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)

The total, free and unprecipitated activity of lysosomal (acid DNAase, acid RNAase, acid phosphate, acid beta-galactosidase) and peroxisomal (catalase, oxidase of D-amino acids) enzymes were studied in dog kidney cortex during storage of the tissues in solution of rheopolyglucin and under conservation of the kidney tissue by transrenal gas perfusion in hypothermia within 3 and 7 days. Labilization of lysosomal and peroxisomal membranes was observed during storage both in unperfused and in oxygenated kidney. Mechanisms of formation and functional significance of the alterations observed in structure of lysosomes and peroxisomes are discussed.
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PMID:[Labilization of lysosomal and peroxisomal membranes in the kidneys preserved by transrenal gas perfusion]. 1 22

Postoperative neurological deficit may result from ischaemic or hypoxic hypoxaemia. Postural cerebral hypoperfusion may ensue when a pre-existing asymptomatic vascular anomaly in combination with rotation of the head for surgical positioning compromises cerebral blood flow. CASE REPORT. A 30-year-old man was referred for recraniotomy for glioblastoma. Following uneventful induction of anaesthesia, increased diuresis and progressive hypothermia were observed. The postoperative period was complicated by a seizure, followed by apnoea requiring reintubation of the trachea. A CAT scan revealed global cerebral oedema with subtotal compression of the third ventricle. Intracranial pressure was 60 mm Hg as measured by an epidural probe. On the 1st postoperative day clinical and electroneurophysical signs of brain death were observed; the patient underwent organ explantation the next day. PATHOLOGY. Pathological examination revealed pronounced global hypoxaemic lesions and an S-shaped internal carotid artery with intimal proliferation (Fig. 1). The diagnostic conclusion was cerebral ischaemia following carotid occlusion caused by carotid kinking and completed by surgical positioning (rotation of the head). CONCLUSION. Carotid kinking is a rare abnormality, and patients at risk may not be identified preoperatively. Though it is questionable whether this disaster could have been prevented at all, electroneurophysiological monitoring would have been the only early monitoring system capable of detecting diminishing cerebral blood flow. Although a request for routine intraoperative neurophysiological monitoring seems unrealistic at present, it has to be acknowledged that only such monitoring could have provided the information needed to save this patient.
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PMID:[A fatal intraoperative cerebral ischemia following kinking of the internal carotid artery?]. 163 22

The incidence of renal cell carcinoma with a vena caval tumour thrombus has been reported in the literature, form 4% to 19%. Vena caval involvement causes serious diagnostic and therapeutic problems. Surgical treatment is usually conditioned by the tumor thrombus cranial extension and the possible invasion of the vena caval wall. Using Diagnostic Imaging (ECHO, CAT, MRI) we are able to establish the real presence, dimension and extension of the tumor thrombus, but we can not evaluate precisely its nature or the infiltration of the vena caval wall. We report our own experience in 27 patients with renal cell carcinoma extending into the vena cava (22 cases with tumor thrombus extending under the diaphragm and 5 cases over the diaphragm) and describe our favourite approach for thrombus extending into the right atrium using extracorporeal circulation, profound hypothermia and cardiac arrest (3 cases). From our data, we believe that the vena cava involvement doesn't make the prognosis any worse, if it isn't associated with the infiltration of the vena caval wall and nodal disease.
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PMID:[Surgical treatment of caval thrombosis caused by parenchymal renal neoplasms]. 183 Jun 71

The effect of aminotriazole (AT), inhibitor of catalase activity, on hypothermia and narcosis induced by ethanol and on the acquisition of tolerance to the ethanol hypothermic and narcotic effect was studied. Rats were pretreated with AT (1 g/kg IP) 1 hour before the test dose of ethanol (2.76 g/kg IP) and narcosis time, hypothermia and ethanol blood levels evaluated (first test). For studies on tolerance to ethanol, rats of the first test received daily (for 7 days) a dose of AT (1 g/kg IP) 1 hour before ethanol (2.76 g/kg) given by gavage, and the same parameters evaluated (8th day test). Results were compared to similar groups of rats without AT pretreatment (controls, 1st and 8th day test). Rats pretreated with AT exhibited a shorter narcosis time induced by ethanol but this treatment did not alter the hypothermic effect of ethanol nor ethanol disposal rate. Chronic ethanol treatment induced tolerance to the narcotic and hypothermic effect of ethanol as well as a metabolic tolerance. AT administered daily before the dose of ethanol produced a partial blockade of the development of tolerance to the narcotic effect of ethanol, but did not alter the development of hypothermic or metabolic tolerance. The brain catalase system seems to play a role in narcosis and on the development of tolerance to this effect of ethanol, but not in the hypothermic effect or in the development of tolerance to this ethanol effect. Since the inhibition of liver catalase activity by AT treatment was not correlated with changes in ethanol disposal rate, the liver catalase system appears not to play a role in the metabolic tolerance.
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PMID:Effect of 3-amino-1,2,4-triazole on the hypothermic effect of ethanol and on ethanol tolerance development. 187 89

