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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxytocin (OXY) administered intracisternally to adult male mice produced a significant dose-related (1-4 micrograms) increase in colonic temperatures at an ambient temperature of 25 degrees C. The maximal rise in temperature occurred 30 min after administration of the peptide. The interactive effects on colonic temperature of central OXY with equimolar amounts of neurotensin, bombesin or beta-endorphin or of 2 2 mg/kg of chlorpromazine were investigated. OXY significantly antagonized the hypothermia produced by all of these substances. Pretreatment of mice with haloperidol or naloxone failed to prevent OXY-induced hyperthermia. The hyperthermic action of OXY and the interactive effects of OXY with other peptides on thermoregulation may be physiologically significant during parturition and lactation.
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PMID:Interactive effects of intracisternal oxytocin and other centrally active substances on colonic temperatures of mice. 294 25

To investigate the mechanism by which ACTH secretion is inhibited during hypothermia, hypophysial portal blood was collected from euthermic and hypothermic rats, and the concentrations of corticotropin-releasing factor (CRF), vasopressin (AVP), and oxytocin (OT) were measured by RIA. Whereas CRF levels in portal plasma were not different in the two groups, AVP and OT levels were significantly lower in hypothermic rats. The concentration of AVP and OT in peripheral plasma was also significantly lower in hypothermic rats compared with euthermic controls. The pituitary responsiveness to CRF during hypothermia was tested in vivo and in vitro. In pentobarbital-anesthetized male rats injected iv with 0.1 or 1.0 nmol CRF, the ACTH response was significantly smaller in hypothermic compared with euthermic animals. However, hemipituitaries superfused at 31 C released the same amount of ACTH in response to 1 nM CRF as hemipituitaries superfused at 37 C (31 C, 541 +/- 90 pg; 37 C, 563 +/- 29 pg) despite reduced baseline secretion (31 C, 77 +/- 10 pg/10 min; 37 C, 114 +/- 14 pg/10 min; P less than 0.05). The data suggest that the inhibition of ACTH secretion during hypothermia is mediated by decreased hypothalamic secretion of AVP and OT which in turn decreases the pituitary responsiveness to CRF.
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PMID:Inhibition of corticotropin release during hypothermia: the role of corticotropin-releasing factor, vasopressin, and oxytocin. 298 77

The relative dependence or independence of the secretion of the neurohypophysial hormones, arginine vasopressin and oxytocin, was investigated using a wide variety of stimuli reported to cause the secretion of one or the other hormone. Differences in species, animal preparations, sampling techniques, assays, and other factors make comparison of many previous studies difficult. The aim of this study was to overcome these problems by using the same methodology, animal species, and assays to compare vasopressin and oxytocin release. To further strengthen the analysis, determinations of vasopressin and oxytocin were done in the same blood samples. The results demonstrated that during simultaneous release of both hormones, vasopressin is released in greater proportion following restraint stress, hemorrhage, isotonic hypovolemia, and nicotine, whereas oxytocin is released in greater proportion following endotoxin or hypertonic saline. Vasopressin was released without oxytocin following diethylstilbestrol. Oxytocin was released without concomitant vasopressin release following exercise, hypothermia, hyperthermia, labour, and lactation. Neither oxytocin nor vasopressin release was observed following thyroid-releasing hormone or insulin-induced hypoglycemia. These data illustrate the marked flexibility of the hypothalamo-neurohypophysial system that regulates secretion of vasopressin and oxytocin.
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PMID:Simultaneous and independent release of vasopressin and oxytocin in the rat. 337 May 33

Sixteen peptides were injected intracerebroventricularly to test their effects on rectal temperature of rabbits in a thermoneutral environment. In initial tests 5 micrograms alpha-MSH, ACTH(1--24), oxytocin, vasopressin and glucagon altered body temperature while ACTH(1--10), cholecystokinin, contraceptive tetrapeptide, gastrin, insulin, interferon, leupeptin, LHRH, panhibin (somatostatin), and proctolin did not. Bombesin also altered body temperature but in no consistent direction. In further tests on the effective peptides 1.25--5.0 micrograms alpha-MSH and ACTH(1--24) produced dose-related decreases in rectal temperature as great as 1.0 degrees C. The same doses of oxytocin and glucagon produced small, prolonged hyperthermias which did not exceed 0.4 degrees C. Vasopressin caused rapid development of small increases in rectal temperature; temperature returned to normal in 2--3 hr. The results suggest that five of the peptides tested may have roles in central mediation of normal body temperature, hypothermia, hyperthermia and fever.
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PMID:Central administration of peptides alters thermoregulation in the rabbit. 724 7

