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)

Combined azaperone and metomidate anaesthesia has been used in 86 surgical procedures on 84 piglets, either as such or deepened and prolonged. 51 animals were sacrificed at the end of the procedure as planned before. The anesthesia allowed the performance of various short and long operations. Out of the 33 remaining pigs, submitted to 35 operations, 4 died during the procedure of a technical fault; 2 did not recover from a deep hypothermia (below 10 degrees C); 1 died from the hepatic coma induced through the operative procedure. The other 26 awoke and recovered spontaneous breathing within 1-4 h following the type of anaesthesia and operating procedure they had submitted, which dured from 15 to 330 min.
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PMID:Combined azaperone and metomidate anaesthesia in liver transplantation in the pig. 0 80

Hypothermia is a grave prognostic finding in hepatic coma. Occasionally, it is found in patients whose conditions are stabilized clinically or are improving. When hypothermia occurs, the patients usually die within 24 to 48 hours. All of the patients described herein who eventually improved sufficiently to be discharged from the hospital achieved normal temperatures.
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PMID:Hypothermia, a grave prognostic sign in hepatic coma. 76 Jun 72

The spontaneous course of the galactosamine-hepatitis in the guinea-pig (750 and 1000 mg/kg GalN iv respectively) is characterized by a terminal hypoglycemia together with hypothermia and arterial hypotension fifty-nine hours on average after GalN-application. Preventing hypoglycemia and hypothermia by continuous intravenous infusion of a glucose solution and by increasing room temperature, the animals do not develop hepatic coma, but show an increasing disturbance of the righting reflex and survive at least seventy-two hours. Plasma biochemical tests and liver histology reflect severe hepatic damage. A twofold increase of the liver weight is caused by raised water and lipid content combined with a concomitant depletion of liver glycogen. Pharmacological studies with 14C-Pentobarbital result in a distinctly diminished clearance and in a prolonged half life while the cytochrome P-450 content of the liver shows a moderate decrease. In animal models of acute liver failure the possible incidence of hypoglycemia, arterial hypotension and hypothermia should be considered.
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PMID:[Galactosamine-induced acute liver failure in the guinea pig--spontaneous course and controlled study conditions]. 371 20

The criteria of brain death established by Japanese Society of EEG in 1974, necessitates a prerequisite; be applicable only to "acute destructive, primary gross lesion of brain". Namely, because of insufficient clinical data, secondary brain lesion such as post-anoxia, intoxication, metabolic coma and some kinds of CNS infection were excluded for the object to determine brain death. The criteria published by others also describe that etiology of coma should be clarified, and that careful measures are necessary to diagnose brain death if the cause of coma is unknown. In the present study, it was investigated that whether a clinico-pathological entity of brain death could exist universally regardless of the etiology, and by what means it could be defined clinically. The patients suffering from nondestructive, secondary brain lesions and who showed "brain death-like state" were selected for the study. ("Brain death-like state" requires coma, dilated nonreactive pupis and arrest of respiration concomitantly for more than 6 hours.) And 25 patients were collected, whose underlying diseases were post-anoxia or shock, CO intoxication, Paraquat poisoning, near-drowning or suffocation, hepatic coma, accidental hypothermia and sepsis, with or without the episode of cardiac arrest. Though all the patients died from 1 to 13 days after the insult, clinical signs of brain death-like state were not always irreversible. Isoelectric EEG was obtained on that state in 11 patients and repeated EEG revealed no return on those patients. But another 5 patients showed EEG activity when brain death was strongly suspected clinically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain death in secondary brain lesion]. 665 91

The completely hepatectomized rat has frequently been used as a model to study changes in the economy of norepinephrine (NE) and dopamine (DA) in hepatic coma. Hypothermia characteristically develops in hepatectomized rats and also occurs in patients in hepatic coma and is associated with improved survival in both. The aims of the present study were to measure both release and uptake of NE and release of DA in brain in warm (37 degrees C) and cool (30-32 degrees C) rats at 3-5 h after laparotomy or hepatectomy. Ventriculocisternal perfusions of the brain were performed on rats under basal conditions and during releases evoked by 40 mM K+. Basal releases of NE and DA and evoked release of DA were greater in the warm hepatectomized rats than in all other groups. In some studies, 10(-5) M amitriptyline was added to the perfusates to assess whether neuronal uptake was changed after hepatectomy. Uptake of released NE was equally robust in cool hepatectomized as in cool laparotomized rats but could not be measured in warm hepatectomized rats because of amitriptyline toxicity in these rats. Decreases in NE and increases in DA content were found in most areas of the brain after perfusion. Increased releases of NE and DA may contribute to the pathogenesis of hepatic encephalopathy.
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PMID:Releases of norepinephrine and dopamine in ventriculocisternal perfusions in hepatectomized and laparotomized rats. 859 26

Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. When ICP increases above 20 mmHg it may damage neurons and jeopardize cerebral perfusion. If such a condition persists, treatment is indicated. Control of ICP requires measurement, which can only be performed invasively. Standard techniques include direct ventricular manometry or measurement in the parenchyma with electronic or fiberoptic devices. Displaying the time course of pressure (high-resolution ICP tonoscopy) allows assessment of the validity of the signal and identification of specific pathological findings, such as A-, B- and C-waves. When ICP is pathologically elevated--at or above 20-25 mmHg--it needs to be lowered. A range of treatment modalities is available and should be applied with consideration of the underlying cause. When intracranial hypertension is caused by hematoma, contusion, tumor, hygroma, hydrocephalus or pneumatocephalus, surgical treatment is indicated. In the absence of a surgically treatable condition, ICP may be controlled by correcting the patient's position, temperature, ventilation or hemodynamics. If intracranial hypertension persists, drainage of CSF via external drainage is most effective. Other first-tier options include induced hypocapnea (hyperventilation; paCO2 < 35 mmHg), hyperosmolar therapy (mannitol, hypertonic saline) and induced arterial hypertension (CPP concept). When autoregulation of cerebral blood flow is compromised, hyperoncotic treatment aimed at reducing vasogenic edema and intracranial blood volume may be applied. When intracranial hypertension persists, second-tier treatments may be indicated. These include 'forced hyperventilation' (paCO2 < 25 mmHg), barbiturate coma or experimental protocols such as tris buffer, indomethacin or induced hypothermia. The last resort is emergent bilateral decompressive craniectomy; once taken into consideration, it should be performed without undue delay.
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PMID:Prevention and treatment of intracranial hypertension. 1828 35

There is evidence to suggest that integrity of the neurovascular unit may be compromised in acute liver failure (ALF). In order to address this issue from a molecular standpoint, expression of an array of genes coding for key cerebrovascular endothelial cell and tight junction proteins were measured by reverse transcription-polymerase chain reaction in cerebral cortex of rats with ischemic liver failure resulting from hepatic devascularization (portacaval anastomosis followed 24h later by hepatic artery ligation) compared to appropriate sham-operated controls. Expression of P-glycoprotein, endothelin-1, von Willebrand factor, caveolin-1, occludin, and the endothelial nitric oxide synthase isoform (eNOS) were measured in brain extracts from rats with ALF at coma/edema stages of encephalopathy. The effects of mild hypothermia (35 degrees C) sufficient to prevent cerebral edema in ALF animals on the expression of these genes were also studied. Brain edema and hepatic coma in normothermic ALF rats was accompanied by selective increases in expression of eNOS. Expression of occludin and von Willebrand factor mRNAs were decreased at coma/edema stages of encephalopathy in ALF rats whereas, expression of other cerebrovascular endothelial cell markers endothelin-1, P-glycoprotein, and caveolin-1 were unaffected. Mild hypothermia led to normalization of brain water content and of eNOS mRNA. However, the correlation between increased eNOS expression and encephalopathy/edema grade was poor suggesting the existence of additional mechanisms. These findings underscore the multifactorial nature of brain edema/encephalopathy mechanisms in ALF and question the role of BBB breakdown as a major pathogenetic factor.
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PMID:Alterations in expression of genes coding for proteins of the neurovascular unit in ischemic liver failure. 2020 Nov 30

Acute liver failure (ALF) or fulminant hepatic failure represents a serious life-threatening condition. ALF is characterized by a significant liver injury that leads to a rapid onset of hepatic encephalopathy (HE). In ALF, patients manifest rapid deterioration in consciousness leading to hepatic coma together with an onset of brain edema which induces high intracranial pressure that frequently leads to herniation and death. It is well accepted that hyperammonemia is a cardinal, but not the sole, mediator in the pathophysiology of ALF. There is increasing evidence that neurosteroids, including the parent neurosteroid pregnenolone, and the progesterone metabolites tetrahydroprogesterone (allopregnanolone) and tetrahydrodeoxycorticosterone (THDOC) accumulate in brain in experimental models of ALF. Neurosteroids in ALF represent good candidates to explain the phenomenon of "increased GABAergic tone" in chronic and ALF, and the beneficial effects of benzodiazepine drugs. The mechanisms that trigger brain neurosteroid changes in ALF are not yet well known, but could involve partially de novo neurosteroidogenesis following activation of the translocator protein (TSPO). The factors that contribute to TSPO changes in ALF may include ammonia and cytokines. It is possible that increases in brain levels of neurosteroids in ALF may result in auto-regulatory mechanisms where hypothermia may play a significant role. Possible mechanisms that may involve neurosteroids in the pathophysiology of HE, and more speculatively in brain edema, and inflammatory processes in ALF are suggested.
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PMID:GABAergic neurosteroids: the "endogenous benzodiazepines" of acute liver failure. 2204 Nov 64