PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Hypothermia, Induced”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMedDate not supplied

Some pharmacological correlations of hypothermia induced by anticholinesterasics.

The investigations have been performed on Wistar rats intoxicated with paraoxon in toxic sublethal doses. There have been measured the variations of rectal temperature at various time periods following the anticholinesterase agent. The authors established the pharmacodynamic correlations of paraoxon-induced hypothermia with cholinesterase reactivators (toxogonin, isonitrosine), anticholinergic substances (atropine, butylscopolamine), carbamic anticholinesterase (eserine, neoeserine) and chlorpromazine. The efficiency of atropine and cholinesterase reactivators in antagonization of hypothermia induced by organophosphorics on the one hand, and only of atropine against hypothermia induced by carbamates on the other hand allow the hypothesis of a central cholinergic mechanism, predominantly muscarinic, involved in hypothermia induced by anticholinesterasics and of a direct correlation of this mechanism with phosphorylation or carbamylation processes of cerebral cholinesterases.

Animals↗
PubMed1975

Is taurine-induced hypothermia in the rat mediated by 5-HT?

Intraventricular administration of taurine in the rat caused hypothermia, the extent of which was directly dependent upon the thermal gradient between the body and the environment. Pre-treatment of animals with p-chlorophenylalanine, which depleted most of the brain serotonin, strongly reduced the hypothermia induced by taurine. Pre-treatment with alpha-methyltyrosine induced hypothermia and sedation in animals. When this was followed by a taurine injection, they exhibited a decrease in body temperature which fitted the curve relating thermal gradients to hypothermic responses. It is suggested that taurine induced hypothermia in rat is mediated in part by central 5-HT systems.

Animals↗
PubMed1977

Mechanisms of amitriptyline induced hypothermia in the rat.

Effects of amitriptyline on rectal temperature of male rats were studied at the ambient temperature of 25 degrees C. Drugs were administered intraperitoneally. Amitryptyline elicited a dose related hypothermia. The hypothermia was attenuated by phenoxybenzamine 10 mg/kg, haloperidol 2 mg/kg, diphenhydramine 5 mg/kg, atropine 20 mg/kg, and cyproheptadine 5 mg/kg. Propranolol, at a dose of 5 mg/kg, had no effect on the hypothermia. Theophylline 50 mg/kg and dibutyryl cyclic AMP 20 mg/kg inhibited the hypothermia produced by anitriptyline. Pretreatment with parachloroamphetamine (PCA), 2 or 5 mg/kg daily for 3 days, strongly antagonized the hypothermia. In addition, pretreatment with parachlorophenylalanine (PCPA), 100 mg/kg daily for three days, reduced the brain 5-hydroxytryptamine (5-HT) concentration to 20% of the control level and completely blocked the hypothermia response. When brain 5-HT concentration recovered to 50% of the control level in PCPA treated rats following the administration of 10 mg/kg 5-hydroxytryptophan (5-HTP) the hypothermia induced by amitriptyline was restored. However, the administration of 5-HT, 5 mg/kg, to PCPA treated rats did not increase brain 5-HT concentration or restore the amitriptyline induced hypothermia (AIH). Results suggest that amitriptyline interacts with several transmitter substances to produce hypothermia. Since the ability of amitriptyline to produce hypothermia was correlated with brain 5-HT content, 5-HT might play an important role in the mediation of AIH.

Amitriptyline↗
PubMed1975

Metabolic and respiratory responses during Helox-induced hypothermia in the white rat.

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.

Animals↗
PubMed1977

The possible role of dopamine in phenothiazine-induced hypothermia in rats: an application to DA hypothesis of schizophrenia.

Hypothermic effects of d-Amphetamine, chlorpromazine, a variety of other phenothiazines, ET495 and haloperidol in rats at 4 degrees C were measured separately and in combination. All the drugs produced some hypothermia. Among the phenothiazines, degree of hypothermia induced was found to be correlated with relative effectiveness of the drug as an antipsychotic agent. Hypothermic effects of each of the phenothiazines in combination with d-Amphetadrugs as an antipsychotic agent. Hypothermic effects of each of the phenothiazines in combination with d-Amphetamine was greater than for either drug alone. Hypothermic effects of the combination CPZ with Amphetamine was potentiated by haloperidol but blocked by ET495. The evidence supports a model of neuronal feedback loops either within the central DA mesolimbic pathway or between the mesolimbic and nigrostriatal DA systems. The establishment of interdependency between antipsychotic and hypothermic effects of phenothiazines offers promise not only to a greater understanding of the mechanisms underlying these effects, but the possibility of an objective test for screening new materials for antipsychotic effectiveness.

