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

We have demonstrated previously that mild intraischemic hypothermia confers a marked protective effect on the final histopathological outcome. The present study was carried out to evaluate whether this protective effect involves changes in the degree of local cerebral blood flow reductions, tissue accumulation of free fatty acids, or alterations in the extracellular release of glutamate and dopamine. Rats whose intraischemic brain temperature was maintained at 36 degrees C, 33 degrees C, or 30 degrees C were subjected to 20 minutes of ischemia by four-vessel occlusion combined with systemic hypotension. Levels of local cerebral blood flow, as measured autoradiographically, were reduced uniformly in all experimental animals at the end of ischemia by gas chromatography after tissue extraction and separation by thin layer chromatography. A massive ischemia-induced accumulation of individual free fatty acids was observed in animal groups whose intraischemic brain temperature was maintained at either 36 degrees C or 30 degrees C. Extracellular neurotransmitter levels were measured by microdialysis; the perfusate was collected before, during, and after ischemia. In rats whose intraischemic brain temperature was maintained at 36 degrees C, dopamine and glutamate increased significantly during ischemia and the early period of recirculation (by 500-fold and sevenfold, respectively). In animals whose brain temperature was maintained at 33 degrees C and 30 degrees C, the release of glutamate was completely inhibited, and the release of dopamine was significantly attenuated (by 60%). These results suggest that mild intraischemic hypothermia does not affect the ischemia-induced local cerebral blood flow reduction or free fatty acid accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1989 Jul
PMID:Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain. 256 5

The article discusses the results of study of central hemodynamics in patients with acquired aortic valvular diseases who were operated on under conditions of hypothermia without perfusion. The minute circulation volume reduced at a temperature of 26.8 degrees C to 63% of the initial level. The stroke volume did not change practically. The changes of the values of central hemodynamics in the stages of hypothermia (active and passive cooling) were irregular in character. No essential inhibiting effect of hypothermia on the cardiovascular activity was noted.
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PMID:[Central hemodynamics during correction of acquired aortic defects without artificial blood circulation]. 261 65

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

The use of cardiopulmonary bypass, deep hypothermia and circulatory arrest has decreased the risks of hemorrhage, tumor embolization, incomplete thrombus resection, and warm hepatic and renal ischemia associated with resection of renal cell carcinoma extending into the inferior vena cava above the hepatic veins. Patients about to undergo this operation frequently have significant coronary artery and carotid artery disease, and are at risk for perioperative myocardial infarction and stroke. Preoperative evaluation of the coronary artery and carotid artery circulation by coronary angiography, duplex carotid artery scan and digital subtraction carotid angiography is recommended. Depending upon the severity and location of the cardiovascular disease a sequential or simultaneous operation may be performed. This surgical approach can be used in selected patients to facilitate complete tumor thrombectomy with a low operative risk.
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PMID:Cardiovascular evaluation before circulatory arrest for removal of vena caval extension of renal carcinoma. 272 26

Hypothermia protects tissue function in ischemia. This study determined if selective brain cooling inhibits cerebral cortical lactate accumulation and thus accounts for imporved neurologic outcome after complete cerebral ischemia in dogs. The brain was selectively cooled (hippocampal temperature 33 degrees C) by nasal lavage with water at 5 degrees C. Control dogs received nasal lavage with water at 39 degrees C. Mean +/- SEM rectal temperature in both groups was 39 +/- 1 degree C prior to ischemia. Selective brain cooling before and during 10 minutes of cardiac arrest was associated with significantly improved neurologic function and 100% survival, whereas normothermic cardiac arrest produced marked neurologic dysfunction and 100% mortality. Cerebral cortical lactate accumulation was measured in a complementary series of dogs exposed to the same two treatments but with the addition of six cerebral cortical brain biopsies taken before, during, and immediately after cardiac arrest. Brain and rectal temperatures of dogs in the brain biopsy protocol were similar to those of dogs in the recovery protocol. There was no difference detected in cerebral lactate accumulation during ischemia between brain-cooled and control dogs. Thus, reduction in cortical brain lactate during ischemia cannot account for the postischemic functional protection afforded by preischemic selective brain cooling.
Stroke 1989 Jun
PMID:Protection from cerebral ischemia by brain cooling without reduced lactate accumulation in dogs. 272 44