Canine thyroid tissue (CTy) was subjected to hyperbaric oxygen culture (HOC) under conditions that affect immunoalteration in murine thyroid tissue (MTy). Survival of autografts and allografts implanted under the kidney capsule was determined after 21 days by 125I uptake and histology. Unlike MTy, autograft CTy subjected to normothermic HOC (95% O2, 5% CO2; 1.76 kg/cm2) for 48 h did not survive (0/8) whereas decrease of culture duration to 24 h resulted in autograft CTy survival (3/3). Under hypothermia (5 degrees C), HOC could be extended to 7 days with autograft CTy survival (3/3 after 4 days and 3/3 after 7 days). Allograft CTy after 24 h of normothermic HOC and 7 days of hypothermic HOC was rejected. Indicators of oxygen free radical injury were determined:catalase activity was comparable in MTy and CTy (means 14.82 and 6.3-10.8 mm/mg protein, respectively) but superoxide dismutase activity was low in CTy (means 0.01-0.29 and 4.75 U/mg protein, respectively). Malondialdehyde content after 48 h of normothermic HOC was higher in CTy than in MTy (means 2215 and 1275 nmol/g, respectively). The results show that CTy is injured by HOC under conditions tolerated by MTy, and that this difference is related to the greater sensitivity of CTy to oxygen free radical injury.
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PMID:A comparison of the effects of hyperbaric oxygen culture on survival of murine and canine thyroid gland grafts. 191 Apr 28

It has been proposed that ethanol can be oxidized in brain via the peroxidatic activity of catalase and that centrally formed acetaldehyde may mediate several of the psychopharmacological actions of ethanol. The present study was designed to investigate the role of brain catalase in the mediation of ethanol-induced narcosis, hypothermia and lethality in rats. Rats were pretreated with the catalase inhibitor 3-amino-1,2,4-triazole (AT) or saline. Five hours later, animals in each pretreatment group received IP injections of ethanol (3 or 4 g/kg). Ethanol-induced narcosis was significantly attenuated in AT-pretreated rats compared to the saline control group. As well, AT pretreatments reduced significantly the lethal effect of these ethanol doses. However, AT-pretreated ethanol-injected animals significantly reduce their body temperature as compared to the saline-ethanol animals. Blood ethanol determinations revealed that AT did interfere with ethanol metabolism. AT inhibits significantly brain catalase activity at all doses used in this study. The results indicate a role for brain catalase in ethanol effects. Furthermore, they suggest that catalase may be involved in the oxidation of ethanol in brain and that centrally formed acetaldehyde may play a role in ethanol-induced narcosis and lethality, but not hypothermia.
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PMID:Effect of 3-amino-1,2,4-triazole on ethanol-induced narcosis, lethality and hypothermia in rats. 192 13

Cytotoxicity resulting from the interaction of fluorescent light from a flow hood with Hepes-buffered cell culture medium at room temperature was demonstrated. Toxicity was prevented by keeping both cells (V79 Chinese hamster) and medium shielded from direct fluorescent light ("dark conditions") or by supplementing the medium with 10 micrograms/ml catalase; this suggests that extracellular hydrogen peroxide is a major cause of the lethal effect under "lighted conditions." No sensitization resulted from the exposure of cells in a sodium bicarbonate (SBC)-buffered medium to fluorescent light, nor in a catalase supplemented SBC-buffered medium. The Hepes/light reaction during routine cell manipulations presensitized cells to hypothermia damage in the dark with the presensitization being more severe for 5 than for 10 degrees C hypothermic exposure. Presensitization was prevented by performing the complete experiment under dark conditions or by supplementing the medium with 10 micrograms/ml catalase. However, catalase did not improve the hypothermic survival when experiments were performed under dark conditions. Hence, 10 micrograms/ml catalase does not protect cells from hypothermic (5 and 10 degrees C) damage per se, but rather from Hepes/light sublethal damage which interacts with hypothermic sublethal damage to result in lethal lesions. Additionally, under dark conditions, superoxide dismutase (SOD), allopurinol, catalase plus SOD, DMSO, or mannitol did not improve survival when present during hypothermic storage, suggesting that extracellular superoxide anion, hydrogen peroxide, or hydroxyl radicals are not the cause of cell killing under conditions of pure hypothermia uncomplicated by prehypothermic ischemia or hypoxia.
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PMID:Factors influencing survival of mammalian cells exposed to hypothermia. V. Effects of hepes, free radicals, and H2O2 under light and dark conditions. 201 62

