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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type A Aortic Dissection is a medical-surgical emergency which requires prompt diagnosis and adequate treatment. Since its inception--more than 40 years ago--the surgical treatment has evolved up until now, when it offers an immediate solution to the high mortality rate due to complications, with acceptable morbidity and mortality rates. This improvement is due also to better diagnostic techniques, postoperative management and profound hypothermia with circulatory arrest. The basic techniques to achieve this consist of resection of the entry tear and closure of the false lumen and repair of the aortic regurgitation when present. Failure of them--proximally or distally--leads to persistence of the false lumen and the possibility of complications or late reoperations. The long-term follow-up, monitorized by non-invasive methods, is mandatory to decide the proper management.
Rev Esp Cardiol 1996
PMID:[Surgery of type A acute aortic dissection. Past, present and future]. 905 38

The neuropharmacological profile of the total fungal extract of F. moniliforme (FM) has been investigated. FM produced dose related decrease in spontaneous motor activity (SMA) and exploratory activity, potentiated pentobarbitone hypnosis and the anticonvulsant actions of phenobarbitone and phenytoin against MES seizures, potentiated PTZ and tryptamine seizures, antagonised reserpine induced syndrome, attenuated tetrabenazine and morphine induced catalepsy and potentiated haloperidol catalepsy. FM showed per se antinociceptive activity and potentiated morphine analgesia. It increased rectal temperature, antagonised reserpine and apomorphine hypothermia and potentiated the hyperthermic response of haloperidol and 5-hydroxytryptophan (5-HTP) and hypothermic response of betaphenylethylamine (PEA) and L-dopa. FM had no per se effect on amphetamine lethality, but enhanced the lethality induced by morphine in aggregated animals. Stereotypy by amphetamine was potentiated while that of apomorphine was not affected. The behavioural response of 5-HTP and L-dopa was potentiated. FM had no effect on swim induced behavioural despair. The effect on aggressive behavior was complex, and while the cumulative aggressive score was reduced, the onset of fighting behaviour and contact period was increased. It also inhibited clonidine induced auto mutilation. Since earlier investigation had shown that FM, like nialamide, induced non-selective inhibition of monoamine oxidase (MAO), the results were compared with those induced by nialamide. A comparative profile of action reveals that the neuropharmacological action of FM are qualitatively similar to those induced by nialamide, and likely to be due to inhibition of MAO. The investigation has practical implications because F. moniliforme is a common contaminant of cereals and fruits.
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PMID:Neuropharmacological studies on Fusarium toxins--I: Total toxin extract from Fusarium moniliforme. 906 73

The effects of the GABAA receptor antagonists, pentylenetetrazol, bicuculline, and picrotoxin, the glycine antagonist, strychnine, and the NMDA receptor antagonist, memantine, on ethanol-induced behavioral sleep and body temperature were investigated. Pentylenetetrazol, bicuculline, and picrotoxin given prior and following ethanol reduced the behavioral sleep and potentiated the hypothermia caused by ethanol. However, convulsions appeared when bicuculline, but not pentylenetetrazol and picrotoxin, were given following ethanol. After the reversal of unconsciousness in rats without convulsions the animals remained awake throughout the experiments without motor incoordination, hyperexcitability, and sedation, but they were in hypothermia within 12 h. The glycine antagonist, strychnine, given prior or after ethanol had virtually no effect on ethanol-induced behavioral sleep and hypothermia. Ethanol given prior or following strychnine failed to antagonize strychnine-induced convulsions. The NMDA receptor antagonist, memantine, given following ethanol potentiated the behavioral sleep and had virtually no effect on hypothermia induced by ethanol. It is suggested that the ethanol-induced behavioral sleep may be attributed to its ability to enhance the GABAergic mechanisms and to inhibit NMDA-mediated excitatory responses. However, the ethanol-induced hypothermia may be ascribed solely to the facilitation of GABAergic transmission. Further, it is postulated that a bidirectional inhibitory system subserves the regulation of behavioral sleep and convulsions. However, one-way inhibitory system underlies the ethanol-induced hypothermia.
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PMID:Opposite effects of GABAA and NMDA receptor antagonists on ethanol-induced behavioral sleep in rats. 908 18

