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

1. The effect of various agents injected into the cerebral ventricles of the mouse, upon the tremor and hypothermia produced by oxotremorine (0.5 mg/kg i.p.) was studied. 2. Acetylcholine (0.1-10 mug) produced a dose-dependent potentiation of oxotremorine tremor in contrast to the multiphasic effect it had on the accompanying hypothermia. Both tremor and hypothermia were antagonised by very small doses (0.1-10 ng) of atropine. 3. Dopamine and apomorphine (0.1-10 mug) had no significant effect on oxotremorine tremor. A dose-dependent potentiation of hypothermia was, however, observed. 4. Noradrenaline (0.1-10 mug), phentolamine and propranolol (0.1-10 mug) produced no significant effect on tremor and inconsistent results were obtained on hypothermia. 5. Neither tremor nor hypothermia were affected by 5-hydroxytryptamine (1-20 mug). 6. Oxotremorine tremor appears to be due solely to the activation of cholinergic pathways, whereas the production of hypothermia is brought about via a system involving both cholinergic and dopaminergic components. 5-Hydroxytryptamine is not involved.
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PMID:Modification of oxotremorine tremor and hypothermia by injections of drugs into the cerebral ventricles of the mouse. 101 35

1. Hypothermia induced by infusion of noradrenaline into the hypothalamus of 2-3 week old chicks, within their thermoneutral range, was considerably potentiated by lowering ambient temperature. 2. Noradrenaline-induced hypothermia was associated with reduced carbon dioxide elimination and reduced blood lactate concentrations whereas leg temperature, electromyographic activity, plasma NEFA and plasma glucose concentrations were increased. 3. Mechanisms postulated to explain the phenomenon are inhibitory and facilitatory effects of noradrenaline on some, but not all, heat production and heat loss mechanisms. Increased electromyographic activity after intrahypothalamic noradrenaline is assumed to be due to lack of effect of noradrenaline on spinal thermosensitive centres; increased plasma NEFA concentration may be due to inhibition of NEFA utilization.
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PMID:Effects of noradrenaline infused into the chick hypothalamus on thermoregulation below thermoneutrality. 114 57

The isolated rabbit heart was perfused according to the Langendorff technique. Prostaglandins in the effluent from the organ were identified by use of thin layer chromatography and assayed on the rat stomach strip. The effect of alterations of the physical and chemical conditions of the perfusion medium on the overflow of prostaglandins from the heart was studied. In addition, the capacity of noradrenaline and acetylcholine to release prostaglandins was tested. Acidosis, hyperthermia, hypothermia, hypotension, hyperosmoaarity and increased [K+] OR [Ca++] levels, while all inducing marked changes in the mechanical activity of the heart, did not induceporstaglandin release. Hypoxia, on the other hand, stimulated the liberation of prostaglandins. Noradrenaline was a potent agent for stimulation of prostaglandin release, in the absence of alpha- and betaadrenergic receptor blockade. Acetylcholine was also found to liberate prostaglandins, by activation of muscarinic receptors. The prostaglandin releasing capacity of acetylcholine was about 3 times weaker than that of noradrenaline. It is concluded that the release of prostaglandins from the rabbit heart is not dependent on the mechanical activity of the organ. Furthermore, it is suggested that prostaglandins released by hypoxia may play an important roli in the development of reactive hyperemia. Finally it is stated that the release of prostaglandins from the heart caused by acetylcholine may constitute the negative link in an endogenous prostaglandin mediated feed-back inhibition of the release of acetycholine from parasympathetic nerve endings.
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PMID:Prostaglandin release and mechanical perfromance in the isolated rabbit heart during induced changes in the internal environment. 115 28

1 The mechanism of the cataleptic effect of metoclopramide was analyzed by using drugs which alter the activity of dopaminergic or cholinergic neurones or the content of psi-aminobutyric acid in the central nervous system of rats. 2 The cataleptic effect of metoclopramide (20 mg/kg) was antagonized by apomorphine (10 mg/kg) and by atropine (50 mg/kg). Aminoxyacete acid (AOAA, 25-50 mg/kg) potentiated the catalepsy induced by metoclopramide (5 mg/kg). 3 Metoclopramide alone did not alter the rectal temperature of rats. It did not alter the AOAA-induced hypothermia, but it partially antagonized apomorphine-induced hypothermia. 4 Metoclopramide induced a six-fold increase in striatal homovanillic acid (HVA) concentration, but it did not change the dopamine or noradrenaline content in the brain of rats. Apomorphine decreased the striatal HVA concentration in control and in metoclopramide-treated rats. Atropine and AOAA did not alter the metoclopramide-induced increase in striatal HVA concentration. 5 The results suggest that metoclopramide produces catalepsy by blocking striatal dopamine receptors.
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PMID:Inhibition by apomorphine of the metoclopramide-induced catalepsy and increase in striatal homovanillic acid content. 123 23

