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)

Neurologic complications after severe brain injuries are the result of primary injuries in the moment of impact and secondary injuries which evolve over the minutes and days later. According to statistics, secondary injuries were documented in about 90 percent of patients who died after traumatic brain injury. Low oxygen delivery in hypotension, hypoxia, oedema, intracranial hypertension or changes in cerebral blood flow all account for development of secondary injuries. Primary injuries are more or less complete, but secondary injuries could be prevented with adequate therapy. Understanding mechanisms of secondary injuries could help identify potentially beneficial therapies. Important elements of therapy are: head position, normoglycemia, osmotherapy, normal body temperature, optimal blood pressure, adequate oxygenation, barbiturate therapy. Neutral head and neck position is recommended to prevent intracranial hypertension. Hyperglycemia with less ATP leads to ishaemic acidosis, hypoglycemia enhances decomposition of phospholipids and release of fat acids, what makes the cellular damage worse. Normocapnia is recommended and adequate oxygenation (PaO2 higher than 90%). To prevent dehydration and electrolyte imbalance, serum electrolytes should be examined every 4-6 h as well as osmolarity. Moderate therapeutic hypothermia could be of benefit, and maintaining of optimal blood pressure (MAP above 90 mmHg), especially in the first period after injury. As these have a lot of adverse effects, barbiturates are recommended only when conventional therapies show no effect. Patients should be hydrated well before induction of barbiturates. In organized trauma centers and with adequate intensive care the mortality from traumatic brain injury decreased from 50% in 1970, to about 30% now days.
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PMID:[Prevention of secondary brain injuries]. 1501 66

A 15-year-old female with short intestine syndrome due to chronic intestinal pseudo-obstruction associated with kidney failure underwent a multivisceral (stomach-duodenum-jejunum-ileum-pancreas-liver) and kidney transplant. She had required parenteral nutrition for the last 5 years, with numerous complications such as sepsis from the central catheter, deep venous thrombosis, severe liver dysfunction, pancytopenia due to bone marrow failure, and severe malnutrition. Surgery lasted 15 hours and was free of complications other than hypothermia, which worsened after revascularization of the grafts. Replacement of 6 units of blood products and crystalloids was required. Biochemical and hemodynamic variables were stable, apart from the development of hypernatremia, hyperglycemia, and lactic acidosis. The anesthetic approach included preoperative assessment of problems related to chronic parenteral nutrition (liver dysfunction, coagulopathy, and restricted venous access), the prevention of hypothermia, correction of electrolyte imbalance and the acid-base status, treatment of reperfusion syndrome, and the replacement of fluids and blood products to maintain circulatory homeostasis and assure sufficient splanchnic perfusion.
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PMID:[Anesthesia for a pediatric multivisceral transplant]. 1507 2

As we commemorate the 25th anniversary of the journal Peptides, it is timely to review the functional significance of the bombesin (BB)-like peptides and receptors in the CNS. Over two decades ago we published an article in the journal Peptides demonstrating that BB-like peptides are present in high densities in certain rat brain regions (such as the paraventricular nucleus of the hypothalamus). Subsequently, one of the mammalian forms of BB, gastrin-releasing peptide (GRP) containing cell bodies were found in the suprachiasmatic nucleus of the hypothalamus and nucleus of the solitary tract of the hindbrain. Another related peptide, namely neuromedin (NM)B, was detected in the olfactory bulb and dentate gyrus. BB and GRP bind with high affinity to BB(2) receptors, whereas NMB binds with high affinity to BB(1) receptors. The actions of BB or GRP are blocked by BB(2) receptor antagonists such as (Psi(13,14)-Leu(14))BB whereas PD168368 is a BB(1) receptor antagonist. Exogenous administration of BB into the rat brain causes hypothermia, hyperglycemia, grooming and satiety. BB-like peptides activate the sympathetic nervous system and appear to modulate stress, fear and anxiety responses. GRP and NMB modulate distinct biological processes through discrete brain regions or circuits, and globally these peptidergic systems may serve in an integrative or homeostatic function.
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PMID:Bombesin-like peptides and associated receptors within the brain: distribution and behavioral implications. 1513 70