In the present study we examined the impact of glycolysis and glucose oxidation on myocardial calcium control and mechanical function of fatty acid-perfused rat hearts subjected to hypothermia rewarming. One group (control) was given glucose (11.1 mM) and palmitate (1.2 mM) as energy substrates. In a second group glycolysis was inhibited by iodoacetate (IAA, 100 microM) and replacement of glucose with pyruvate (5 mM), whereas in the third group glucose oxidation was stimulated by administration of dichloroacetate (DCA, 1 mM) and insulin (500 microU/ml). All groups showed a rise in myocardial calcium ([Ca]total in response to hypothermia (10 degrees C). However, [Ca]total was significantly lower both in IAA- and DCA-treated hearts, as compared to controls (2.20 +/- 0.22 and 2.94 +/- 0.20 v 3.83 +/- 0.29 nmol/mg dry wt., P < 0.025). The reduced calcium load in the treated hearts was correlated with higher levels of high energy phosphates. Following rewarming control and DCA-treated hearts still showed elevated [Ca]total, whereas IAA-treated hearts [Ca]total was not different from the pre-hypothermic value. All groups showed a reduction in cardiac output following rewarming. Furthermore, the control group, in contrast to both IAA- and DCA-treated hearts, showed a significant reduction in systolic pressure. These results show that hypothermia-induced calcium uptake in glucose and fatty acid-perfused rat hearts was reduced by two different metabolic approaches: (1) inhibition of glycolysis by IAA while simultaneously by-passing the glycolytic pathway by exogenous pyruvate: and (2) stimulation of glucose oxidation by DCA. Thus, glycolytic ATP is not an essential regulator of sarcolemmal calcium transport under the present experimental conditions. Instead, we suggest that a change in oxidative substrate utilization in favour of carbohydrates may improve myocardial calcium homeostasis during hypothermia and rewarming.
J Mol Cell Cardiol 1997 Feb
PMID:Stimulation of carbohydrate metabolism reduces hypothermia-induced calcium load in fatty acid-perfused rat hearts. 914 Aug 12

From January 1989 through June 1996, 29 patients underwent surgical repair of type A acute aortic dissection. Mean age was 59 +/- 13.5 years (range 25-76 yrs) and 21 patients (72.4%) were male. Nineteen patients (65.5%) had systemic hypertension and 3 (10.3%) Marfan syndrome. One patient (3.4%) had prior surgical repair of descending aortic dissection and CABG. Six patients (20.7%) were operated on in shock. The dissection was limited to the ascending aorta (DeBakey type II) in 12 patients (41.4%). Eleven patients (37.9%) had severe aortic regurgitation. Replacement of the ascending aorta was performed in all cases and extended to include the transverse arch in one. Twenty-three patients (79.3%) were operated upon using a tubular graft (sacron-21, homograft-2) with aortic valve resuspension. In the remaining 6 (20.7%) the aortic valve and root were replaced using a Bentall procedure, modified with a homograft in 3 cases. Five patients (17.2%) had associated surgery: CABG (4) and closure of aortic-atrial fistula (1). Mean cardiopulmonary bypass time was 134 minutes (range 70 to 285 min) and aortic cross-clamp time was 58 minutes (range 23 to 93 min). Hypothermic circulatory arrest for open distal anastomosis was used in 26 patients (89.7%) (mean time 22 min; range 10 to 32 min), with retrograde cerebral perfusion in the last 4 years (18 cases; 62.1%). Hospital mortality was 17.2% (5 patients). Eight patients (27.6%) had hospital morbidity: reexploration for bleeding (4 cases), CVA (3), A-V block necessitating permanent pacemaker (1). The mean time of hospitalization was 18 days (range 9 to 81 days). In the follow-up period (mean 38 mths; range 4 to 94 mths), 2 patients died (CVA and gastrointestinal bleeding) and 4 required hospitalization (perforated duodenal ulcer, peritonitis, suspected endocarditis, supraventricular tachyarrhythmia-1 patient each). All 22 survivors (75.9%) returned to the functional status they had prior to the dissection and 18 of them (81.8%) are in NYHA functional class I. Type A acute aortic dissection is a complex pathology and the postoperative mortality remains significant, but surgery permits good functional recovery and an active life for the survivors.
Rev Port Cardiol 1997 Jun
PMID:[Surgery for acute type-A aortic dissection]. 930 6