Changes in rectal and skin temperatures following intraventricular injection of biogenic amines and related substances were investigated in rats. Intraventricular injection of norepinephrine in a small dose (6 mug) produced a slight elevation of rectal temperature, but in larger amounts (25-50 mug) resulted in a dose-dependent hypothermia which was associated with a marked rise of skin temperature. No change was observed in plasma free fatty acid and glucose levels and oxygen consumption after intraventricular injection of norepinephrine (25 mug). Intraventricular injection of imipramine and safrazine produced a slight fall in the rectal temperature. Norepinephrine-induced hypothermia was more pronounced in rats pretreated with safrazine and less in rats pretreated with alpha-methyl-p-tyrosine, as compared with that in controls. Intraventricular injection of 6-hydroxydopamine (0.75-250 mug) brought about a marked dose-dependent hypothermia. The second injection of 6-hydroxydopamine 5 days after the first injection had no effect on the body temperature. Norepinephrine injection 2 days after the second injection of 6-hydroxydopamine produced a more pronounced hypothermia than the change in control rats without pretreatments. Haloperidol did not affect the hypothermia induced by 6-hydroxydopamine. Intraventricular injection of dopamine and L-DOPA showed less effect that norepinephrine had. Intraventricular injection of phenoxybenzamine prior to norepinephrine blocked the hypothermia and skin temperature elevation which are normally observed following norepinephrine injection, while propranolol given in the same way showed less or no effect. Intraventricular injection of phenylephrine produced a dose-dependent hypothermia, whereas no dose-response relationship was obtained by isoproterenol. These results suggest that in the rat the hypothermic effect of norepinephrine injected intraventricularly is mediated by an action of central alpha-receptor. At high and low ambient temperatures hypothermia was similarly observed following intraventricular injection of 5-hydroxytryptamine (25 mug) as at normal room temperature. On the other hand, norepinephrine (25 mug) produced a rise in rectal temperature at high ambient temperature and a marked fall at low ambient temperature. The hypothermic effect of norepinephrine was not different between cold-adapted ones at room temperature. From the results the role of norepinephrine and other biogenic amines in the brain in thermoregulatory processes was discussed.
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PMID:[Role of brain biogenic amines in the central thermoregulatory mechanism of the rat (author's transl)]. 124 80

To determine the ability of intraoperative hypothermia to modify changes in the plasma protein component of the acute-phase response (APR) and the plasma hormone component of the endocrine response (ER) to surgical injury, 20 patients undergoing coronary artery surgery were randomised to an intraoperative blood temperature of 28 degrees C or 20 degrees C during cardiopulmonary bypass (CPB). Serial measurements of pack-cell-volume corrected concentrations (PCVCC) of five plasma proteins (albumin, prealbumin, transferrin, caeruloplasmin, ferritin) and six plasma hormones (adrenaline, noradrenaline, cortisol, triiodothyronine, thyroxine, and thyroid-stimulating hormone) were obtained twice preoperatively, seven times during surgery, six times in the 24 hours following surgery, and a further four times until the seventh postoperative day. A more profound level of intraoperative hypothermia significantly reduced the plasma adrenaline response to CPB but not the other components of the ER or APR.
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PMID:The effects of systemic intraoperative hypothermia on the acute-phase and endocrine response to cardiac surgery. 163 76