Mice were rendered tolerant to the hypothermic effect of ethanol by forcing them to inhale ethanol vapor for 3 days. One day after withdrawal, tolerance was assessed by determining the response of the mice to an acute 3 g/kg IP challenge dose of ethanol. Thirty minutes before the injection of ethanol, saline or peptide solution was SC injected. The peptides studied were des-Gly9-Arg8-vasopressin (a peptide with reduced peripheral endocrine activities), oxytocin, and analogs and fragments of these peptides. None of the peptides, with the possible exception of oxytocin, affected body temperature in naive animals or the acute hypothermic response to ethanol in non-tolerant mice. Des-Gly9-Arg8-vasopressin enhanced the expression of tolerance to ethanol hypothermia; shorter fragments of vasopressin did not share this effect. Oxytocin attenuated the expression of tolerance but this may been due to an interaction with the acute effects of ethanol.
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PMID:Effects of peptides related to neurohypophyseal hormones on ethanol tolerance. 724 30

Two series of experiments were done to investigate the mechanism underlying arginine8-vasopressin (AVP)-induced barrel rotation in rats. In the first series, the effect of intracerebroventricular (ICV) administration of various neurohypophyseal hormone antagonists on AVP-induced barrel rotation was studied. The more vasopressin was given, the more the rats exhibited barrel rotation. ICV pretreatment with a V1 vasopressin receptor antagonist, d(CH2)5[Tyr(Me)2]AVP, prevented barrel rotation, while similar treatment with a V2-antagonist, d(CH2)5[dIle2Ile4]AVP, did not affect vasopressin-induced barrel rotation. However, Des-Gly,NH2d(CH2)5[Tyr)Me2)Thr4Orn8]-vasotocin, a specific oxytocin antagonist, potentiated the effect of AVP on barrel rotation. The second experiment was performed in rats equipped with a telemetry system to measure heart rate (HR), core temperature (CT), and gross locomotor activity. Also, in this experiment the incidence of AVP-induced barrel rotation was dose-dependent, as was the number of rats that died. Barrel rotation was accompanied by a significant decrease in CT and HR, while rats that did not develop hypothermia did not show barrel rotation. These results suggest that a V1 receptor is involved in barrel rotation. Since AVP-induced hypothermia is also mediated by a V1 receptor, it is postulated that hypothermia is a prerequisite for barrel rotation to occur. Further experiments are needed to substantiate this hypothesis.
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PMID:Barrel rotation induced by central arginine8-vasopressin treatment: involvement of neurohypophyseal peptide receptors. 811 25

Vasopressin immunostaining in the lateral septum of the European hamster (Cricetus cricetus L.) disappears in autumn, at the time of the first appearance of hypothermic periods characteristic to hibernation. Previous results have shown that chronic administration of vasopressin in the lateral septum during winter prevents the expression of hypothermic periods, suggesting a role for this peptide in hibernation. It is now observed that acute infusion of vasopressin, and in 50% of the cases, of a specific vasopressin V1 receptor agonist, during a hypothermic period results in an immediate termination of hypothermia. Infusion of oxytocin or a vasopressin V2 receptor agonist were without effect. The results indicate that the seasonal variation in central vasopressin activity, possibly through an interaction with V1 receptors, may play an important role in the expression of hibernation in the European hamster.
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PMID:Induction of arousal in hibernating European hamsters (Cricetus cricetus L.) by vasopressin infusion in the lateral septum. 813 Oct 59