Because of advances in surgical and cardiopulmonary bypass techniques it is now possible to definitively repair the vast majority of congenital heart disease in infancy or childhood. Although the majority of survivors do not have obvious cerebral sequelae, there is increasing disquiet about the high incidence of acute neurological events in the immediated postoperative period as well as evidence that at long-term follow-up there are subtle cognitive and motor deficits in many. Some children are more at risk of neurodevelopmental problems, either because of their cardiac (e.g. , extensive aortopulmonary collaterals) or cerebrovascular (e.g., the propensity to large vessel dissection) anatomy or because of genetic predisposition (e.g., to prothrombotic disorders). The incidence may vary with the surgery (e.g., the Fontan operation) and the cardiopulmonary bypass technique necessary to achieve an adequate technical repair (e.g., low or no flow at deep hypothermia). Recognition of the population at risk will lead to prevention of serious sequelae. Data collected in adults may be misleading, and many pediatric units have developed their own practice, but recent studies in animal models of child surgery and in children have produced some evidence to guide management to ensure the optimal cerebral as well as cardiac outcome. Pump flow should be maintained at least 30 ml/kg/min where possible, with inotropic support to maintain blood pressure if necessary. If pump flow must be lowered or circulatory arrest is essential, thorough cerebral cooling to deep hypothermic temperatures is mandatory; a pH-stat strategy may make this easier, but an alpha-stat strategy may be better in those operations that can be performed at moderate hypothermia. There is no evidence that the available pulsatile pumps offer an advantage. Tissue oxygenation may reach critical levels and a high hematocrit and oxygen tension may reduce the risk of significant hypoxia. There is a risk of embolization in children, which can be reduced with membrane oxygenators and careful monitoring; the role of arterial filtration remains controversial. The only protective agent that can currently be recommended is methylprednisolone to protect the spinal cord (e.g., in operations on the aortic arch). Further studies are needed in this important area.
Pediatr Cardiol
PMID:Recognition and prevention of neurological complications in pediatric cardiac surgery. 963 58