Animals↗
PubMedDate not supplied

The effect of lesions of dopaminergic and serotonergic systems on apomorphine-induced hypothermia in the rat.

Bilateral lesion of caudate nucleus or substantia nigra as well as brain transsection between telencephalon and diencephalon potentiates the body temperature fall produced by apomorphine (5 mg/kg). A lesion of nucleus accumbens septi did not prevent the hypothermia, but slightly shortened its duration. Electrolytical and chemical (with 5,6-dihydroxytryptamine) lesions of both dorsal and medial raphe nuclei alleviated the hypothermia produced by apomorphine. The lesion of medial raphe nucleus did not affect, while the lesion of dorsal raphe nucleus prevented the hypothermia induced by apomorphine or piribedil (25 mg/kg). The results show that dopaminergic neurons of telencephalon are not involved in the mechanism of induction of apomorphine hypothermia, while the neurons of dorsal raphe nucleus participate in it.

5,6-Dihydroxytryptamine↗
PubMed1978

Imipramine antagonism of apomorphine-induced hypothermia: a non-dopaminergic interaction.

Imipramine antagonized high dose apomorphine-induced hypothermia, and did not modify small dose apomorphine-induced hypothermia. It is suggested that apomorphine-induced hypothermia is the result of two effects. The first, induced by small doses of apomorphine, and antagonized by pimozide and sulpiride, is probably related to dopaminergic receptor stimulation. The second, induced by high doses of apomorphine, and antagonized by imipramine, is probably not related to dopaminergic receptor stimulation.

Animals↗
PubMed1976

A comparison between the hypothermia induced by intra-ventricular injections of thyrotropin releasing hormone, noradrenaline or calcium ions in unanaesthetized cats.

1 The hypothermia produced by intraventricular injections of thyrotropin releasing hormone (TRH) in unanaesthetized cats has been investigated. 2 TRH is more potent than either noradrenaline or calcium ions. It is estimated that the equi-potent molar ratio for TRH: noradrenaline:calcium is 1:900:27,000. 3 TRH injections is also produce profuse salivation, tachypnoea, cutaneous vasodilatation and frequently defaecation and vomiting. It is considered that the increased respiration is a major cause of the hypothermia. 4 Prior administration of phentolamine antagonized noradrenaline-induced hypothermia but did not affect hypothermia produced by TRH or calcium ions. Pretreatment with alpha-methyltyrosine did not affect the hypothermia induced by TRH, calcium ions or noradrenaline. 5 The calcium antagonists verapamil and xylocaine did not antagonize hypothermia induced by an injection of calcium ions. 6 The constituent amino acids of TRH did not produce hypothermia either individually or collectively. Thyroxine sodium produced a rise in temperature that was slow in onset, consistent with its known metabolic effects. TSH produced a small hypothermia unrelated to dose.

Animals↗
PubMed1978

Reduction of cerebral blood flow and oxygen consumption with a combination of barbiturate anaesthesia and induced hypothermia in the rat.

The influence of phenobarbitone anaesthesia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) during hypothermia (23 degrees C & 27 degrees C) was studied in the rat, using a modification of the Kety & Schmidt (1948) technique and arterio-venous differences for oxygen. Phenobarbitone (150 mg/kg) was found to decrease CMRo2 by 40-60% during hypothermia, when compared to N2O anaesthesia. At a body temperature of 23 degrees C, and during phenobarbitone anaesthesia, CMRo2 was reduced to about 15% of normal control value (about 10.3 ml.100g-1). CBF was reduced to about 50% of the phenobarbitone control value but was similar to the value obtained with N2O anaesthesia at 22 degrees C. It is concluded that the combination of phenobarbitone anaesthesia and hypothermia results in a more pronounced reduction in cerebral metablic rate for oxygen than can be achieved by administration of barbiturates to normothermic animals, or by reducing body temperature by 15 degrees C during superficial anaesthesia.

Anesthesia, General↗
PubMed1979

An improved method for inducing hypothermia and rewarming.

