Systemic hypothermia

Clifton G. L. (1995) Systemic hypothermia in treatment of severe brain injury a review and update. J. Neurotrauma 12, 923-927. 

In several animal studies severe adverse effects of hypothermia were clotting abnormalities and coagulopathy (22,42). In baboons, systemic hypothermia led to increased bleeding times (43). In men the enzymatic reactions of the coagulation cascade were shown to be strongly inhibited by hypothermia (44,45). However, severe clotting abnormalities have... 

CoolCap Study Group, Selective head cooling with mild systemic hypothermia after neonatal encephalopathy multicentre randomized trial, Lancet, 2005,365 663-670. 

CCK is found in the digestive tract and the central and peripheral nervous systems. In the brain, CCK coexists with DA. In the peripheral nervous system, the two principal physiological actions of CCK are stimulation of gaU. bladder contraction and pancreatic enzyme secretion. CCK also stimulates glucose and amino acid transport, protein and DNA synthesis, and pancreatic hormone secretion. In the CNS, CCK induces hypothermia, analgesia, hyperglycemia, stimulation of pituitary hormone release, and a decrease in exploratory behavior. The CCK family of neuropeptides has been impHcated in anxiety and panic disorders, psychoses, satiety, and gastric acid and pancreatic enzyme secretions. 

O Connor, J.V., Wilding, T., Farmer, P Sher, J., Ergin, M.A., Griepp, R.B. (1986). The protective effect of profound hypothermia on the canine central nervous system dunng one hour of circulatory arrest. Ann. Thorac. Surg. 41, 255-259. 

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. 

Systemic effects of nickel exposure include hyperglycemia, increased levels of plasma glucagon, damage to the pancreatic islet cells, decreased body weight, reduced food and water intake, and hypothermia (NAS 1975 USEPA 1980 USPHS 1993). Acute administration of nickel salts caused prompt hyperglucagonemia and subsequent hyperinsulinemia in rats, rabbits, and guinea pigs (WHO... 

Although the precise mechanism for the hypothermia induced by chlordecone is unknown, data suggest a role of central nervous system (CNS) dopaminergic or a-noradrenergic activity in... 

Exercise is not without risks these include sudden cardiac death, hyperthermia, hypothermia, hypoglycaemia, hypo-natraemia, a reduction in the effectiveness of the immune system, overuse injury and interference in the reproductive system in females. Whether severe physical activity affects the reproductive system in males is sometimes discussed but these are no reports in the scientific literature. 

Degenerative changes were observed in the liver and kidney of rodents exposed to high one-time concentrations of 0.26-1.4g/mL Nonspecific changes in the blood were also observed. Nervous system effects, including excitation, impairment of locomotor activity, listlessness, hypothermia, and convulsions, were observed in mice before death following inhalation exposure to 2 g/rsf ... 

Injection studies have shown that nickel can decrease body temperature (Gordon 1989 Gordon et al. 1989 Hopfer and Sunderman 1988 Watanabe et al. 1990). Because nickel also disturbs the circadian rhythm of temperature regulation, this decrease is thought to result from an effect on the central nervous system. It has been speculated that nickel may mimic the effect of calcium on the hypothalamic thermoregulatory center resulting in hypothermia (Hopfer and Sunderman 1988). 

Serious reactions such as blood dyscrasias, agranulocytosis, leukocytopenia, thrombocytopenia, cholestatic jaundice, neuroleptic malignant syndrome (NMS), constipation or paralytic ileus, priapism, QT prolongation and torsades de pointes, seizure, systemic lupus erythematosusdike syndrome, and temperature regulation dysfunction (heatstroke or hypothermia) occur rarely. 

The major signs of toxicity are ataxia, analgesia, mydriasis (less prominent in monkeys at lower doses), and profound central nervous system (CNS) depression lasting from several hours to several days, depending on dose. At higher doses, the CNS depression may be preceded by CNS stimulation and convulsions. Marked hypothermia at an intravenous dose of 1 mg/kg, hypotension, and respiratory depression are other significant effects of this compound. DMHP produces a... 

All five muscarinic receptor subtypes have been detected in the central nervous system. The roles of Mx through M3 have been analyzed by means of experiments in knockout mice. The Mx subtype is richly expressed in brain areas involved in cognition. Knockout of Mx receptors was associated with impaired neuronal plasticity in the forebrain, and pilocarpine did not induce seizures in Mx mutant mice. The central nervous system effects of the synthetic muscarinic agonist oxotremorine (tremor, hypothermia, and antinociception) were lacking in mice with homozygously mutated M2 receptors. Animals lacking M3 receptors, especially those in the hypothalamus, had reduced appetite and diminished body fat mass. 

Like many other neuropeptides, NT serves a dual function as a neurotransmitter or neuromodulator in the central nervous system and as a local hormone in the periphery. When administered centrally, NT exerts potent effects including hypothermia, antinociception, and modulation of dopamine neurotransmission. When administered into the peripheral circulation, it causes vasodilation, hypotension, increased vascular permeability, increased secretion of several anterior pituitary hormones, hyperglycemia, inhibition of gastric acid and pepsin secretion, and inhibition of gastric motility. It also exerts effects on the immune system. 

NT receptors can be blocked with the nonpeptide antagonists SR142948A and meclinertant (SR48692). SR142948A is a potent antagonist of the hypothermia and analgesia produced by centrally administered NT. It also blocks the cardiovascular effects of systemic NT. 

NPY produces a variety of central nervous system effects, including increased feeding (it is one of the most potent orexigenic molecules in the brain), hypotension, hypothermia, respiratory depression, and activation of the hypothalamic-pituitary-adrenal axis. Other effects include vasoconstriction of cerebral blood vessels, positive chronotropic and inotropic actions on the heart, and hypertension. The peptide is a potent renal vasoconstrictor and suppresses renin secretion, but can cause diuresis and natriuresis. Prejunctional neuronal actions include inhibition of transmitter release from sympathetic and parasympathetic nerves. Vascular actions include direct vasoconstriction, potentiation of the action of vasoconstrictors, and inhibition of the action of vasodilators. 

Narcosis due lo CO is characterized by mental disturbances which may range from confusion, mania, or drowsiness to deep coma, headache, sweating, muscle twitching, increased intracranial pressure, pounding pulse, low blood pressure, hypothermia, and sometimes papilloedcina. The basic mechanisms by which carbon dioxide induces narcosis is probably through interference with the intracellular enzyme systems, which are all sensitive to pll changes. 

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