In the feline intestine studies have implicated superoxide (O.-) and other oxygen derived free radicals as initiators of injury as measured by increased capillary permeability during the reperfusion period. Biochemical mechanisms of this free radical generation include: xanthine oxidase dependent O.- production, hydrogen peroxide (H2O2) formation by superoxide dismutase (SOD), hydroxyl radical (OH-) production via the Haber-Weiss reaction, and lipid radical formation from membrane peroxidation. Pathological consequences of these events include inflammatory neutrophil infiltration, damage to the collagen and mucosal basement membrane, increased capillary permeability, edema, cell degeneration and necrosis. Animal models of neonatal necrotizing enterocolitis (NNEC) indicate that intestinal injury occurs after the etiologic factors (hypothermia, hypoxia) are removed. In order to determine the role of active oxygen species in the pathogenesis of NNEC, weanling hamsters and neonatal piglets were cold stressed and activities of pro/antioxidant enzymes were determined, and histopathologic and ultrastructural studies were performed. Cold stressed weanling hamsters showed a 55.7% (P less than 0.05) decrease in xanthine dehydrogenase/xanthine oxidase activity ratio. Light microscopy revealed scattered colonic mucosal erosions and submucosal edema in 50% of cold stressed animals. Transmission electron microscopy demonstrated degeneration of colonic mucosal epithelial cells, enlarged intracellular spaces, cytoplasmic vacuolization, and nuclear membrane swelling. The colonic serosa was also edematous and infiltrated with bacteria. Large intestinal tissue from cold stressed neonatal piglets showed a significant increase (P less than 0.05) in Mn and Cu, Zn, SOD, CAT, GSH-Red, total GSH, and Glc6-PD at 0 and 12 hrs. post stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal post-ischemic reperfusion injury: studies with neonatal necrotizing enterocolitis. 259 24

The release of oxygen free radicals from ischemic myocardium has been implicated as a causative factor of cardiac dysfunction after thermal injury. In this study, isolated coronary perfused guinea pig hearts were used to determine if free radical scavengers improve left ventricular (LV) intrinsic contractile response to burn shock. Parameters measured included peak isovolumic LV pressure (LVP) and maximal rate of LVP rise (+dP/dtmax) and fall (-dP/dtmax) at a constant preload. Control animals were immersed in body temperature water and divided into four groups: Group 1, untreated N = 10; Group 2, control animals treated with unbound superoxide dismutase (SOD), N = 5; Group 3, control animals treated with ficoll-SOD, N = 5; and Group 4, control animals treated with PEG-SOD, N = 5. Scald burn equivalent to 45% of total body surface area was produced in 64 animals. Fluid resuscitation was initiated immediately after burn in all animals, and animals were then divided into seven burn experimental groups. In Group 5, 10 animals were treated with fluid alone, lactated Ringer's, 4 mL/kg/% burn. Burned animals in Group 6 (N = 10) received a reduced volume of Ringer's 2 mL/kg/% burn plus unbound-SOD, 50 mg/kg; 10 animals in Group 7 received this volume of Ringer's plus ficoll-SOD, 50 mg/kg. In groups 8, 9, and 10 animals were given fluid, lactated Ringer's, 2 mL/kg/% burn plus varying doses of PEG-SOD (Group 8: N = 9, 1,000 U; Group 9: N = 10, 6,000 U; Group 10: N = 5, 12,000 U). In Group 11 (N = 10), animals received SOD-PEG, 6,000 U, plus catalase, CAT-PEG, 6,000 U, given with 4 mL/kg/% burn lactated Ringer's solution. Hypotension, hypothermia, and hemoconcentration were similar in all animals after thermal injury, regardless of treatment regimen. Burn hearts showed significantly lower LVP, +dP/dt max, and -dP/dt max than control hearts (P less than 0.05). Compared to controls, coronary pressure and coronary vascular resistance were significantly higher in all treated burn groups. There was no significant difference in heart rate or time to peak pressure or time to maximal contraction or relaxation among the groups. Left ventricular function curves for burned hearts were shifted downward and to the right of curves obtained from control hearts (P less than 0.01), regardless of scavenger treatment. PEG-SOD, 6,000 U, improved left ventricular contractility (+dP/dt) at maximal levels of end-diastolic pressure but deficits in left ventricular pressure and relaxation persisted.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of oxygen-derived free radicals in burn-induced myocardial contractile depression. 322 Aug 65

Previous studies have demonstrated that reactive oxygen species are involved in ischemic injury. The present work was undertaken to determine in vivo the role of xanthine oxidase in the oxygen free radical production during rat liver ischemia and to examine the activity of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) during the same period. Our results indicate a 4-fold increase in xanthine oxidase activity between 2 and 3 hours of normothermic ischemia, in parallel with a decrease in cell viability. Moderate hypothermia delays both events. Under the same conditions, the activity of oxygen radical scavenging enzymes remains unchanged. Moreover, we have compared in vitro the susceptibility of isolated liver cells to an oxidative stress induced by O2.-, H2O2 and .OH. Our results reveal that endothelial cells are much more susceptible to reactive oxygen species than hepatocytes, probably because they lack H2O2-detoxifying enzymes. These findings suggest that xanthine oxidase might play a major role in the ischemic injury mainly at the level of the sinusoidal space where most endothelial cells are located.
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PMID:Deleterious effects of xanthine oxidase on rat liver endothelial cells after ischemia/reperfusion. 748 47


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