Choreoathetosis, seizures, and impaired mental development continue to occur in children undergoing cardiopulmonary bypass (CPB) and profound hypothermia with or without circulatory arrest. Although there is some evidence that the hypothermia itself may be causing these neurologic problems, skepticism remains because of lack of evidence from experimental studies simulating the clinical setting. In this experimental study, we examined the effect of profound and moderate hypothermia on the brain while maintaining normal flow rates during CPB. Ten adult mongrel dogs equally divided into two groups were anesthetized and subjected to CPB and varying levels of hypothermia (group 1, < or = 15 degreesC; group 2, < or = 2 degreesC). Both groups were kept at the desired temperature for 1 hour prior to rewarming and discontinuation of CPB. The dogs were euthanized 4-6 weeks later and neuropathologic studies were performed. The mean CPB flow rates during cooling and at the desired rectal temperature were comparable in both groups: group 1, 108 +/- 10 ml/kg/min versus 106 +/- 7 ml/kg/min in group 2 (p = NS) and 95 +/- 12 ml/kg/min in group 1 versus 101 +/- 5 ml/kg/min in group 2 (p = NS). Because of the difference in temperature between the two groups, the mean cooling time (onset of CPB to desired rectal temperature) was longer in group 1 (70 +/- 14 minutes) than in group 2 (28 +/- 11 minutes, p = 0.007). Hence, the total mean CPB time was also longer in group 1 (198 +/- 25 minutes) than in group 2 (143 +/- 13 minutes, p = 0.002). The lowest mean blood and rectal temperature achieved in group 1 were 11 +/- .9 degreesC and 12 +/- 1 degreesC versus 29 +/- .4 degreesC (p < 0.001) and 30 +/- .6 degreesC (p = 0.001), respectively, in group 2 (p = 0.001). Neuronal loss and degeneration was noted in all dogs in group 1 ranging from 2 to 8 cells per 1000 cells counted compared to none in group 2 (p = 0.05). These lesions occurred in both the basal ganglia and the cortex, although they were more marked in the caudate when compared to the cortex and cerebellum. Both in the cortex and in the caudate, neuronal loss was more marked around the capillaries. We conclude that the use of profound hypothermia of < or =15 degreesC and maintenance of normal flow rates during cooling at this temperature for 1 hour produces neuronal loss and degeneration in the brain. These lesions being more marked around capillaries points to the vulnerability of the neurons, probably because of their high lipid content to injury from the cold perfusate.
Pediatr Cardiol
PMID:Experimental evidence of cerebral injury from profound hypothermia during cardiopulmonary bypass. 970 64

Atrial fibrillation (AF) commonly develops after cardiac valvular surgery. The objective of this study was to identify risk factors for postoperative AF following valvular surgery. A cohort of 915 consecutive adult patients undergoing isolated valvular surgery with preoperative sinus rhythm was analyzed. Univariate and independent multivariate risk factors for postoperative AF were determined. A second cohort of 305 patients with the same inclusion criteria was used to validate the multivariate predictors. Patients studied had a mean age of 56.1 +/- 14.7 years, 57.9% were men, 79.6% had a normal left ventricular ejection fraction, and their mean left atrial size was 46.2 +/- 9.3 mm. The incidence of postoperative AF was 36.7%. Independent predictors of postoperative AF included: advanced age (odds ratio [OR] 1.506 per decade, 95% confidence interval, [CI] 1.35 to 1.68, p = 0.0001); mitral stenosis (OR 2.066, CI 1.21 to 3.52, p = 0.0077); left atrial enlargement (OR 1.468, CI 1.07 to 2.01, p = 0.0165); use of systemic hypothermia (OR 0.572, CI 0.422 to 0.776, p = 0.0003); and a history of cardiac surgery (OR 0.676, CI 0.465 to 0.981, p = 0.0393). Among these variables, advanced age, mitral stenosis, and left atrial enlargement were confirmed as independent risk factors in the validation cohort.
Am J Cardiol 1998 Oct 01
PMID:Analysis of risk factors for development of atrial fibrillation early after cardiac valvular surgery. 978 73

