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

Changes in evoked spinal cord potential (ESCP) and in local spinal cord blood flow (local SCBF) were measured simultaneously in eight dogs in the course of systemic cooling and rewarming using a water mattress. PaCO2 was maintained at 35-40 mm Hg (temperature-uncorrected values) by adjusting ventilatory volume every 1 degree C change of esophageal temperature under N2O (60%)-O2-isoflurane (1.15%) anesthesia. Local SCBF and arterial blood pressure decreased and ESCP latencies increased linearly with the decrease in body temperature to 23-24 degrees C. The conductive ESCPs (non-synaptic components) showed temporary augmentation in amplitude before eventual decrease under cooling. These showed a tendency to return to the precooling baselines after the initiation of rewarming. These results demonstrate that conductive ESCPs could be available for intraoperative monitoring of spinal function under hypothermia down to 23-24 degrees C.
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PMID:Effects of systemic cooling and rewarming on the evoked spinal cord potentials and local spinal cord blood flow in dogs. 816 Sep 87

We examined the perception of thermal comfort in six male subjects immersed in water at 28 degrees C (study I) and 15 degrees C (study II), breathing either room air (AIR) or a normoxic mixture containing 30% N2O (N2O). Immersions were terminated if esophageal temperature (Tes) decreased by 2 degrees C from resting levels or to 35 degrees C. At regular intervals, subjects rated their perception of thermal comfort on a 21-point scale (thermal comfort vote, TCV; +10 = very, very hot, 0 = neutral, -10 = very, very cold). For similar decreases in Tes from resting preimmersion values (mean +/- SD = -0.90 degrees +/- 0.13 degrees C and -0.92 degrees +/- 0.15 degrees C during the AIR and N2O trials in study I, and -0.90 degree +/- 0.22 degree C and -0.89 degree +/- 0.27 degree C during the AIR and N2O trials in study II), subjects perceived the immersions as less cold during the N2O trials. The median TCVs for the AIR condition of -5 in study I and -7.75 in study II, were significantly lower than those reported by the subjects for the respective N2O conditions (1.75 in study I and -5.5 in study II). It is concluded that behavioral adjustments required for maintaining thermal balance may be diminished during narcosis due to the altered perception of thermal discomfort. Assuming that the effect of inert gas narcosis on thermoregulatory responses is similar to that of N2O, then combined with the significant attenuation of heat gain mechanisms by anesthetic gases, the attenuation of the perception of thermal comfort may represent a significant factor in the etiology of hypothermia observed in compressed air divers.
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PMID:Perception of thermal comfort during narcosis. 818 May 69

Menkes disease is a rare, sex-linked recessive disorder characterized by kinky hair, convulsion, mental retardation, bone and connective tissue lesions, and hypothermia. These symptoms have been attributed to suppression of copper-dependent enzymes resulting from copper deficiency. We report a case of a 7-month-old infant with Menkes disease who underwent repair of inguinal hernia. Anesthesia was maintained with sevoflurane-N2O-O2, and the operation was carried out uneventfully. Although the patient had been medicated with anticonvulsants preoperatively, transient seizure occurred in the recovery room. We also discuss pathophysiology and anesthetic management of a patient with Menkes disease.
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PMID:[Anesthetic management of an infant with Menkes disease]. 823 Jul 25

Spinal-sciatic evoked responses (ScER) have been used successfully to monitor the integrity of the anterior spinal cord during spinal surgery. To evaluate the effects of hypercarbia, hypocarbia, induced hypotension, and hypothermia on the ScER, ten swine anesthetized with ketamine were subjected to varying levels of PaCO2, hypothermia, and induced hypotension. During variation of one physiologic variable, the other variables were closely regulated. There were no significant changes associated with variations in PaCO2. Decreasing temperature provided a consistent increase in latency (r = -0.78, P < 0.001) with no significant alteration in amplitude. Graded hypotension caused little increase in latency (3.2% at 30 mm Hg). The amplitude decrease averaged 23% at 60 mm Hg with a maximal decrease of 50% at 30 mm Hg. To study inhaled anesthetics, 21 swine anesthetized with ketamine were subjected to nitrous oxide (50% and 70%). After termination of the nitrous oxide, one of the potent inhaled anesthetics (n = 7 each) was administered in 0.25 minimum alveolar concentration (MAC) increments. Nitrous oxide caused a significant decrease in amplitude (average 43% and 61% at 50% and 70%) with minimal changes in latency. There was a dose-dependent decrease in amplitude and increase in latency with all inhaled anesthetics. The ScER disappeared at 1.0 MAC with all anesthetics. There were no differences between effects of equipotent concentrations of inhaled anesthetics. These findings may be helpful in the interpretation of the ScER response during anesthesia and surgery.
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PMID:Physiologic and anesthetic alterations on spinal-sciatic evoked responses in swine. 842 1

