Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microwave irradiation of 6 kw at 2450 MHz for 300 msec was sufficient to completely inactivate mouse brain cholinesterase and choline acetyltransferase. After this method of sacrifice, the acetylcholine contents of mouse brain regions, given in nanomoles per gram, were found to be: striatum, 81; medulla-pons, 44; diencephalon-midbrain, 34; hippocampus, 31; cerebral cortex, 26; and cerebellum, 17. Sodium pentobarbital caused a dose-dependent increase in whole brain acetylcholine. A maximal increase of 81% in whole brain was seen at 15 minutes with 80 mg/kg of sodium pentobarbital. The increase in acetylcholine after sodium pentobarbital treatment was not caused by anoxia from respiratory depression or by hypothermia. All brain regions except the cerebellum exhibited an increase in acetylcholine after pentobarbital treatment. Fifteen minutes after treatment, cerebellar acetylcholine was significantly decreased. However, at the time when half of the animals had regained the righting reflex, the unconscious mice showed an increase in cerebellar acetylcholine which was statistically significant as compared to control. The relative accumulation rate of acetylcholine calculated for cerebral cortex and hippocampus was higher than that for striatum although the absolute rate of accumulation of ACh was higher in the striatum. Thus, after sodium pentobarbital treatment, the cerebral cortex and hippocampus exhibit a greater cholinergic response than the striatum.
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PMID:Use of 300-msec microwave irradiation for enzyme inactivation: a study of effects of sodium pentobarbital on acetylcholine concentration in mouse brain regions. 0 94

Spontaneous contractions of the adult rabbit isolated testicular capsule were found to be influenced by moderate hyperthermic and hypothermic temperature changes. The decrease in testicular capsular spontaneous contractions resulting from an exposure to 32, 40 and 42 degrees C have been shown to be influenced by the addition of NE, ACh and PGF2 alpha. Of the three neurohumoral agents studied, NE was found to cause the greatest increase and re-initiation of testicular capsular tone during both hypothermia and hyperthermia. These data indicate that endogenous levels of neurohumoral agents may play an important role in the maintenance of testicular capsular tone during exposure to hyperthermic or hypothermic conditions.
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PMID:Response of the rabbit isolated testicular capsule at hypothermic and hyperthermic temperatures to norepinephrine, acetylcholine and prostaglandin F2 alpha. 53 85

The effects of hypothermia (4 degrees C) on the components of the cholinergic system of the ileal longitudinal muscle and the adherent Auerbach's plexus of the guinea pig ileum have been investigated. Acetylcholine (ACh) content of the muscle was determined by pyrolysis-gas chromatography. It decreased from 119 to a fairly steady level of 16 nmol/g of wet tissue during the first 72 h of cold storage at 4 degrees C under anoxic conditions. Concomitantly, responsiveness to intramural electrical stimulation decreased by 72%. Cholinesterase (ChE) and choline acetyltransferase (ChA) activities each dropped by 40% during this period. However, the de novo synthesis of ACh over the period of study did not change significantly. The response of the preparation to the exogenously applied ACh remained fairly constant suggesting that the changes in the cholinergic receptor are not accountable for the decrease in responsiveness to intramural stimulation. From the results of this study, it has been concluded that cold storage for 5 days leads to: (1) a significant decline in ACh content within 72 h of storage; (2) a decrease in ChE and ChA activities; (3) no significant effect on the cholinergic receptor; and (4) a decrease in responsiveness to intramural electrical stimulation which is probably due to a malfunction of the ACh-releasing mechanism.
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PMID:Effects of cooling on the levels of acetylcholine, cholinesterase, choline acetyltransferase and the intramural electrical stimulation on the guinea pig ileum. 62 70

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

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

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

To characterize the hypothermia-induced changes in the activity and kinetic constants for muscarinic receptors, we investigated the effects of hypothermia on the onset and offset of action of phenoxybenzamine from the muscarinic receptors of the longitudinal muscle of the guinea-pig isolated ileum. At 37 degrees C, the onset of phenoxybenzamine action was very rapid (less than 5 min) and there was no apparent recovery of the response to ACh 70 min after washing off the phenoxybenzamine. However, the onset at 24 degrees C was very slow (30 min) and there was a complete recovery of the response to ACh 40 min after washing off the unoccluded phenoxybenzamine. We concluded that the lack of reversibility of the effects of phenoxybenzamine at 37 degrees C is due to the predominance of covalent binding between the receptors and phenoxybenzamine whereas at 24 degrees C the blockade of the muscarinic receptor by phenoxybenzamine is mainly due to simple occlusion.
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PMID:The effects of hypothermia on the blockade of muscarinic receptors by phenoxybenzamine. 339 77