Recent studies have suggested that topical hypothermia may be unnecessary during coronary bypass operations because of possible pulmonary complications resulting from phrenic nerve damage. This study was undertaken to determine whether topical hypothermia is necessary for optimal myocardial protection when distribution of the cardioplegic solution is heterogeneous because of coronary occlusions. Twenty pigs were subjected to 120 minutes of ischemic arrest with multidose potassium crystalloid cardioplegia (4 degrees C). During arrest, the mid-left anterior descending coronary artery was occluded with a snare that was released on reperfusion. Ten of these pigs received topical hypothermia and 10 others served as controls. Hearts protected with topical hypothermia had lower temperatures in the left anterior descending (7.0 degrees +/- 0.7 degree C versus 18.5 degrees +/- 0.5 degree C; p less than 0.05) and circumflex regions (8.9 degrees +/- 0.5 degree C versus 15.5 degrees +/- 0.5 degree C; p less than 0.05). The pH values were higher in hearts protected with topical hypothermia in both the left anterior descending (7.36 +/- 0.09 versus 6.73 degrees +/- 0.07; p less than 0.05) and circumflex regions (7.40 +/- 0.07 versus 7.05 +/- 0.07; p less than 0.05). Topical hypothermia also resulted in better preservation of postischemic stroke work index (0.64 +/- 0.06 versus 0.40 +/- 0.08 gm-m/kg; p less than 0.05) and wall motion scores (1.0 +/- 0.3 hypothermia versus 1.8 +/- 0.4 no hypothermia; p less than 0.05). We conclude that topical hypothermia affords maximal myocardial protection when coronary occlusions are present and should be used during all coronary operations.
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PMID:Importance of topical hypothermia during heterogeneous distribution of cardioplegic solution. 275 57

A standard murine model was used to determine whether acute pretreatment exposures to hypoxia could alter ultimate hypoxic survival time. Adult male albino mice (Mus musculus) weighing 25-30 g were subjected to three pretreatment hypoxic exposures (4.5% O2, balance N2) of increasing duration (90, 120, and 150 seconds) with 300 seconds of normoxia between each pretreatment exposure and before testing of hypoxic survival time. Acute pretreatment exposures to hypoxia significantly increased mean +/- SEM hypoxic survival time from 108 +/- 4 to 403 +/- 42 seconds. Mean +/- SEM blood glucose concentrations increased significantly from 201 +/- 19 to 397 +/- 10 mg/dl immediately after hypoxic pretreatment. A significant increase in mean +/- SEM blood ketone concentrations, from 0.15 +/- 0.01 to 0.40 +/- 0.08 mM, was detected in the blood 1,800 seconds but not 300 seconds after hypoxic pretreatment. However, pretreatment with exogenous glucose or ketones alone, to mimic the blood levels seen after hypoxic pretreatment, failed to increase hypoxic survival time. In contrast, mice pretreated with hypoxic exposures plus the exogenous substrate beta-hydroxybutyrate had an increased mean +/- SEM hypoxic survival time of 749 +/- 48 seconds and a decreased body temperature. Stepwise Cox regression analyses with body temperature as a fixed covariate suggest that this decrease in body temperature has a partial role in, but can not fully account for, the increased hypoxic survival time. These data suggest that sequential exposures to hypoxia induce metabolic changes that protect against the lethal effects of hypoxia, perhaps by altering substrate mobilization and utilization and/or by inducing a hypometabolic hypothermia.
Stroke 1989 Sep
PMID:Hypoxia-induced increases in hypoxic tolerance augmented by beta-hydroxybutyrate in mice. 277 83