If the efficacy of hypothermia and barbiturates in ameliorating ischemic brain injury lies in reducing the cerebral metabolic rate of oxygen (CMRO2), the greater efficacy of mild hypothermia (34 degrees C) compared with barbiturates is inconsistent with the 15-20% reduction of CMRO2 caused by mild hypothermia compared with 50% caused by barbiturates. This paradox, we hypothesized, derives from the fact that whereas barbiturates lower CMRO2 associated with EEG activity or thiopental (TP)-suppressible CMRO2, not essential for cellular viability, hypothermia lowers CMRO2 associated with providing energy, i.e., adenosine triphosphate, to maintain transmembrane ion gradients or TP-nonsuppressible CMRO2, essential for neuronal viability. To test this hypothesis, we measured whole brain cerebral blood flow (CBF) and CMRO2 in two groups of rats mechanically ventilated with 70% N2O/30% O2 before and after TP-induced isoelectric EEG. In the normothermic group (n = 7), measurements were made at a brain temperature (Tb) of 38 degrees C, while in the hypothermic group (n = 7), they were made at 34 degrees C. In the normothermic group, TP-induced isoelectric EEG reduced CMRO2 by 50%, from 7.92 +/- 1.05 to 3.95 +/- 0.70 ml 100 g-1 min-1 (mean +/- = SD). Thus, at 38 degrees C, TP-suppressible and TP-nonsuppressible CMRO2 were both 50 +/- 4% of total CMRO2. In the hypothermic group, decreasing Tb from 38 to 34 degrees C caused a 17% decline in CMRO2, from 7.62 +/- 1.92 to 6.28 +/- 1.22 ml 100 g-1 min-1 (p > 0.05). AT 34 degrees C, TP infusion lowered CMRO2 to 2.15 = 0.46 ml 100 g-1 min-1. At 34 degrees C, TP-suppressible and TP-nonsuppressible CMRO2 values were 64 +/- 7% and 36 +/- 8% of total CMRO2, respectively. TP lowered CBF by 50% at both 38 and 34 degrees C. In conclusion, mild hypothermia selectively lowers TP-nonsuppressible CMRO2 associated with the maintenance of viability rather than EEG-associated or TP-suppressible CMRO2.
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PMID:Suppression of cerebral metabolic rate for oxygen (CMRO2) by mild hypothermia compared with thiopental. 871 94