A hypothermia and rewarming system combining body surface and ventilatory heat exchange is described. The method utilizes body surface heat exchange through conduction, convection, and black body radiation, and ventilatory heat exchange across the lung surface through conduction, convection, and water evaporation. The system consisted of a chamber in which the temperature was maintained at a desired level (+/- 2.5 degrees C) using a refrigeration-heat pump unit. Chamber temperatures during cooling and rewarming were -15.5 +/- 2.7 degrees C and 43.2 +/- 2.3 degrees C, respectively. Inhalate temperatures during cooling were -8.2 +/- 6.5 degrees C and during rewarming they were 41.5 +/- 0.3 degrees C. Helium (100%) was supplied to the chamber, while the animal was ventilated with 20% O2 + 80% He. Under these conditions, the cooling and rewarming rates were 0.33 +/- 0.06 degrees C/min and 0.20 +/- 0.04 degrees C/min, respectively, at 38--21 degrees C. The system provided for rapid cooling and rewarming with no evidence of any untoward effects.

Animals↗
PubMed1977

Induced hypothermia in dogs with acute myocardial infarction and shock.

Acute myocardial infarction with shock (AMI/S) was produced in 46 anesthetized "closed-chest" dogs by catheter injection of metallic mercury into the circumflex coronary artery. Twenty-four dogs were kept normothermic and 22 were maintained at 32 degrees C. Nine of the latter were rewarmed to 37 degrees C. and the experiments then were terminated, so that true survival time was arbitrarily shortened. Including these dogs, the survival time was three times longer than in the normothermic series (p less than 0.001). Hypothermia reduced heart rate (HR) by 34 percent, oxygen consumption by 38 percent, and myocardial oxygen consumption by an estimated 30 to 40 percent, while cardiac output (CO), stroke volume, and stroke work were unchanged. Left ventricular end-diastolic pressure (LVEDP) was reduced by 40 percent during hypothermia (p less than 0.05) and increased by 60 percent on rewarming. HR during rewarming increased substantially more than CO and thereby significantly reduced stroke volume.

Acute Disease↗
PubMed1979

The effect of aminosteroid, ORG 6001, on hypothermia induced ventricular fibrillation in the cat.

1 The effect of the antidysrhythmic aminosteroid, ORG 6001, on hypothermia-induced ventricular fibrillation was investigated in cats anaesthetized with pentobarbitone. 2 ORG 6001 (total dose, 10 mg/kg, by intravenous injection) reduced both the incidence of fibrillation and the temperature at which it occurred. The number of animals that survived to 16 degrees C was increased. 3 This protective effect of ORG 6001 could not be explained by changes in respiratory acidosis, plasma concentrations of sodium and potassium, or by changes in the action potential of excised hypothermic ventricular muscle. The hypothermia-induced elevation of blood lactate was less in cats treated with the aminosteroid. 4 Over a limited temperature range, ORG 6001 prolonged the P wave and QRS duration and shortened the QTc interval. ST segment elevation was slightly reduced in the drug-treated group. J deflections were observed but were not correlated with the development of fibrillation. 5 The onset of fibrillation was not considered to be due to temperature differences between the myocardium and arterial blood or between localized areas of the left ventricular wall.

17-Ketosteroids↗
PubMed1977

Changes in plasma glucose, FFA, corticosterone, and thyroxine in He-O2-induced hypothermia.

Unanesthetized, male rats were exposed to normal air (NA), or NA and a 4 h-exposure of He-O2 (79% helium, 21% oxygen) at ambient temperature (Ta) of 22 or - 10 degrees C. Blood samples from each individual were taken from a chronically implanted carotid cannula at 1) preexposure, 2) during exposure, 3) 2.5 h after exposure, and 4) 19-20 h after exposure. Exposure to He-O2 at 22 degrees C caused an increase in plasma free fatty acids (FFA) and corticosterone of 45% and 49%, respectively, with little change in plasma glucose and thyroxine. Exposure to He-O2 at 10 degrees C for 3 h invariably induced hypothermia with body temperature (Tb) decreased to 23.7 +- 0.5 degrees C (N = 10). During hypothermia, plasma glucose, FFA, and corticosterone were significantly higher (P LESS THAN 0.05) than those at preexposure and those after exposure to NA at -10 degrees C. During spontaneous recovery from hypothermia, at Ta = 19 degrees C and NA, glucose, corticosterone, and thyroxine returned to normal, but FFA remained significantly higher than at preexposure. The ability of animals to rewarm spontaneously from hypothermia and the quick return of metabolic substrates and hormones to normal after rewarming indicates the preservation of regulatory mechanisms for metabolism at depressed Tb when hypothermia is induced by He-O2 and cold.

Animals↗