Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although it has been known for a long time that pronounced hypothermia has a protective effect on the brain during ischemia, and that severe hyperthermia damages neuronal tissue, knowledge of human brain temperature is very limited. The recent findings by two independent research groups, that even small differences in brain temperature significantly influence the degree of neuronal damage following cerebral ischemia, became the incentive for measuring brain temperature in neurosurgical patients. The temperature of the lateral ventricle, epidural space, membrana tympani and rectum were measured with copper-constantan thermocouples. During the implantation of an intraventricular catheter for measuring intracranial pressure, a temperature gradient of 0.4-1.0 degrees C between the lateral ventricle and the epidural space was noted. Continuous measurements for 1-5 days showed that the rectal temperature usually adequately reflects the temperature of the epidural space, although the temperature of the membrana tympani followed changes in epidural temperature more closely. However, at times, and in one patient during most of the time, the temperature of the epidural space was up to 1 degree C above rectal temperature. The relevance of these findings for the care of neurosurgical patients is discussed in relationship to what is known about brain temperature from animal experiments.
 ...
PMID:Epidural temperature and possible intracerebral temperature gradients in man. 233 25

Induced circulatory arrest is a technique used to provide a period of operative stability in a variety of surgical procedures that might otherwise be technically unfeasible. The use of hypothermia and barbiturates for protection against cerebral ischaemia during circulatory arrest is reviewed against a background of the pathophysiology of cerebral ischaemia and possible future therapies are also suggested.
 ...
PMID:The anaesthetic management of circulatory arrest. 240 29

The influence of YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]-carbonyl]-L-histidyl-L-prolinamide dihydrate), a new thyrotropin releasing hormone (TRH) analogue, on morphine-induced hypothermia, development of cerebral ischemia and analgesia was investigated in rodents. YM-14673, in doses not affecting the normal rectal temperature, antagonized morphine-induced hypothermia in mice. Morphine-induced hypothermia was also antagonized by administration of TRH, in doses increasing normal rectal temperature. Morphine increased the appearance rate of convulsions in rats subjected to bilateral occlusion of the carotid artery. YM-14673, unlike TRH, reduced the appearance rate of convulsions increased by morphine in the ischemic rats. Morphine-induced analgesia measured by the hot plate method was not affected by both YM-14673 and TRH. Naloxone antagonized the effect of morphine in the 3 models. These results suggest that YM-14673 possesses physiological opioid antagonistic properties.
 ...
PMID:Effects of YM-14673, a new TRH analogue, on responses to morphine in rodents. 251 20

To assess the augmented delta quotient (ADQ) monitor as a monitor of cerebral function during cardiac surgery, we monitored during operation the electroencephalograms of 48 young subjects (aged 2 weeks to 19 yr). We found ADQ patterns produced by cardiopulmonary bypass, hypothermia and general anaesthetic agents correlated with those obtained from a compressed spectral array (CSA) monitor and could be differentiated from changes caused by cerebral ischaemia, except in the youngest group of patients (less than or equal to 18 months) undergoing deep hypothermia (19.4 (SD 0.8) degrees C nasopharyngeal). In all other age groups the ADQ proved to be a simple monitor of the adequacy of cerebral perfusion. Neurological deficit occurred only if the ADQ was abnormal during hypotension for a period exceeding 7 min. ADQ evaluation of cerebral function was limited by events which produced artificially normal ADQ readings such as low amplitude EEG activity and the described isoflurane effect that was demonstrated to occur in some cardiac patients. The results obtained by the ADQ were comparable to those obtained by compressed spectral array and the ADQ was easier to use and interpret.
 ...
PMID:Clinical evaluation of the augmented delta quotient monitor for intraoperative electroencephalographic monitoring of children during surgery and cardiopulmonary bypass for repair of congenital cardiac defects. 260 75

The effects of indeloxazine hydrochloride [(+/-)-2-[(inden-7-yloxy)methyl]morpholine hydrochloride, YM-08054], a new cerebral metabolic enhancer, on learned behavior and central monoaminergic function were compared to those of other cerebral metabolic enhancers in animals. Indeloxazine enhanced passive learned behaviour in rats and ameliorated cerebral ischemia-induced learned disturbances in gerbils. Reserpine-induced hypothermia in mice, ponto-genicullo-occipital (PGO) waves in reserpinized cats and caudate spindle activity in cats were reduced by the administration of indeloxazine, suggesting that the drug possesses facilitatory effects on central monoaminergic systems. In contrast, piracetam, calcium-hopantenate, idebenone and bifemelane had no significant effect on learned behavior or central monoaminergic function, with the exception of bifemelane which antagonized reserpine-induced hypothermia. These results are in contrast to the findings that all tested cerebral metabolic enhancers, including indeloxazine, prolonged the survival time of mice subjected to anoxia. The greater effect of indeloxazine to other cerebral metabolic enhancers, in facilitating learned behavior, may be attributable to its broader effects on central monoaminergic systems.
 ...
PMID:Pharmacological effects of indeloxazine, a new cerebral activator, on brain functions distinct from other cerebral metabolic enhancers. 261 13

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.
 ...
PMID:Protection from cerebral ischemia by brain cooling without reduced lactate accumulation in dogs. 272 44