The present study describes a method for rapidly cooling the whole body via its blood pool and tests whether cooling instituted after ischemia has begun can still limit infarction. We also evaluated whether the cardiac protection seen with cooling could be added to that from ischemic preconditioning. Recently it was reported that lowering myocardial temperature by only several degrees greatly slows the extent of myocardial infarction in the beating heart experiencing regional ischemia. To further explore the potential of hypothermia for myocardial protection, rabbits underwent either a 30-, 45- or 60-min coronary artery occlusion and 3-h reperfusion. Blood from a carotid artery was allowed to circulate through a heat exchanger immersed in ice water and return to a jugular vein until the blood temperature in the left atrium reached the target temperature of 35 or 32 degrees C. Furthermore, to elucidate the mechanism of hypothermia's protection, we also examined its effect on isolated cardiomyocytes. Rewarming began upon reperfusion in all protocols. Cooling to 32 degrees C before a 30-min ischemia reduced infarct size from 37.3 +/- 2.5% (n = 6) of the risk zone in normothermic controls to 3.6 +/- 0.3% (n = 6). When cooling was begun 10 or 20 min after the onset of ischemia infarct size was still significantly smaller [8.1 +/- 1.2% and 22.8 +/- 1.8%, respectively (n = 6 in each group)]. Less but significant protection was also seen with cooling to 35 degrees C. Cooling caused only mild bradycardia and hypotension and no apparent arrhythmias. Forty-five min of regional ischemia caused 50.7 +/- 3.3% (n = 6) of risk zone to infarct in untreated hearts. Preconditioning with 5-min ischemia/10-min reperfusion reduced infarct size to 27.5 +/- 2.5% (n = 6). Cooling to 32 degrees C starting 20 min after the onset of ischemia protected the heart (28.7 +/- 2.6% infarction, n = 8), and this protection could be added to the effect from ischemic preconditioning (6.3 +/- 2.3% infarction, n = 6). In the myocyte model, hypothermia and ischemic preconditioning delayed the progressive increase in osmotic fragility that occurs during simulated ischemia in an additive way, but only hypothermia delayed the appearance of contracture suggesting that different mechanisms are involved. Hence blood pool cooling was easily induced and well tolerated and protected the beating heart against infarction even when hypothermia was started after the onset of coronary occlusion. We conclude that hypothermia might be a simple and useful therapy for patients presenting with acute myocardial infarction.
Basic Res Cardiol 1998 Oct
PMID:Mild hypothermia reduces infarct size in the beating rabbit heart: a practical intervention for acute myocardial infarction? 983 49

It was the aim of the present study to investigate the influence of Bretschneider's cardioplegia on norepinephrine (NE) release [determined by high pressure liquid chromatography (HPLC) and electrochemical detection] in isolated perfused guinea-pig hearts. The following resulted were noted. (1) Calcium-dependent exocytotic NE release evoked by electrical field stimulation (12 Hz, 1 min) was completely suppressed after only 3 min of normothermic (37.5 degrees C) Bretschneider's cardioplegia. (2) Stop-flow ischemia is associated with a substantial calcium-independent, non-exocytotic NE release, which is regarded as a sodium-dependent carrier-mediated process. Accordingly, it is inhibited by blockers of the sodium/proton-exchanger (e.g. amiloride) and the neuronal uptake1-carrier (e.g. desipramine). Compared with stop-flow ischemia alone, cardioplegia with 3 min of Bretschneider's histidine-tryptophan-ketoglutarate (HTK)-solution preceding stop-flow enhanced NE release at all stop-flow durations (10-90 min) investigated (e.g. after 30 min of normothermic Bretschneider's cardioplegia: 1070+/-41 pmol/g, n = 45, v stop-flow alone: 764+/-48 pmol/g, n = 27, P<0.05). The NE concentrations determined in the cardiac effluent upon reperfusion followed a typical first order kinetic indicating that the transmitter release had already occurred during stop-flow. Hypothermia reduced NE release in a temperature-dependent manner down to intramyocardial temperatures of 2 7.5 degrees C. NE release evoked by Bretschneider's cardioplegia still exceeded that induced by stop-flow ischemia alone by up to 60%. The NE release evoked by Bretschneider's cardioplegia and stop-flow ischemia was calcium-independent. However, it was significantly reduced by desipramine and amiloride, but both agents had a more pronounced inhibitory effect on NE release evoked by stop-flow ischemia alone. (3) This difference may be due to an intrinsic effect of Bretschneider's HTK-solution, as continuous administration of normothermic Bretschneider's HTK-solution induced a substantial NE release which was neither calcium-dependent nor inhibited by blockade of either uptake1 or sodium/proton-exchange. It is concluded that Bretschneider's cardioplegia is not neuroprotective, as it even augments the stop-flow ischemia-induced nonexocytotic NE release.
J Mol Cell Cardiol 1999 Jan
PMID:Influence of Bretschneider's cardioplegia on norepinephrine release from isolated perfused guinea-pig hearts. 1007 18


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