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

Venous plasma noradrenaline, adrenaline, dopamine, corticosterone, glucose and free fatty acid concentrations were measured in anaesthetized rabbits during hypovolaemia, hypothermia and a combination of these. The anaesthetic used was Hypnorm, which contains fentanyl and fluanisone. In the hypovolaemia group blood was shed via the venous cannula until the mean arterial pressure was 50 mmHg. The rabbits in the hypothermia group were cooled in iced water to a central temperature of 32 degrees C, and the rabbits in the combined hypovolaemia-hypothermia group were bled until hypovolaemic and then cooled in iced water to a central temperature of 32 degrees C. Rewarming was done in dry air at 43 degrees C. Bleeding and hypothermia activated the sympathicoadrenal system, causing a rise in the noradrenaline and adrenaline concentrations, as well as a rise in corticosterone. There were no significant differences in plasma noradrenaline and adrenaline values between the groups, whereas hypovolaemia alone also increased the dopamine concentration. In the hypothermia group the amount of corticosterone after cooling and rewarming was higher than in the combined group. Hypothermia and hypovolaemia increased the level of free fatty acids and blood glucose, which in the hypovolaemia group remained higher after volume replacement than in the other groups. Hypothermia in both groups increased the mean arterial pressure. In conclusion, the results suggest that hypothermia may prevent some harmful effects of hypovolaemia, e.g. by correcting mean arterial pressure, thus preventing the mortality seen in the hypovolaemia group.
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PMID:Plasma catecholamines, corticosterone, glucose and fatty acids concentrations and mean arterial pressure and body temperature in haemorrhagic hypovolaemia, hypothermia and a combination of these in the rabbit. 223 47

A group of five hyperthermia-related deaths is presented in which urinary noradrenaline (NA) concentrations were elevated (172.1 +/- 119.4 ng/ml) compared with a control group of rapid violent deaths (43.7 +/- 26.1 ng/ml). Urinary adrenaline (A) concentrations were not elevated in the hyperthermia cases, nor were there any significant differences in urinary dopamine (DA) concentrations between the two groups. All except one of the hyperthermia victims were under the influence of ethanol. It is suggested that a combination of heat stress and ethanol consumption was responsible for the elevated urinary NA in the hyperthermia cases, reflecting increased sympathetic nervous system activity. A combination of high urinary NA with low A seems to be characteristic of hyperthermia fatalities, in contrast to hypothermia deaths, where both NA and A are usually elevated.
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PMID:Urinary catecholamines in hyperthermia-related deaths. 227 17

Metabolic indicators of myocardial ischaemia were measured in coronary sinus blood in six patients undergoing coronary artery bypass grafting (CABG). Five arterial and coronary sinus blood samples were taken in each case--one before cardiopulmonary bypass (CPB), and three during and one after CPB. Moderate hypothermia with topical cardiac cooling and cold cardioplegia were used. Myocardial infarction occurred perioperatively in two patients. Myocardial lactate production was not found before CPB in any patient, but it was common during CPB. Adenosine, inosine and hypoxanthine were released into the coronary sinus blood, but their release did not correlate significantly with lactate production. Myocardial noradrenaline production showed positive correlation with lactate levels (p less than 0.05). Release of adrenaline from the myocardium during CABG was also demonstrated. Myocardial catecholamine production was especially seen in the patients with myocardial infarction. Myocardial catecholamine release seemed to be the most sensitive of the studied biochemical indicators of myocardial ischaemia during CABG.
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PMID:Biochemical indicators of myocardial ischaemia during coronary artery bypass grafting. 235 86

To investigate the effects on the central nervous system of severe cold stress with and without chlorpromazine, guinea pigs were treated with chlorpromazine or 0.9% NaCl and exposed to -20 degrees C or +23 degrees C for 1 h. Hypothalamic noradrenaline (NA), dopamine (DA), 5-hydroxy-tryptamine (5-HT), 3-methoxy-4-hydroxyphenyl ethylene glycol (MHPG), homovanillinic acid (HVA) and 5-hydroxy-indoleacetic acid (5-HIAA) were determined by high-performance liquid chromatography. Serum, urinary and vitreous fluid catecholamines, muscle and liver glycogen, and blood glucose were also measured. Chlorpromazine caused distinct hypothermia at -20 degrees C and slight hypothermia at +23 degrees C. The rise in hypothalamic MHPG, 5-HIAA and MHPG/NA and in 5-HIAA/5-HT ratios in the cold indicate increased noradrenergic and serotonergic activity. The latter was inhibited by chlorpromazine and a drug-induced inhibition of noradrenergic neurons could not be ruled out. Chlorpromazine increased the turnover of DA at room temperature and the same tendency was seen in the cold. The hypothermic animals had low serum catecholamines, indicating diminished sympathetic activity. The chlorpromazine-treated cold-exposed animals did not react to the environmental stress by sympathetic activation, as urinary NA and adrenaline were not elevated, but DA was excreted by all the drug-treated animals. Vitreous fluid NA and DA were elevated as an indicator of cold stress, and no drug effect was seen in this fluid.
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PMID:Chlorpromazine-induced alterations in hypothalamic amine metabolism and stress responses in severe cold. 247 37