Amitraz is an insecticide/acaricide of formamidine pesticides used worldwide to control ectoparasites in animals. Amitraz poisoning is a rare disorder characterized by central nervous system (CNS) and respiratory depression, bradycardia, hypotension, hypothermia, hyperglycemia,nausea and vomiting. Poisoning may occur either by oral inhalation and dermal route. In this study, we present seven pediatric patients with amitraz poisoning. The initial symptoms were unconsciousness, dizziness and vomiting; and emerged within 30-150 minutes. The length of stay in the intensive care unit (ICU) was between 18-62 hours.
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PMID:Amitraz poisoning: clinical and laboratory findings. 1518 Dec 99

The aggravating effect of hyperglycemia on ischemic brain injury can be mimicked in a model of in vitro ischemia (IVI) using murine hippocampal slice cultures. Using this model, we found that the damage in the CA1 region following IVI in the absence or presence of 40 mm glucose (hyperglycemia) is highly temperature dependent. Decreasing the temperature from 35 to 31 degrees C during IVI prevented cell death, whereas increasing the temperature by 2 degrees C markedly aggravated damage. As blockade of the mitochondrial permeability transition (MPT) is equally effective as hypothermia in preventing ischemic cell death in vivo, we investigated whether inhibition of MPT or of caspases was protective following IVI. In the absence of glucose, the MPT blockers cyclosporin A and MeIle4-CsA but not the immunosuppressive compound FK506 diminished cell death. In contrast, following hyperglycemic IVI, MPT blockade was ineffective. Also, the pan-caspase inhibitor Boc-Asp(OMe)fluoromethyl ketone did not decrease cell death in the CA1 region following IVI or hyperglycemic IVI. We conclude that cell death in the CA1 region of organotypic murine hippocampal slices following IVI is highly temperature dependent and involves MPT. In contrast, cell death following hyperglycemic IVI, although completely prevented by hypothermia, is not mediated by mechanisms that involve MPT or caspase activation.
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PMID:The temperature dependence and involvement of mitochondria permeability transition and caspase activation in damage to organotypic hippocampal slices following in vitro ischemia. 1614 40

Neuroprotection of patients with acute ischemic stroke should start at the scene and continue in the ambulance with the assessment and treatment of the airway, breathing, circulation, body temperature, and blood glucose. The key goal in eligible patients should be fast vessel recanalization with intravenous recombinant tissue-type plasminogen activator Results from a meta-analysis suggest that systemic thrombolysis is effective when given within 4.5 hours after stroke onset. The time window extends to 6 hours for patients undergoing intravascular thrombolysis. Acute stroke patients should be admitted to stroke care units. A crucial component of neuroprotection is the prevention of secondary brain damage, which can be caused by hypoxemia, hypotension, hyperthermia and hyperglycemia. This can be achieved by avoiding complications, e.g. aspiration, and intensive control of oxygenation, hydration and blood pressure, body temperature, blood glucose, and cardiac monitoring. Neuroprotective agents are designed to try to salvage brain tissue within the penumbra. Thus far, despite promising preclinical studies, clinical trials with neuroprotective drugs in acute ischemic stroke have been disappointing. However, we have been able to identify many of the factors that were responsible for these failures, and better-designed clinical trials with neuroprotective drugs should look more promising. Mild induced hypothermia is another form of neuroprotective treatment that is currently being investigated in acute stroke.
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PMID:Neuroprotection in acute ischemic stroke. 1625 52

Erycibe henryi Prain ("Ting Kung Teng"), a species of Convolvulaceae, has been used in Chinese medicine to relieve pain involving the musculoskeletal system, such as arthritis, sciatica, and traumatic tissue swelling. E. henryi can be mistaken for another herbal plant, Tripterygium wilfordii Hook F, used to treat gouty arthritis. We report here three cases of E. henryi poisoning. All three cases presented with vomiting, diarrhea, salivation, diaphoresis, lacrimation, and rhinorrhea; two patients also had miosis, hypothermia, bradycardia, hypotension, and ventricular tachyarrhythmias. Laboratory abnormalities included leucocytosis, hyperglycemia, hyperamylasemia, hypocalcemia, and transiently elevated liver enzymes, creatinine and creatinine phosphokinase. The active constituents of E. henryi include several tropane alkaloids, which exhibit cholinergic activities. Gastrointestinal disturbances and ventricular tachyarrhythmias may occur with ingestion of either E. henryi or T. wilfordii, but the cholinergic symptoms can help to differentiate them.
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PMID:Acute Erycibe henryi Prain ("Ting Kung Teng") poisoning. 1649 97