To improve the surgical results of aneurysms of the transverse aortic arch, it is essential to select the optimal support technique to protect the cerebral ischemia during the aortic arch occlusion. In the four year period between 1983 and 1987, 21 consecutive patients had surgical correction of aneurysms of the transverse aortic arch at our institution. The causes of aneurysms were dissection (type A) in 16 patients and arteriosclerosis in 5 patients. Seven patients had emergency operation for frank or impending rupture. Two method for cerebral protection were employed during the period of arch exclusion. In Group I, 11 patients underwent selective cerebral perfusion both to innominate and left common carotid arteries via one roller pump at a rate of 600 ml/min (25 degrees C). The average cerebral perfusion time was 70.4 +/- 20.5 minutes. In Group II, 10 patients underwent deep hypothermia (15 degrees C to 20 degrees C) and total circulatory arrest to allow repair of the transverse aortic arch. The concomitant AVR was performed in two patients and CABG in one patient. The average cerebral arrest time was 35.2 +/- 3.4 minutes. Two out of 10 patients had additional cerebral perfusion because cerebral ischemic time exceeded over 45 minutes. There were three early deaths (14.3%) in this series. The causes of early death were bleeding in two patients and renal failure in one patient. There were no cerebral complications in both groups. The duration of extracorporeal bypass necessary for cooling and rewarming phase in Group II was longer than that in Group I.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Clinical study on surgical treatment of aortic arch aneurysm using selective cerebral perfusion or hypothermic circulatory arrest]. 273 49

We have determined whether lowering brain temperature during the acute recirculation period following transient cerebral ischemia would influence the extent of ischemic neuronal injury. Anesthetized rats underwent 10 min of bilateral carotid artery occlusion combined with systemic hypotension (50 mmHg). Four animal subgroups were investigated, including non-ischemic controls; rats whose postischemic brain temperature was maintained at 36 or 30 degrees C starting 5 min into the recirculation period; and rats in which postischemic hypothermia was begun 30 min into the recirculation period. In all cases, intra-ischemic brain temperature was 36 degrees C and body temperature was held at 36-37 degrees C throughout. Three days following the ischemic insult, the CA1 sector of the hippocampus was severely damaged in normothermic rats (36 degrees C). In contrast, when postischemic brain temperature was decreased to 30 degrees C starting 5 min into the recirculation period, normal-appearing pyramidal neurons were present throughout the CA1 hippocampus. A beneficial effect of postischemic hypothermia was not demonstrated when brain cooling was initiated 30 min into the recirculation period. These results demonstrate that postischemic hypothermia can markedly protect CA1 pyramidal neurons from injury following transient ischemia. The 'therapeutic window' for postischemic hypothermia was found to be narrow under the present experimental conditions.
 ...
PMID:Postischemic moderate hypothermia inhibits CA1 hippocampal ischemic neuronal injury. 277 Nov 74

Using the bilateral carotid artery occlusion model of cerebral ischemia in the gerbil, we studied the effect of moderate hypothermia (30 to 31 degrees C) on the postischemic production of prostanoids (cyclooxygenase pathway) and leukotrienes (lipoxygenase pathway) and accompanying changes in cerebral edema formation. Hypothermia capable of slowing central evoked potential conduction time was studied over the course of 40 minutes of cerebral ischemia and for up to 2 hours of reperfusion. The successful induction of cerebral ischemia was confirmed by somatosensory evoked potential amplitude changes. Measurements of 6-ketoprostaglandin F1 alpha (PGF1 alpha) and leukotriene B4 (LTB4) (radioimmunoassay) and cerebral edema (specific gravity) were made at early (10 minutes) and late (2 hours) reperfusion times. Although both white and gray matter showed no early significant difference in edema accumulation between normothermic and hypothermic gerbils at 10 minutes of reperfusion, hypothermic animals demonstrated significantly less white matter edema (specific gravity, 1.0397 +/- 0.0010 vs. 1.0341 +/- 0.0012, P less than 0.01) and gray matter edema (specific gravity, 1.0408 +/- 0.0009 vs. 1.0365 +/- 0.0008, P less than 0.01) by 2 hours of reperfusion. Production of PGF1 alpha was not significantly different between normothermic and hypothermic animals during the reperfusion period; however, hypothermic gerbils demonstrated significantly lower production of LTB4 at 10 minutes reperfusion time compared to normothermic animals (1.49 +/- 0.79 vs. 5.28 +/- 1.49 pg/mg of protein, P less than 0.05). This difference between the two groups in LTB4 levels was no longer detectable at 2 hours of reperfusion time.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Moderate hypothermia reduces postischemic edema development and leukotriene production. 282 45

The metabolic effects of graded whole body hypothermia on complete global cerebral ischemia and recirculation was investigated in the cat. Hypothermia was induced to one of three levels prior to ischemia; T = 26.8 degrees +/- 0.5 degrees C (n = 4), T = 32.1 degrees +/- 0.2 degrees C (n = 5), and T = 34.6 degrees +/- 0.3 degrees C (n = 6), and maintained constant throughout 16 min of ischemia and 1.5-2 h of recirculation. Intracellular cerebral pH and relative concentrations of high-energy phosphate metabolites were continuously monitored, using in vivo 31P nuclear magnetic resonance (NMR) spectroscopy. Except for the first 4 min of ischemia, no significant differences were detected in the response of adenylate intensities and intracellular pH to ischemia and recirculation between the hypothermic groups. The three hypothermic groups were then pooled into one group, and the data compared to previously published data from a normothermic group, T = 38.4 degrees +/- 0.6 degrees C (n = 14), and a hyperthermic group, T = 40.6 degrees +/- 0.2 degrees C (n = 9), subjected to the identical ischemic and NMR measurement protocols. The hypothermic animals exhibited a statistically significant reduction of cerebral intracellular acidosis, both during ischemia and recirculation, as well as a more rapid return of adenylate intensities during recirculation, compared to the normothermic or hyperthermic groups. The data thus suggest that mild hypothermia has an ameliorative affect on brain energy metabolism and intracellular pH under conditions of complete global cerebral ischemia and recirculation.
 ...
PMID:The metabolic effects of mild hypothermia on global cerebral ischemia and recirculation in the cat: comparison to normothermia and hyperthermia. 292 Dec 88


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>