Neuroendocrine response to stress stimuli is aimed to maintain body homeostasis. The activation of the neuroendocrine system is accomplished mainly by two ways: by feedback regulation based on the recognition of altered metabolic homeostasis by appropriate receptors sending the signal into the CNS, and by forward regulation involving a direct stimulation of the neuroendocrine system by a central command coming from an activated brain regulatory center. With regard to mechanisms of neuroendocrine activation, the signal specificity and site of its origin are of particular importance. The significance of the signal in neuroendocrine responses has been evaluated in three different stress conditions: hypoglycemia, surgical trauma and dynamic physical exercise. The stimulus inducing neuroendocrine response during hypoglycemia is the glucopenia. The signal for the activation of the neuroendocrine response is generated in glucosensitive cells which are not located in a single brain structure (hypothetical glucostat). The signal for growth hormone, vasopressin and oxytocin release is produced in brain structures protected by the blood-brain barrier, that for ACTH release in regions both protected and unprotected by the barrier, while the signal for prolactin release is generated in tissues lacking the blood-brain barrier. The neuroendocrine response during surgical trauma is activated by a signal formed in the damaged tissue reaching the CNS by neural pathways. Moreover, cytokins may participate on endocrine stimulation in those surgical interventions in which a large amount of bacterial endotoxins is released. During a complicated surgery, e.g. during a bypass other signals and modifying factors, such as hypothermia, dilution of blood, hypoperfusion of organs, rewarming of the body and hormone degradation in the oxygenator are important. On the On the other hand, during a short-term dynamic exercise, a forward regulation by a central signal from the activated CNS motor center comes into play with the consequent release of catecholamines, growth hormone, etc. In the control of some other hormones (beta-endorphin, partly ACTH) and especially during a long term exercise, neural signals from working muscles (feedback) are also involved. During a static exercise mainly catecholamines triggered by signals from working muscle cells are activated. The understanding of the signal and mechanisms of neuroendocrine activation during stress is indispensable for selective modulation of physiological and pathological responses.
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PMID:[Activation of the neuroendocrine system during changes in homeostasis during stress conditions]. 868 9

The role of central vasopressin V1 receptors in grooming behavior induced by vasopressin and oxytocin was studied in male rats of the Wistar strain. The intracerebroventricular (ICV) injection of vasopressin (3 micrograms/5 microliters) induced hypothermia and enhanced novelty-induced grooming behavior. Enhanced grooming but not hypothermia was also induced by ICV injection of oxytocin (3 micrograms/5 microliters). The central administration of a selective vasopressin V1 receptor antagonist prevented the stimulating action of vasopressin on novelty-induced grooming and its hypothermic effect. The ICV injection of a selective vasopressin V2 receptor antagonist failed to affect vasopressin-induced grooming and hypothermic effect. An increase in core temperature was observed in oxytocin-injected animals pretreated with the vasopressin V1 receptor antagonist. Furthermore, pretreatment with the antagonist did not affect grooming induced by oxytocin. These results suggest that enhancement of grooming behavior and influence on thermoregulation are differently regulated by central receptors for vasopressin and oxytocin.
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PMID:The block of central vasopressin V1 but not V2 receptors suppresses grooming behavior and hypothermia induced by intracerebroventricular vasopressin in male rats. 939 41

Neuropeptides affect adaptive central nervous system processes related to opiate ethanol and cocaine addiction. Oxytocin (OXT), a neurohypophyseal neuropeptide synthesized in the brain and released at the posterior pituitary, also is released in the central nervous system (CNS). OXT acts within the CNS and has been shown to inhibit the development of tolerance to morphine, and to attenuate various symptoms of morphine withdrawal in mice. In rats, intravenous self-administration of heroin was potently decreased by OXT treatment. In relation to cocaine abuse, OXT dose-dependently decreased cocaine-induced hyperlocomotion and stereotyped grooming behavior. Following chronic cocaine treatment, the behavioral tolerance to the sniffing-inducing effect of cocaine was markedly inhibited by OXT. Behavioral sensitization to cocaine, on the other hand, was facilitated by OXT. OXT receptors in the CNS--mainly those located in limbic and basal forebrain structures--are responsible for mediating various effects of OXT in the opiate- and cocaine-addicted organism. Dopaminergic neurotransmission--primarily in basal forebrain structures--is another important biochemical mediator of the central nervous system effects of OXT. Tolerance to ethanol (e.g. hypothermia-inducing effect of ethanol) also was inhibited by OXT.
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PMID:Oxytocin and addiction: a review. 992 46


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