Neurologic complications after severe brain injuries are the result of primary injuries in the moment of impact and secondary injuries which evolve over the minutes and days later. According to statistics, secondary injuries were documented in about 90 percent of patients who died after traumatic brain injury. Low oxygen delivery in hypotension, hypoxia, oedema, intracranial hypertension or changes in cerebral blood flow all account for development of secondary injuries. Primary injuries are more or less complete, but secondary injuries could be prevented with adequate therapy. Understanding mechanisms of secondary injuries could help identify potentially beneficial therapies. Important elements of therapy are: head position, normoglycemia, osmotherapy, normal body temperature, optimal blood pressure, adequate oxygenation. barbiturate therapy. Neutral head and neck position is recommended to prevent intracranial hypertension. Hyperglycemia with less ATP leads to ishaemic acidosis, hypoglycemia enhances decomposition of phospholipids and release of fat acids, what makes the celulare damage worse. Normocapnia is recommended and adequate oxygenation (PaO2 higher than 90%). To prevent dehydration and electrolyte imbalance, serum electrolytes should be examined every 4-6 h as well as osmolarity. Moderate therapeutic hypothermia could be of benefit, and maintaining of optimal blood pressure (MAP above 90 mmHg), especiallz in the first period after injury. As thez have a lot of adverse effects, barbiturates are recommended only when conventional therapies show no effect. Patients should be hydrated well before induction of barbiturates. In organized trauma centers and with adequate intensive care the mortality from traumatic brain injury decreased from 50% in 1970, to about 30% nowdays.
...
PMID:[Prevention of secondary brain injury]. 1652 33

Cardiopulmonary bypass (CPB) is associated with surgical stress, hypothermia, hyperoxia, enhancement of neuroendocrine outflow, and administration of glucogenic catecholamines that are associated with glucogonolysis and glucogenesis that result in hyperglycemia. The hyperglycemic state during CPB has been associated with adverse outcomes, such as infection, neurological impairment, cardiac dysfunction, prolonged hospitalization, and higher mortality rates. This report justifies vigilant monitoring of blood glucose levels and a rational protocol for the treatment of hyperglycemia of all open heart surgical patients that may improve post-CPB surgical outcomes.
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PMID:Hyperglycemia as an effect of cardiopulmonary bypass: intra-operative glucose management. 1692 93

Maneb, manganese ethylene-bis-dithiocarbamate, is a fungicide pesticide used in the agriculture and bulb flower culture sector. Toxicological effects for humans have been reported in literature and are diverse. They vary from allergic reactions (dermatitis, conjunctivitis, and bronchitis), central nervous system effects (muscarinic, nicotinic, central and extrapyramidal) and renal toxicity (acute renal failure).A 7-year old girl was admitted to the pediatric intensive care unit because of status epilepticus. Physical examination showed respiratory insufficiency, convulsions, and severe hypothermia (32.5 degrees C). The patient was intubated and her convulsions were successfully treated with benzodiazepines. Except for a combined metabolic and respiratory acidosis and hyperglycemia, diagnostic investigations on admission (full blood count, electrolytes, liver and renal functions, cerebrospinal fluid investigation, toxicology screening of blood and urine for barbiturates and benzodiazepines, blood culture, herpes PCR, and a CT scan of the brain) were normal. Within 24 hours, there was a complete recovery of all neurological signs. Within 72 hours, the patient was discharged from the hospital. Liquid chromatography-mass spectrometric investigation of her blood showed amounts of maneb, which can explain all symptoms and signs. However, effects of this magnitude on the central nervous system have not previously been reported in humans.
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PMID:Life threatening central nervous system manifestations and hypothermia due to maneb intoxication in a child: a case report. 1716 99


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