UMLS:C0020672 - FACTA Search

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

The purpose of this study was to determine the effect of selective modulation of brain temperature in the experimental settings of permanent and reversible middle cerebral artery (MCA) occlusion in Sprague-Dawley rats. Three models of proximal MCA occlusion were used, in which the effect of brain-temperature modulations could be studied. These included (a) permanent MCA occlusion with an initial 30-min period of hypotension (30 or 36 degrees C x 4 h), (b) permanent MCA occlusion alone (30, 36, or 39 degrees C x 2 h), and (c) 2 h of reversible MCA occlusion (30, 36, or 39 degrees C x 2 h). In the transient MCA occlusion series, intra- and postischemic cortical blood flow was assessed using a laser-Doppler flowmeter placed over the dorsolateral cortex. After a 3-day survival, all rats were perfusion fixed for histopathological analysis and the determination of infarct volume. In animals with permanent MCA occlusion plus hypotension, no significant difference in infarct volume was demonstrated between the 30 and 36 degrees C groups. In rats with permanent MCA occlusion without hypotension, significant differences in infarct volume were again not demonstrable, but an interaction between infarct area and temperature class was shown by repeated-measures analysis, indicating that hypothermia altered the topographic pattern of the cortical infarct. With 2 h of reversible MCA occlusion, there was a statistically significant reduction in infarct volume in the 30 degrees C group compared to 39 degrees C rats. Although intra- and postischemic CBF were not significantly different among the three temperature groups, the cortical infarct volume was positively correlated with postischemic CBF. The postischemic CBF, in turn, was positively correlated to the intraischemic brain temperature and was negatively correlated to CBF during the ischemic period. These findings demonstrate that moderate manipulations of brain temperature have a greater influence on the resulting cortical infarction in the setting of transient focal ischemia than in the context of permanent vascular occlusion.
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PMID:The significance of brain temperature in focal cerebral ischemia: histopathological consequences of middle cerebral artery occlusion in the rat. 156 34

Cerebral protection by hypothermia is commonly attributed to cerebral metabolic suppression. However, at temperatures below 28 degrees C, the relationship of temperature to cerebral metabolic rate of oxygen consumption (CMRO2) has not been well characterized. Accordingly, the relationship between brain temperature and CMRO2 was determined in eight dogs during cooling from 37 to 14 degrees C while the EEG was continuously monitored. Cardiopulmonary bypass was initiated and control measurements were made at 37 degrees C during anesthesia with nitrous oxide 50-60% inspired and morphine sulfate 2 mg.kg-1 intravenously (iv). Upon cooling to 27 degrees C, the nitrous oxide was discontinued and the morphine was antagonized with naloxone 2 mg iv. Measurements were repeated at 27, 22, 18, and 14 degrees C and in four dogs again at 37 degrees C after nitrous oxide 50-60% had been reestablished at 27 degrees C along with administration of morphine sulfate 2 mg.kg-1. For each temperature interval, the temperature coefficient (Q10) for CMRO2 was calculated (Q10 = CMRO2 at x degrees C divided by CMRO2 at [x - 10] degrees C). Between 37 and 27 degrees C the Q10 was 2.23, but between 27 and 14 degrees C the mean Q10 was doubled to 4.53. With rewarming to 37 degrees C, CBF and CMRO2 returned to control levels, and brain biopsies revealed a normal brain energy state. During cooling, the EEG developed burst suppression at or below 22 degrees C. With further cooling, the periods of suppression increased; however, burst activity continued in seven of eight dogs even at 14 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The relationship among canine brain temperature, metabolism, and function during hypothermia. 206 37

