fresp was not altered. Upon naloxone administration, TCS were reduced because heat production was decreased (VO2 fell) and heat dissipation was enhanced further by increased vasodilatation (elevated TW) and a substantial (greater than 10-fold) increase of fresp (gular fluttering). Results demonstrate that morphine caused hyperthermic TC changes in adult Pekin ducks by increasing heat production while, at the same time, minimizing heat loss by vasoconstricting the peripheral vasculature and inhibiting respiration.