We investigated the earliest time at which irreversible damage takes place after hypoxia-ischemia in the Levine preparation of rats. In 60 rats anesthetized with chloral hydrate and maintained at one of three body temperatures, we unilaterally ligated the left common carotid artery and placed electrodes in the striatum to measure impedance (reflecting the extracellular space) during hypoxia, recovery, and/or cardiac arrest. We measured blood gases and pH at regular intervals during hypoxia in 47 rats and assessed blood-brain barrier function with Evans blue and tissue damage using Na+:K+ ratios. Shortly after hypoxia, impedance normalized in 24 rats without brain damage (normal Na+:K+ ratios, 4 hours of recovery). Sustained elevation of striatal impedance during recovery in six rats was related to an elevated Na+:K+ ratio and a disrupted blood-brain barrier. Damage was not obviously related to blood gases, pH, or the net reduction of the extracellular space during hypoxia. Hypothermia in 17 rats prevented impedance changes, and no striatal damage was found. Thus, irreversible brain damage very likely occurs during or very shortly after hypoxia. Persistent reduction of the extracellular space indicates tissue damage and can be used to monitor potential in vivo therapeutic measures.
Stroke 1989 Oct
PMID:Rat striatal cation shifts reflecting hypoxic-ischemic damage can be predicted by on-line impedance measurements. 279 69

To evaluate intraoperative changes in myocardial performance during valvular operations, ventricular functional measurements were obtained in 16 patients before and after elective cardiac valvular replacement. Six patients had mitral regurgitation, four had mitral stenosis, and six had calcific aortic stenosis; all patients underwent isolated mitral or aortic valve replacement. Cold potassium crystalloid cardioplegia, topical hypothermia, and low-flow systemic hypothermia were employed uniformly. Just before and 10 minutes after cardiopulmonary bypass was discontinued, left ventricular pressure and volume data were recorded at four to five different steady-state levels of filling produced by blood infusion or withdrawal from the aortic cannula (mean end-diastolic pressure range, 10-22 mm Hg; mean end-diastolic volume range, 120-168 ml). Portable first-pass radionuclide ventriculography and simultaneous micromanometry were used for construction of left ventricular pressure-volume loops from which stroke work and end-diastolic volume were calculated. Two-dimensional transesophageal echocardiograms also were recorded, and epicardial pacing maintained heart rate as constant as possible. As compared with prebypass measurements, echocardiographic left ventricular wall volume changed insignificantly after the valvular procedures (178-181 ml/m2, p greater than 0.5). The stroke work-end-diastolic volume relationship before and after operation was highly linear in all studies (mean = 0.97). The slope and x intercept of this relationship did not change significantly after operation, indicating a stable level of left ventricular function (from 12.7 x 10(4) to 10.0 x 10(4) ergs/ml and from 67 to 57 ml, respectively; p greater than 0.3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of left ventricular functional preservation during isolated cardiac valve operations. 280 86

We looked at FiO2, choice of anesthetic, nutritional status, and body temperature in a gerbil model of forebrain ischemia to determine their effect on data interpretation, ischemic outcome, and extent of pharmacologic protection. We subjected 484 gerbils to 5 minutes of forebrain ischemia under different experimental conditions. The gerbils were anesthetized with 3% halothane and inspired 21% O2, 37% O2 and 60% N2O, or 97% O2. Six groups of gerbils pretreated with 200 mg/kg phenytoin or 2 ml/kg polyethylene glycol (vehicle) underwent ischemia in the fasted or fed state. Three groups of gerbils receiving no pretreatment underwent ischemia with rectal temperatures of 32-33 degrees C, 34-35 degrees C, or 37 degrees C. We counted intact neurons in the CA1 hippocampal sector in brains fixed on Day 7 after ischemia. t tests of square-root-transformed cell counts were used to assess the effect of hypothermia, and analysis of variance of the transformed data was used to test for the effects of phenytoin, FiO2, and nutritional status. Phenytoin pretreatment provided significant protection from CA1 neuron loss in all groups tested (p less than 0.001), but the degree of protection varied from 20% to 44%. In spite of significantly higher serum glucose concentrations in fed than in fasted gerbils (173 and 118 mg/dl, respectively), we found no significant effect of nutritional status upon neuron loss in phenytoin- or vehicle-pretreated gerbils. An FiO2 of 21% significantly decreased the number of viable neurons in both vehicle- and phenytoin-pretreated groups (p less than 0.03), despite the lack of an effect of hypoxemia on arterial blood gases.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1989 Nov
PMID:Conditions for pharmacologic evaluation in the gerbil model of forebrain ischemia. 281 90


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