Arginine vasopressin (AVP) has been reported to have an antipyretic effect in the ewe and guinea pig near term. Perfusions with AVP of sites in the septal region also reduced fever in non-pregnant sheep. In the present experiments adult rabbits with third cerebral ventricular or septal cannulas were restrained in a 23 degree C environment, and rectal temperature was recorded every 10 min. Fever induced by IV administration of leukocytic pyrogen was not reduced by AVP (25-100 ng) given intraventricularly 20 min later. Doses of 1-5 micrograms AVP injected into the septum likewise were not antipyretic but actually caused an increase in fever. This augmentation of the febrile response is consistent with results of previous studies in this laboratory in which AVP increased hyperthermia in a hot environment and enhanced hyperthermic responses to PGE2. The data from these experiments provide no evidence that central AVP is an endogenous antipyretic in rabbits; rather, it may be that central AVP augments fever in this species.

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PubMedDate not supplied

Hyperthermic effect of prostacyclin injected into the third cerebral ventricle of the cat.

Prostaglandin E2 may not be solely responsible for hyperthermia produced by central administration of sodium arachidonate. To determine its effect, if any, on body temperature prostacyclin sodium salt, another product of prostaglandin endoperoxides, was injected into the third cerebral ventricle of unrestrained, unanesthetized cats while deep body temperature was recorded automatically. Doses of 2--25 microgram, in a volume of 0.05 ml saline solution, did not appreciably alter body temperature. A 100 microgram dose produced hyperthermia in five of six animals. Administration of 1 mg prostacyclin caused prolonged hyperthermic responses in four cats with a maximum increase in temperature of at least 2.1 degrees C. Prostaglandin E1 (1 microgram) produced hyperthermic responses which were intermediate between responses to 100 and 1000 microgram prostacyclin. Indomethacin (2 mg/kg), given IV to two cats during recovery from prostacyclin-induced hyperthermia, did not hasten the rate of recovery. These results indicate that, if a sufficient concentration of prostacyclin is achieved at a central site of action after injection of arachidonate or during pathologic processes which release arachidonic acid, prostacyclin could contribute to the development of hyperthermia.

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PubMedDate not supplied

Effects of centrally administered pentazocine and ethylketocyclazocine on thermoregulation in the cat.

The mechanisms for the biphasic response of unrestrained cats to centrally administered pentazocine were examined by injecting 1 mg pentazocine into the third cerebral ventricle at various ambient temperatures (TaS). The initial phase was hyperthermia at Ta = 34 degrees C, but at Ta = 22 degrees C hypothermia, which was enhanced at Ta = 0 degrees C, developed. The second phase was an increase in body temperature that occurred at all three TaS. No evidence was seen of compensatory thermoregulatory effector activity during development of either phase. The first phase can be attributed to general depression of thermoregulation whereas the second phase was likely due to an increase in the level about which body temperature was regulated. Ethylketocyclazocine (250-1000 micrograms) caused a very similar, dose-related change in temperature, neither phase of which, as reported previously for pentazocine, was reduced by a large dose of nalaxone. Thus both agonists appear to act on the same receptors to alter thermoregulation in the cat. These receptors are distinct from the naloxone-sensitive receptors stimulated by morphine.

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PubMedDate not supplied

Thermoregulatory effects of (D-ala2)-methionine-enkephalinamide in the cat. Evidence for multiple naloxone-sensitive opioid receptors.

(D-ala2)-methionine-enkephalinamide (DAME) was injected into the third cerebral ventricle of unrestrained cats. At ambient temperature (Ta) = 22 degrees C, 3.1-50 micrograms caused dose-related hyperthermias. As dosage was increased, the hyperthermias diminished and in some cats hypothermia developed. Hyperthermia was not due to pyrogenic contamination or prostaglandin synthesis since it was not altered by pretreatment with a large IV dose of indomethacin. However, pretreatment with naloxone did cause a dose-related reduction in the hyperthermia. A low dose of DAME (12.5 micrograms) also caused hyperthermia at Ta = 4 and 32 degrees C, indicative of an increase in the level about which body temperature was regulated. On the other hand, a dose of 200 micrograms, which caused hyperthermia Ta = 22 and 32 degrees C, usually caused hypothermia at Ta = 4 degrees C, perhaps due to impairment of thermoregulatory control mechanisms. The response to DAME in the cold was reduced by naloxone pretreatment or reversed by subsequent injection of naloxone. Differences in hyperthermic patterns over a range of TaS and the lack of hypothermogenic action of morphine indicate that DAME alters thermoregulation in the cat by acting on morphine-insensitive, but naloxone-sensitive receptors. Central injection of beta-endorphin (5-50 micrograms) caused a dose-related hyperthermia. (Des-tyr1)-leucine-enkephalin (10-250 micrograms) was weakly hyperthermogenic, and kyotorphin (500 micrograms) did not consistently alter body temperature.

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PubMedDate not supplied

[Effects of different feeding patterns on the activities of histidine and D.O.P.A. decarboxylases in rat stomach (author's transl)].

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