Thermoregulation In Rabbits Research Articles

Presence of cholinoceptors in mesencephalic raphe nuclei concerned in thermoregulation in rabbits.

The thermal effects of cholinomimetics and cholinoceptor blocking agents microinjected into mesencephalic nucleus raphe medianus (NRM) were investigated in rabbits to determine the nature and role of these cholinoceptors in thermoregulation. Microinjection of cholinoceptor agonists, carbachol and pilocarpine, into NRM resulted in significant hyperthermia which could be blocked by local pretreatment with chlorisondamine (a nicotinic receptor blocker) as well as by ethybenztropine (a muscarinic receptor blocker). Intracerebroventricular pretreatment with LM 5008 (serotonin reuptake blocker) significantly inhibited the carbachol-induced hyperthermia. Both nicotinic and muscarinic cholinoceptors are present in mesencephalic NRM which may be involved in thermoregulation in rabbits. Activation of these cholinoceptors in NRM results in hyperthermia which seems to be due to an inhibition of a serotonin sensitive hypothalamic heat loss mechanism.

Effects of brain monoamine depletions on thermoregulation in rabbits.

Biochemical analyses revealed that 5,7-dihydroxytryptamine- (5,7-DHT) treated and 6-hydroxydopamine- (6-OHDA) treated rabbits, respectively, had a significant reduction in diencephalic 5-hydroxytryptamine (5-HT) and norepinephrine (NE) with minimal alterations in the other monoamines. Both 5,7-DHT-treated and 6-OHDA-treated animals, although showing the maintenance of normal body temperatures, did exhibit specific alterations in the thermoeffector outputs. The 5-HT-depleted animals displayed an increase in ear skin blood flow, respiratory heat loss, and metabolism at both ambient temperatures (Ta) of 22 and 2 degrees C. The NE-depleted animals displayed a decrease in metabolism at all levels of Ta tested. Also, the peripheral temperature threshold for the onset of heat loss responses were displaced to higher values than in control animals. In addition, the prostaglandin E1-induced fever was attenuated after the pretreatment of rabbits with either 5,7-DHT or 6-OHDA. The data indicate that brain levels of 5-HT and NE alter, in an apparently reciprocal fashion, the thermoregulatory responses of rabbits. Also, the integrity of 5-HT and NE pathways in brain is vital for the full functioning of a prostaglandin in producing a fever.

Effects of dopaminergic antagonist and agonist on thermoregulation in rabbits.

1. The effects of dopaminergic antagonist haloperidol and agonist apomorphine on the thermoregulatory responses of unanaesthetized rabbits to different ambient temperatures (Ta) of 2, 22 and 32 degrees C were assessed. 2. I.V. administration of haloperidol produced dose-dependent hypothermia at 2 and 22 degrees C Ta. At 2 degrees C Ta the hypothermia was due to a decrease in metabolic heat production. At 22 degrees C Ta the hypothermia was brought about by a decrease in metabolism and an increase in ear blood flow. However at 32 degrees C Ta, there was an increase in rectal temperature in response to haloperidol application; this hyperthermia was due to a decrease in both the ear blood flow and respiratory evaporative heat loss (Eres). 3. I.V. administration of apomorphine produced dose-dependent hyperthermia at all the ambient temperatures studied. At 2 degrees C Ta the hyperthermia was due to an increase in metabolism. At both 22 and 32 degrees C, the hyperthermia was brought about by an increase in metabolic heat production and a decrease in ear blood flow. Also, there was an increase in Eres in response to apomorphine at 22 degrees C Ta. 4. The data, in general, indicate that dopamine agonist activates all effector pathways which modulate the autonomic processes of thermoregulation (i.e. respiratory heat loss, peripheral vasomotor tone and metabolism), and that the dopamine antagonist inhibits the activity in all three effector pathways. Such a clear pattern of results is readily expressible in terms of the 'Bligh' model dealing with the aminergic mechanisms of temperature regulation.

Thermoregulation in rabbits during fever.

1. We have studied the effect of fever on the efficacy of the thermoregulatory control system in conscious rabbits. 2. The control system was challenged by a series of systemic thermal loads produced by the intravenous infusion of hot or cold isotonic solutions. The time integral of the consequent upward or downward displacement of brain temperature was used as an index of the response of the control system. Steady-state fever was induced by intravenous infusion of plasma containing leucocyte pyrogen. 3. With cold loads there was a linear relation between load and response. The regression coefficients were not significantly changed by fever in any of the six rabbits. Wth hot loads given to afebrile rabbits the regression of response on load was generally not statistically significant, but the responses were not demonstrably greater in the febrile state. 4. We were not able to demonstrate impairment in the capacity of the febrile animal to compensate for systemic thermal loads.

Interrelation between monoaminergic and cholinergic mechanisms in the hypothalamic thermoregulatory centre of rabbits

The intracerebroventricular injection of acetylcholine, carbachol and physostigmine induced hyperthermia in rabbits while muscarinic agents, pilocarpine and oxotremorine produce a biphasic thermal response consisting of an immediate hyperthermia followed by a delayed hypothermia. An involvement of central nicotinic receptors in the acetylcholine-induced hyperthermia is suggested, since it is blocked by intracerebroventricular pretreatment with chlorisondamine and (+)-tubocurarine and not by atropinization. On the other hand, stimulation of central muscarinic receptors in the hypothalamus are concerned in the delayed hypothermia induced by pilocarpine as it is blocked by prior central atropinization. Intracerebroventricular injection of catecholamines, viz. noradrenaline, adrenaline and dopamine, results in a hyperthermic response due to activation of α-adrenoceptors in the hypothalamus, since norepinephrine hyperthermia is blocked by intracerebroventricular pretreatment with phenoxybenzamine and not by propranolol. Furthermore, a blockade of norepinephrine hyperthermia by pretreatment with chlorisondamine and not by prior atropinization suggests that the activation of central α-adrenoceptors in turn stimulates the cholinergic system which is nicotinic in nature. On the contrary, intracerebroventricular 5-hydroxytryptophan and 5-hydroxytryptamine caused hypothermia which is due to an activation of central muscarinic receptors since it is found to be blocked by prior intracerebroventricular administration of ethybenztropine and not by chlorisondamine pretreatment. On the basis of these observations, an interaction between adrenergic and nicotinic mechanisms as well as between tryptaminergic and muscarinic systems is suggested in the hypothalamic thermoregulation in rabbits for the hyperthermic and hypothermie responses, respectively.