Current evidence points to an important role of N-methyl-D-aspartate (NMDA) receptor activation in the pathogenesis of hypoglycemic neuronal death. MK-801 [dizocilpine maleate, (+)-5-methyl-10,11-dihydro-5H-di[a,d]cyclohepten-5,10-imine] is an anticonvulsant compound also known to be a potent noncompetitive antagonist at NMDA receptors, readily crossing the blood-brain barrier after parenteral administration. Treatment of rats with dizocilpine (1.5-5.0 mg/kg) injected intravenously during profound hypoglycemia (blood glucose levels 1.5-2.0 mM) at the stage of delta-wave (1-4 Hz) slowing of the EEG mitigated selective neuronal necrosis in the hippocampus and striatum, assessed histologically after 1-week survival. The degree of neuroprotection in the striatum and in the CA1 pyramidal cells of the hippocampus was dose dependent. Because of concern for a possible hypothermic mechanism of brain protection by MK-801, core temperature was closely monitored and was found not to decrease significantly. Since CBF is normal or increased in hypoglycemia, a fall in brain temperature during hypoglycemia is unlikely to play a role in the mechanism of the neuroprotection seen with the drug. The findings indicate that in profound hypoglycemia, intravenous administration of the NMDA antagonist dizocilpine, even after the appearance of delta-wave EEG slowing, can reduce the number of necrotic neurons in several brain regions and suggest that the neuroprotective effect of MK-801 is not related to hypothermia.
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PMID:Regional neuroprotective effects of the NMDA receptor antagonist MK-801 (dizocilpine) in hypoglycemic brain damage. 215 10

To ascertain the effect of profound hypothermia on brain function and metabolism, newborn dogs were subjected to surface cooling during which regional cerebral blood flow (rCBF) and glucose utilization (rCGU) were measured with iodo-[14C]-antipyrine and 2-deoxy-[14C]-glucose, respectively. Puppies were anesthetized with nitrous oxide, paralyzed, and their lungs artificially ventilated to maintain arterial normoxia (PaO2 greater than 60 mmHg) and normal acid-base balance (PaCO2 = 35-41 mmHg; pHa = 7.34-7.42). When rectal temperature was decreased from 37 to 20 degrees C, mean arterial blood pressure (MABP) decreased from 75 to 47 mmHg (P less than 0.001) and heart rate from 238 to 64 beats/min (P less than 0.001). Arterial PCO2 was reduced from 38 to 31 mmHg (P less than 0.001) (corrected to 37 degrees C), whereas pHa was unchanged from control (7.40). The electroencephalogram slowed progressively and became isoelectric at 22-25 degrees C. During normothermia (n = 6) blood flow to 16 component structures of brain varied from 17 (occipital white matter) to 65 (medulla) ml.100 g-1.min-1, whereas during hypothermia (n = 6) blood flow was lower in all regions (P less than 0.001) at remarkably uniform levels 8.3-10.3 ml.100 g-1.min-1). Thus, the greatest reductions (range, 16-48% of control) in CBF occurred in those structures with the highest intrinsic flows during normothermia and were proportionately less in low flow structures. Regional CGU also decreased in all brain regions analyzed (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow and glucose utilization during hypothermia in newborn dogs. 281 67