There is no consensus on the optimal level of intraoperative hypothermia during cardiopulmonary bypass (CPB). To assess the effect of systemic cooling on the stress response to CPB, the acute phase and endocrine responses were measured in 20 male patients undergoing elective coronary artery surgery and randomised to an intraoperative blood temperature of 28 degrees C or 20 degrees C. The acute phase response was assessed by changes in the plasma concentration of C-reactive protein (CRP) and the endocrine response by the urinary excretion of the counter-regulatory hormones adrenaline, noradrenaline and cortisol. The groups were comparable with respect to age, anthropometric indices, cross clamp and bypass times. There was no significant difference in the groups in the acute phase response but the endocrine response was attenuated in the 20 degrees C group. These findings may have implications for the severely stressed preoperative patient.
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PMID:Hypothermia and the stress response to cardiopulmonary bypass. 248 24

The central action, particularly potential antidepressant activity of WEB 1881, a new nootropic drug related to piracetam, was investigated in rats and mice. WEB 1881 antagonizes the reserpine- and apomorphine-induced hypothermia, potentiates the behavioral effect of DOPA and dihydroxyphenylserine, as well as the TRH-induced hyperthermia. Piracetam was only effective in the reserpine and DOPA tests. WEB 1881 is inactive in immobility test of Porsolt et al. It enhances the hind limb flexor reflex of the spinal rat, this effect being antagonized by prazosin and cyproheptadine. It exerts no effect on head twitches induced by L-5-hydroxytryptophan. The studied compound increases the noradrenaline and dopamine and turnover in the forebrain and brain stem. WEB 1881 given repeatedly potentiates the clonidine-induced aggressiveness and has no effect on the locomotor hyperactivity induced by D-amphetamine. The results indicate that in a number of tests WEB 1881 acts like other antidepressant drugs (but in others not), moreover, they suggest that this action is--at least partly--mediated by the central noradrenaline system.
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PMID:Antidepressant activities of WEB 1881, a new nootropic agent. 256 89

1. The dose-related effects of the selective alpha 2-adrenoceptor agonists clonidine, UK-14,304 and B-HT 933 on the body temperature of untreated and reserpine-treated mice were investigated. 2. In untreated mice all three agonists induced a dose-related hypothermia. The highest doses of UK-14,304 and B-HT 933, 3 and 100 mg kg-1 respectively, elicited a marked (10 degrees C) hypothermia, whereas the maximal hypothermic effect of clonidine (5.5 degrees C) was less pronounced and reached a plateau at a dose of 0.5 mg kg-1 i.p. 3. Reserpine (2.5 mg kg-1, s.c.) induced a marked hypothermia in the mouse; 18 h after injection body temperature had decreased to only slightly (0.5-1.5 degrees C) above ambient (19 degrees C). 4. All three alpha 2-agonists produced a partial dose-related reversal of reserpine-induced hypothermia; maximal thermogenic responses (9-10 degrees C increases in body temperature) were elicited by doses of 0.2, 0.5 and 16 mg kg-1 i.p. of clonidine, UK-14,304 and B-HT 933 respectively, and the log dose-response curves for all 3 agonists were bell-shaped. 5. Following intracerebroventricular administration to reserpine-treated mice, the thermogenic response to clonidine was more rapid in onset, and the agonist was 20 fold more potent than when injected i.p. 6. The selective alpha 2-adrenoceptor antagonists, idazoxan (0.05-0.5 mg kg-1), Wy 26392 (0.3-5.0 mg kg-1) and yohimbine (0.1-1.6 mg kg-1) given orally attenuated the thermogenic responses to all 3 agonists in reserpinized mice in a dose-related manner. Pretreatment with a single dose of idazoxan (0.3 mg kg-1, orally) elicited a 6 fold parallel shift to the right in the dose-response curve to clonidine. 7. The selective alpha 1-adrenoceptor antagonists, prazosin (10 mg kg-1) and indoramin (3-10 mg kg-1), and the beta-adrenoceptor antagonist, propranolol (10 mg kg-1), only partially attenuated the thermogenic responses to the alpha 2-agonists in reserpinized mice. These effects were variable and not clearly dose-related. 8. Pretreatment of reserpinized mice with the catecholamine synthesis inhibitor, alpha-methyl-p-tyrosine, markedly attenuated (60-95%) the thermogenic response to the noradrenaline uptake inhibitor, desipramine (0.13-12.5 mg kg-1, i.p.), but only slightly reduced (10-35%) that to clonidine (0.032-0.5 mg kg-1, i.p.). 9. These results suggest that alpha2-adrenoceptor agonists reverse reserpine-induced hypothermia via a central mechanism involving activation of postsynaptic alpha 2-adrenoceptors.
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PMID:The thermogenic actions of alpha 2-adrenoceptor agonists in reserpinized mice are mediated via a central postsynaptic alpha 2-adrenoceptor mechanism. 256 88