1. Parallel series of experiments were carried out in the rat and mouse in order to investigate the mechanism(s) underlying the hypothermia induced in rodents by the selective 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). 2. In the mouse, lesioning of central 5-hydroxytryptaminergic neurones (by use of the neurotoxin, 5,7-dihydroxytryptamine; 5,7-DHT) abolished the hypothermic response to 8-OH-DPAT, and depletion of brain 5-hydroxytryptamine (5-HT) levels (with the 5-HT synthesis inhibitor, p-chlorophenylalanine) markedly attenuated the response in this species. These pretreatments did not significantly attenuate 8-OH-DPAT-induced hypothermia in the rat, except for a significant attenuation of the response in 5,7-DHT-lesioned rats at the top dose of 8-OH-DPAT (1.0 mg kg-1, s.c.). 3. Pharmacological pretreatments which facilitate 5-HT release (selective 5-HT uptake inhibitors, precursor (5-hydroxytryptophan) loading, or fenfluramine), markedly attenuated or abolished 8-OH-DPAT-induced hypothermia in the mouse. These pretreatments generally had no significant effect on 8-OH-DPAT-induced hypothermia in the rat. 4. The selective noradrenaline uptake inhibitor, desipramine, had no effect on the hypothermic response to 8-OH-DPAT in either species. The selective dopamine uptake inhibitor, nomifensin, significantly increased the hypothermic response to 8-OH-DPAT in the mouse, but did not affect the response in the rat except at high, motor stimulant doses, when the response was attenuated. 5. These data are consistent with the hypothesis that 8-OH-DPAT-induced hypothermia is mediated by presynaptic autoreceptors in the mouse and by postsynaptic 5-HT1A receptors in the rat. Preliminary data also indicate an involvement of dopamine release in the mouse but not in the rat.
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PMID:Direct evidence for an important species difference in the mechanism of 8-OH-DPAT-induced hypothermia. 183 17

1. The metabolic response to injections of noradrenaline (NA) and saline (control) was investigated in conscious and anaesthetised (sodium pentobarbitone) pouched mice, Saccostomus campestris. 2. NA injection produced a calorigenic response which was significantly greater than that elicited by saline injection in both conscious and anaesthetised animals. 3. This calorigenic response was enhanced by motor activity in conscious pouched mice, but the exclusion of measurements recorded during visible activity eliminated the influence of movement. 4. Anaesthetised pouched mice underwent mild Hypothermia and displayed a retarded metabolic response to NA injection which suggests that anaesthesia affects the expression of NA-induced thermogenesis. 5. The validity of proposed techniques for the measurement of NA thermogenesis is further discussed.
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PMID:Noradrenaline thermogenesis in conscious and anaesthetised pouched mice (Saccostomus campestris). 197 64

The distribution of neuropeptide Y in the brain includes extensive coexistence within adrenaline- and noradrenaline-containing neurons and many of its actions are often associated with adrenergic systems. Since neuropeptide Y immunoreactivity is particularly intense in the preoptic area, one of the principal sites for thermoregulation, we have tested the effects of neuropeptide Y on core temperature in normothermic rats, and rats rendered hypothermic by systemic treatment with adrenergic antagonists. In the normothermic rat, intracerebroventricular administration of 1 microgram of neuropeptide Y did not have a significant effect on core temperature. Intraperitoneal treatment with the alpha 1-adrenoceptor antagonist, prazosin, or the beta-adrenoceptor antagonist, propranolol, caused an immediate and significant hypothermia; the intracerebroventricular administration of 1 microgram of neuropeptide Y, 10 minutes after these drugs, strongly potentiated their hypothermic effect. Although intraperitoneal treatment with the alpha 2-adrenoceptor antagonist, idazoxan, had no hypothermic effect per se, the intracerebroventricular administration of NPY 10 minutes after this antagonist led to a significant decrease in core temperature.
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PMID:Centrally administered neuropeptide Y enhances the hypothermia induced by peripheral administration of adrenoceptor antagonists. 198 Sep 42

Hypothermia may contribute to vascular spasm during bypass surgery. The effect of cooling on the reactivity of the human coronary artery (CA), saphenous vein (SV) and internal mammary artery (IMA) was studied in vitro. In CA and IMA cooling diminished the resting tension and the contraction to potassium, noradrenaline and 5-hydroxytryptamine. In contrast, in SV the contraction to noradrenaline and 5-hydroxytryptamine was augmented by cooling. The effect of cold was reversible. These results demonstrate different effects of hypothermia in CA and the graft vessels. Thus, hypothermia augments the receptor-mediated contraction in SV but depresses it in IMA which thereby resembles CA. The difference is most marked in the contractile response to 5-hydroxytryptamine, which may accumulate during surgery. This may contribute to spasm in the saphenous vein grafts and may be involved in the mechanisms responsible for the inferior patency of SV compared to IMA as a graft vessel.
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PMID:Differential effect of hypothermia on the vascular tone and reactivity of the human coronary artery and graft vessels. 205 21


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