CBF and related parameters were studied in 68 patients before, during, and following cardiopulmonary bypass. CBF was measured using the intraarterial 133Xe injection method. The extracorporeal circuit was nonpulsatile with a bubble oxygenator administering 3-5% CO2 in the main group of hypercapnic patients (n = 59) and no CO2 in a second group of hypocapnic patients. In the hypercapnic patients, marked changes in CBF occurred during bypass. Evidence was found of a brain luxury perfusion that could not be related to the effect of CO2 per se. Mean CBF was 29 ml/100 g/min just before bypass, 49 ml/100 g/min at steady-state hypothermia (27 degrees C), reached a maximum of 73 ml/100 g/min during the rewarming phase (32 degrees C), fell to 56 ml/100 g/min at steady-state normothermic bypass (37 degrees C), and was 48 ml/100 g/min shortly after bypass was stopped. Addition of CO2 evoked systemic vasodilation with low blood pressure and a rebound hyperemia. The hypocapnic group responded more physiologically to the induced changes in hematocrit (Htc) and temperature, CBF being 25, 23, 25, 34, and 35 ml/100 g/min, respectively, during the five corresponding periods. Carbon dioxide was an important regulator of CBF during all phases of cardiac surgery, the responsiveness of CBF being approximately 4% for each 1-mm Hg change of PaCO2. The level of MABP was important for the CO2 response. At low blood pressure states, the CBF responsiveness to changes in PaCO2 was almost abolished. An optimal level of PaCO2 during hypothermic bypass of approximately 25 mm Hg (at actual temperature) is recommended. A normal autoregulatory response of CBF to changes in blood pressure was found during and following bypass. The lower limit of autoregulation was at pressure levels of approximately 50-60 mm Hg. CBF autoregulation was almost abolished at PaCO2 levels of greater than 50 mm Hg. The degree of hemodilution neither affected the CO2 response nor impaired CBF autoregulation, although, as would be expected, it influenced CBF: In 33 women CBF was 55 ml/100 g/min at an Htc of 24%, as compared with 42 ml/100 g/min in 35 men (Htc = 28%). High PaO2 was a vasoconstrictor, the autoregulatory plateau being narrowed. The lower limit of autoregulation was shifted to a higher pressure when PaO2 was low.
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PMID:Brain luxury perfusion during cardiopulmonary bypass in humans. A study of the cerebral blood flow response to changes in CO2, O2, and blood pressure. 308 31

An interstitial microwave antenna system was devised for differential hypothermia treatment. It was evaluated for its ability to induce localized brain hyperthermia in hypothermic monkey. Ten brain hyperthermia trials have been performed in 6 monkeys. Under general anesthesia, the animals were put into ice water bath to keep the total body temperature at 30 degrees C. Following parieto-occipital craniectomy, a microwave antenna of 1.5 mm in diameter was inserted into the brain at depth of 2 cm, and the brain tissue was heated by 2450 MHz microwave irradiation. Thermal distribution was measured by thermistor probes and local cerebral blood flow (1-CBF) before and after heating was simultaneously measured by hydrogen clearance method. After the experiment, the animals were sacrificed and histopathological changes of the heated brain tissue were studied. Under total body hypothermia of 30 degrees C, the maximum cross-sectional diameter of the heated brain to 37 degrees C or above was about 4 cm. The temperature profile on the vertical plane presented a bell-shaped distribution. The 1-CBF of the heated brain increased with the elevation of the brain temperature and the blood flow at 37 degrees C is nearly twice as much as that of 30 degrees C. After one hour DH treatment, necrotic tissue was noted along the antenna axis where the temperature was maintained more than 50 degrees C, and this change was not recognized at a distance of 1 cm from the antenna where the temperature was maintained at 42 degrees C. This study indicates that interstitial microwave hyperthermia system can be used effectively to heat the localized brain tissue.
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PMID:[Fundamental study of differential hypothermia treatment of brain tumor using an interstitial microwave antenna]. 344 98

The effect of moderate whole-body hypothermia (30 degrees C) on transient middle cerebral artery (MCA) occlusion in the rat was evaluated using diffusion- and perfusion-weighted magnetic resonance imaging. Two hours of transient MCA occlusion was induced by intracarotid insertion of a nylon filament under normothermic (n = 14) and hypothermic (n = 7) conditions. Diffusion- and perfusion-weighted imaging were performed before, during, and after focal ischemia from 30 min up to 7 days. In hypothermic animals, scattered neuronal necrosis was localized to select areas of the caudate putamen and the parietal and insular cortex. In contrast, the normothermic ischemic animals exhibited pan-necrosis and infarct encompassing the damaged area. The diffusion and perfusion data measured from caudate putamen indicate that hypothermia causes a significant reduction in the apparent diffusion coefficient of water (ADCw) and CBF values from normothermic control values (p < 0.01). In both normothermic and hypothermic animals after onset of MCA occlusion, ADCw and CBF values in the core of the ischemic region (striatum) significantly declined from the preischemic and homologous contralateral control ADCw and CBF values (p < 0.05). However, ADCw and CBF in the hypothermic group returned toward control more rapidly than in the normothermic group. These results suggest that the protective effect of hypothermia on ischemic cell damage is reflected in the early return of ADCw during reperfusion and the reduction of ischemic cell damage by hypothermia may be mediated by the improved CBF during acute reperfusion.
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PMID:The effect of hypothermia on transient focal ischemia in rat brain evaluated by diffusion- and perfusion-weighted NMR imaging. 806 69