1. The effects of acute and chronic (14 day) administration of the noradrenaline uptake inhibitor, desipramine (DMI), on the thermogenic responses to clonidine in reserpine-treated mice, and on the hypothermic and hypoactivity responses to the alpha 2-agonist, UK-14,304, in untreated mice were examined. 2. Taking the capacity of DMI to delay the onset of reserpine-induced hypothermia as an indicator of noradrenaline (NA) uptake inhibition, the lowest dose of DMI to inhibit uptake significantly for 12 h in the mouse was shown to be between 10 and 20 mg kg-1 orally. 3. Chronic (every 12 h for 14 days), but not acute treatment with DMI (15 mg kg-1, orally), attenuated the thermogenic responses to low doses (0.02-0.225 mg kg-1, i.p.) of clonidine (injected 20 h after the last dose of DMI) in reserpinized mice. 4. Acute DMI administration slightly attenuated the hypothermia and hypoactivity induced by UK-14,304 (0.25-1.0 mg kg-1, i.p.) when injected 2h, but not when injected 18-21h before the agonist. In contrast, 18-21h after withdrawal from chronic DMI both of these responses to UK-14, 304 were markedly attenuated. 5. As the thermogenic response to clonidine in reserpinized mice appears to involve central post-synaptic alpha 2-adrenoceptors, these results suggest that prolonged inhibition of NA uptake decreases the sensitivity of postsynaptic alpha 2-adrenoceptors. The results of the studies using UK-14,304 indicate that central alpha 2-adrenoceptors involved in mediating other behavioural and pharmacological responses to alpha 2-agonists are also down-regulated by chronic inhibition of NA uptake.
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PMID:The effects of acute and chronic desipramine on the thermogenic and hypoactivity responses to alpha 2-agonists in reserpinized and normal mice. 256 89

Hypothermia-induced potentiation of alpha-adrenoceptor-mediated responses of the mouse vas deferens to noradrenaline is mainly caused by inhibition of the sites of loss. However, even after blockade of the sites of loss for noradrenaline or when using methoxamine (which is not a substrate for uptake or metabolism) hypothermia still causes a significant increase in responsiveness. This remaining supersensitivity was shown to be an increased receptor affinity. Furthermore, hypothermia revealed contractile responses to low concentrations of UK 14304 (an alpha 2-agonist).
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PMID:Hypothermia induces supersensitivity of mouse vas deferens to adrenergic agonists: evidence for postjunctional alpha 2-adrenoceptors. 256 66

Medetomidine, (+/-)-4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole, is a very potent, selective and specific full agonist at both pre- and postsynaptic alpha 2-adrenoceptors as demonstrated in several models both in vitro and in vivo. In receptor binding experiments the alpha 2/alpha 1 selectivity ratio of medetomidine is 1620 compared to 260, 220 and 160 for detomidine, clonidine and xylazine, respectively. The alpha 2-adrenoceptor activity of medetomidine resides predominantly in its d-enantiomer (dexmedetomidine). Medetomidine induces a dose-dependent decrease in the release and turnover of noradrenaline, dopamine and serotonin in the CNS as measured by changes in metabolite concentrations or using pharmacological intervention techniques. Inhibition of sympathetic tone in the CNS by medetomidine leads for a characteristic pattern of pharmacodynamic responses including e.g. hypotension, bradycardia, sedation, relief of anxiety, analgesia and hypothermia. The potent, dose-dependent sedative effects of medetomidine have been demonstrated in several classical animal models (e.g. decrease in spontaneous motility in rats and mice, potentiation of barbiturate-induced anaesthesia in rats and mice, induction of sleep in young chicks). At high doses medetomidine has hypnotic of anaesthetic effects, a property which distinguishes it clearly from detomidine, clonidine and other alpha 2-agonists. The pharmacological, neurochemical and behavioral effects of medetomidine can be inhibited by prior, simultaneous of subsequent administration of a selective and specific alpha 2-antagonist, atipamezole. Besides verifying that the main pharmacodynamic effects of medetomidine are alpha 2-mediated, this finding forms a strong basis for the use of atipamezole as a reversing agent against medetomidine-induced effects in veterinary practice.
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PMID:Pharmacological profiles of medetomidine and its antagonist, atipamezole. 257 Dec 75


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