Prenatal exposure to nicotine attenuates stress-induced hyperthermia in 7- to 8-week-old rats upon exposure to a novel environment.

Given that approximately 25% of women in the United States continue to smoke cigarettes during pregnancy, it is important to know if exposure to nicotine during development alters the physiological response of the adult to the "stressors" of everyday life. Our current experiments were carried out to determine if prenatal exposure to nicotine alters "stress-induced hyperthermia" in adult rats upon exposure to a novel environment such as a simulated open field. Forty-eight rats (23 males and 25 females) were exposed to a simulated open field or left in their home cage at 7 to 8 weeks of postnatal life (i.e., adulthood as defined by the ability to reproduce) following prenatal exposure to vehicle or nicotine (6 mg of nicotine tartrate per kilogram of maternal body weight per day) via a maternally implanted osmotic minipump from Day 6 or 7 of gestation. The simulated open field consisted of a 30(W)x60(L)x24(H)-in. white acrylic finish box illuminated by two hanging fluorescent lights and core temperature was measured by telemetry. Exposure to a simulated open field following prenatal exposure to vehicle elicited an increase in core temperature in male and female rats with a magnitude of approximately 1.2 degrees C and a duration of greater than 170 min. Prenatal exposure to nicotine significantly attenuated the thermogenic response of both genders; this was not only evident in the latency, magnitude and duration of the core temperature response but also in the core temperature index determined from the 3-h period following exposure to a simulated open field. Thus, our data provide evidence that prenatal exposure to nicotine attenuates stress-induced hyperthermia in male and female 7- to 8-week-old rats upon exposure to a "stressor" of everyday life (i.e., a novel environment).

Age-dependent core temperature responses of conscious rabbits to acute hypoxemia.

Experiments were carried out on chronically instrumented newborn and older rabbits to characterize their core temperature (T(c)) responses to acute hypoxemia and to differentiate "forced" vs. "regulated" thermoregulatory responses. Three age ranges of kits were studied: 4-6, 9-11, and 28-30 days of age. During an experiment, T(c), selected ambient temperature (T(a)), and oxygen consumption were measured from kits studied in a thermocline during a control period of normoxemia, an experimental period of normoxemia or hypoxemia (fraction of inspired oxygen 0.10), and a recovery period of normoxemia. We reasoned that no change or a decrease in T(a) while T(c) decreased during hypoxemia would indicate a regulated thermoregulatory response, whereas an increase in T(a) while T(c) decreased during hypoxemia would indicate a forced thermoregulatory response. T(c) decreased during acute hypoxemia in the older kits but not in the 4- to 6-day-old kits; the decrease in T(c) was accentuated on postnatal days 28-30 compared with postnatal days 9-11. T(a) decreased or stayed the same during exposure to acute hypoxemia. Our data provide evidence that postnatal maturation influences the T(c) response of rabbits to acute hypoxemia and that the decrease in T(c) during hypoxemia in the older kits results from a regulated thermoregulatory response.

Aminophylline alters the core temperature response to acute hypoxemia in newborn and older guinea pigs.

In newborns and adults of a number of species, exposure to acute hypoxemia produces a "regulated" decrease in core temperature, the mechanism of which is unknown. The present experiments were carried out on chronically instrumented newborn (5-10 days of age; n = 27) and older (25-30 days of age; n = 23) guinea pigs to test the hypothesis that adenosine mediates this regulated decrease in core temperature. During an experiment, core temperature was measured by biotelemetry from animals studied in a thermocline during a control period of normoxemia, an experimental period of normoxemia or acute hypoxemia (fraction of inspired oxygen 0.10), and during a recovery period of normoxemia after an intraperitoneal injection of 10 mg/kg aminophylline (i.e., a nonspecific adenosine antagonist) or vehicle. Core temperature decreased significantly during hypoxemia after vehicle in both newborn and older guinea pigs. After aminophylline, however, newborn guinea pigs failed to significantly decrease their core temperature, whereas older guinea pigs exhibited an attenuated yet significant core temperature decrease during hypoxemia. Our data support the hypothesis that adenosine plays an age-dependent role in mediating the regulated decrease in core temperature that occurs in newborn and older guinea pigs during acute hypoxemia.

Naloxone does not alter the "regulated" decrease in core temperature during hypoxemia in guinea pigs.

In newborns and adults of a number of species, exposure to acute hypoxemia produces a "regulated" decrease in core temperature, the mechanism of which is unknown. The present experiments were carried out in chronically instrumented newborn (5-10 days of age; n = 59) and older (25-30 days of age; n = 61) guinea pigs to test the hypothesis that the endogenous opioids mediate this regulated decrease in core temperature. During an experiment, core temperature, oxygen consumption, and selected ambient temperature were measured in a thermocline (linear temperature gradient of 10-40 degreesC) during a control period of normoxemia, an experimental period of normoxemia or hypoxemia (inspired oxygen fraction 0.10), and during a recovery period of normoxemia following an intraperitoneal injection of naloxone hydrochloride (a nonspecific opioid antagonist; 1, 2, or 4 mg/kg) or vehicle. Naloxone did not significantly alter basal core temperature or the core temperature response to acute hypoxemia in newborn or older guinea pigs. Naloxone did, however, decrease basal oxygen consumption in newborn and older guinea pigs and altered the thermoregulatory effector mechanism used to decrease core temperature during hypoxemia in the newborn guinea pigs. Our data do not support the hypothesis that the endogenous opioids mediate the regulated decrease in core temperature that occurs in newborn and older guinea pigs during exposure to acute hypoxemia.