Twenty-seven dogs, divided into three groups, were subjected to a normothermic ventricular fibrillation (VF) cardiac arrest of 15 min and resuscitated by using cardiopulmonary bypass through the femoral veins and artery (F-F bypass). Group I (n = 15): Cardiac beating did not return in any dogs during an initial 3-min conventional cardiopulmonary resuscitation, but it returned 5.2 +/- 3.8 min (mean +/- S.D.) after the successive initiation of the F-F bypass in all dogs, except in one with bypass trouble. Intermittent burst waves appeared on the electroencephalogram and continuous waves returned, 90.0 +/- 24.7 min and 130.7 +/- 28.1 min after the start of resuscitation, respectively. Values of blood glucose, lactate and potassium 5-15 min after the F-F bypass were significantly higher than those before induction of VF, while those of blood pH, base excess, hemoglobin, hematocrit, platelet and serum protein decreased significantly. Group II (n = 7): Both local cerebral (CBF) and myocardial blood flow (MCBF) returned to the pre-arrest level soon after the initiation of the F-F bypass, even though spontaneous cardiac beating was not yet restored. Closed or open chest cardiac massage could not produce as much blood flow as the F-F bypass did. In the early stage of restoration of spontaneous circulation, temporary interruption of the bypass led to a decrease in both local CBF and MCBF. Group III (n = 5): Spontaneous circulation was restored in all five dogs 5.2 +/- 1.1 min after the institution of the F-F bypass, which was continued for 164 +/- 30 min under mild hypothermia. After intensive care for a subsequent 6-36 h, the animals barked, moved their forelegs and could drink water. The mean neurological deficit score (normal: 0, brain death: 500) was 100.6. However, macroscopic examination of the brain in two dogs with prominent recovery revealed atrophy of the central gyrus and microscopic examination revealed injuries of the vulnerable neurons of the brain.
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PMID:Cardiopulmonary-cerebral resuscitation by using cardiopulmonary bypass through the femoral vein and artery in dogs. 835 24

A model of hypothermic circulatory arrest has been developed in newborn dogs which simulates the procedure used for the operative repair of congenital cardiac defects in human infants. Hypothermic circulatory arrest for 1.0 h causes no brain damage, whereas cardiac arrest for 1.75 h results in damage of the cerebral cortex, basal ganglia and to a lesser extent the claustrum and amygdaloid nucleus. In the present study, we determined regional cerebral blood flow (rCBF) during 24 h of recovery from hypothermic circulatory arrest. Newborn nitrous oxide anesthetized and artificially ventilated dogs were cooled to 20 degrees C and subjected to cardiac arrest by the i.v. injection of KCl for either 1.0 or 1.75 h. Thereafter, animals were resuscitated, rewarmed to 37 degrees C, and rCBF measured with [14C]iodoantipyrine at either 2 or 18 h of recovery. Control animals were rendered hypothermic to 20 degrees C without cardiac arrest for 1.0 or 1.75 h prior to rewarming. No alterations in CBF at either 2 or 18 h of recovery were present in any of 16 analyzed structures in animals previously subjected to hypothermic circulatory arrest compared to controls rendered hypothermic alone. A direct linear correlation existed between mean arterial blood pressure and blood flow within frontal, parietal and occipital cortex, occipital white matter, hypothalamus and cerebellar vermis in puppies arrested for 1.75 h and recovered for 2 h, suggesting a loss of CBF autoregulation at this interval. No such association between blood pressure and CBF was apparent at 18 h of recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional cerebral blood flow following hypothermic circulatory arrest in newborn dogs. 840 84

Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.
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PMID:Cerebral blood flow and metabolism during cardiopulmonary bypass. 846 2

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