We have investigated the ability of three hyperthermic stimuli (PGE2, 5-HT and ACh) to elicit hyperthermia in the Helium-Cold (He-Cold) hypothermic hamster. Hamsters in these conditions are poikilothermic and will passively follow room temperature in a regulated cold room. Animals were injected centrally at AH/POA sites via an indwelling guide tube at body temperatures maintained between 9-12 degrees C. Active sites in the AH/POA were determined prior to the experiment by PGE2 injection. PGE2 injection at an effective AH/POA site immediately reversed the anesthetic induced hypothermia in warm air. Hamsters were induced into hypothermia by the He-Cold induction method and body temperatures were maintained in a 9 degrees C cold room. Colonic temperatures were monitored at 5 minute intervals by a YSI thermistor probe and telethermometer. Central injections of 5-HT (2 micrograms/microliter) and ACh (50 micrograms/microliter) at effective AH/POA sites evoked significant increases in colonic temperature in He-Cold hamsters. PGE2 injections were not different from saline control injections and did not elicit pronounced temperature changes in these animals. Specific blockade of the 5-HT and ACh temperature increases was demonstrated with specific antagonist injections. The results suggest that the central organization of heat-gain mechanisms in the AH/POA is the same as normothermic animals even at temperatures well below those previously investigated.
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PMID:Organization of central hyperthermic mechanisms in helium-cold hypothermic hamsters. 346 74

Hamsters in deep experimentally induced hypothermia, at body temperatures between 7 degrees C and 11.5 degrees C, were microinjected with 5-HT and ACh at brain sites in the anterior-preoptic area of the hypothalamus (AH/POA). ACh or 5-HT was injected into an AH/POA site at different starting core temperatures in different groups of hypothermic hamsters. Colonic temperatures (Tc) were maintained, following He-Cold induction, in a temperature controlled environmental chamber and measured with a YSI thermister probe and YSI telethermometer. Injections of either 5-HT or ACh at Tc's between 7.0 degrees C and 9.0 degrees C elicited only modest increases in Tc i.e., 0.3 degrees C--0.6 degrees C, respectively. As Tc increased, however, to ranges between 9.1 degrees C--10.0 degrees C and in different animals to greater than 10 degrees C both ACh and 5-HT at the same sites elicited significant increases in Tc, 1.5 degrees C for 5-HT and 2.2 degrees C for ACh compared to saline injections. These data suggest that at the lowest Tc's we are observing a "cold block" of temperature sensitive sites in the AH/POA. Increasing the starting Tc beyond 9.0 degrees C however, evokes significant increases in heat-gain following AH/POA injection of either ACh or 5-HT. These data are consistent with Myers' observations concerning the organization of heat-gain mechanisms at AH/POA sites. In addition, they suggest that both the afferent limb of the heat-gain circuit (5-HT) and the efferent limb of the circuit (ACh) are functionally impaired when Tc is close to the physiological limit in the He-Cold hypothermic hamster.
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PMID:ACh and 5-HT stimulated thermogenesis at different core temperatures in the He-Cold hypothermic hamster. 386 62

1. An investigation of central cholinoceptors in the mouse has been made by injecting cholinomimetic drugs into the cerebral ventricles and seeing how their effects were modified by prior administration of atropine-like substances and other drugs.2. Carbachol or oxotremorine injected in small doses intracerebroventricularly into conscious mice caused hypothermia, gross tremor and a variety of parasympathomimetic effects including lachrymation and salivation. Acetylcholine injected in this way was active only in much larger doses.3. Methacholine and pilocarpine also caused a variety of parasympathomimetic effects after intracerebroventricular injection but virtually no hypothermia or tremor.4. Nicotine injected intracerebroventricularly caused mild hypothermia, fine tremor but no parasympathomimetic effects.5. Atropine-like drugs, tricyclic antidepressants and amphetamine antagonized the hypothermia induced by intracerebroventricular carbachol or oxotremorine.6. The sites of action of the atropine-like drugs are in the brain; those of the tricyclic antidepressants and amphetamine are in the periphery probably on heat generating beta-adrenoceptor mechanisms.7. It is concluded that the atropine sensitive cholinoceptors in the brain vary in their sensitivities to cholinomimetic drugs, other than acetylcholine, and may exist in isoreceptor forms.8. Peripheral atropine sensitive cholinoceptors may also exist in isoreceptor forms.
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PMID:Investigation of central cholinergic mechanisms in the conscious mouse. 558 Jun 97


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