Previously the authors showed that hypothermia exerts a greater effect on the cerebral metabolic rate for oxygen (CMRO2) that is associated with the maintenance of cellular viability, or "basal" CMRO2, than on electroencephalogram (EEG)-associated CMRO2 or "functional" CMRO2. On the basis of their findings, the authors hypothesized that the ratio of CMRO2 over a 10 degrees C temperature range (Q10) for basal CMRO2 was greater than that for functional and total CMRO2. They tested their hypothesis by determining the Q10 for basal CMRO2 from 38 degrees C to 28 degrees C. They measured whole-brain cerebral blood flow (CBF) and CMRO2 in six rats during progressive hypothermia at a brain temperature of 38 degrees C and, after induction of an isoelectric EEG signal (50 microV/cm) with thiopental sodium, they repeated the measurements at 38 degrees C, 34 degrees C, 30 degrees C, and 28 degrees C. In a control group (five rats), six sequential measurements of CBF and CMRO2 were made while the animals were anesthetized by 0.5% isoflurane/70% N2O/30% O2 at a brain temperature of 38 degrees C over a time span equivalent to the hypothermic group, that is, approximately 3 hours. The Q10 for basal CMRO2 calculated over 38 degrees C to 28 degrees C was 5.2 +/- 0.92. However, the decrease in basal CMRO2 between 38 degrees C and 28 degrees C was nonlinear on a log plot, revealing a two-component response: a high temperature sensitivity component between 38 degrees C and 30 degrees C with a Q10 of 12.1, and a lower temperature sensitivity component between 30 degrees C and 28 degrees C with a Q10 of 2.8. The combined overall Q10 for basal CMRO2 between 38 degrees and 28 degrees C was 5.2. The energy-requiring processes associated with these high and low temperature sensitivity components of basal CMRO2 have yet to be identified.
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PMID:The Q10 ratio for basal cerebral metabolic rate for oxygen in rats. 875 36

In an earlier study on the effect of mild hypothermia (34 degrees C) on the cerebral metabolic rate for oxygen (CMRO2) in rats, we used norepinephrine (NE) to support arterial blood pressure while inducing isoelectricity on the electroencephalogram (EEG) with thiopental (TP). Even with administration of sufficient TP to reduce a fully active EEG to an isoelectric EEG, CMRO2 was often unchanged. Based on this observation, we hypothesized that NE had activated CMRO2 despite thiopental coma. Therefore, we studied the effect of NE compared with donor blood (DB) infusion to maintain arterial blood pressure during TP-induced isoelectric EEG on whole-brain CBF (H2 clearance) and CMRO2 during normothermia (38 degrees C) and mild hypothermia (34 degrees C) in rats during 70% N2O/30% O2 analgesia. Cerebral blood flow (CBF) and CMRO2 were measured in four groups of rats at 38 degrees C followed by measurements at either 38 degrees C (two groups) or 34 degrees C (two groups) and during TP-induced EEG isoelectricity. Within each of the two groups at 38 degrees C and 34 degrees C, arterial pressure was sustained by either DB (n = 10) or NE (n = 9) infusion. At 38 degrees C, CMRO2 in the DB and NE groups was 7.92 +/- 1.05 and 6.4 +/- 0.80 mL x 100 g-1.min-1 and decreased to 50% of normal (3.95 +/- 0.70 and 3.32 +/- 0.40 mL x 100 g-1.min-1, respectively) during TP isoelectricity for a functional:basal CMRO2 distribution of 50% +/- 4% and 50% +/- 4%. At 34 degrees C, CMRO2 values in the DB and NE groups were 6.31 +/- 1.41 and 5.41 +/- 2.02 mL x 100 g-1.min-1, respectively. During TP-induced isoelectricity, CMRO2 values in both groups were reduced to 2.37 +/- 0.43 and 3.55 +/- 1.27 mL x 100g-1.min-1, respectively, resulting in a functional:basal CMRO2 distribution of 61%:38% in the DB group and the reverse, or 27%:73%, in the Ne group. Basal CMRO2 was significantly (P < 0.05) larger in the NE-infused rats. These results suggest that NE infusion, by increasing CMRO2 during mild hypothermia, could nullify its protective effects in the ischemic brain.
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PMID:Norepinephrine activation of basal cerebral metabolic rate for oxygen (CMRO2) during hypothermia in rats. 894 97

Although inhalation of nitrous oxide (N2O) causes hypothermia in rats, there is a paucity of information as to whether tolerance develops to this effect. The purpose of this study was to determine whether tolerance to N2O hypothermia develops within a single administration as well as over repeated administrations. Temperature was measured telemetrically by implanting intraperitoneal thermal sensors/transmitters in male Long-Evans rats. Experimental rats received an initial 2-h exposure to 60% N2O and became hypothermic relative to controls breathing placebo gas. Only a few rats demonstrated evidence of acute tolerance over the 120 min. Over the next 10 days, the experimental rats received five additional 30-min exposures to 60% N2O and five 30-min exposures to placebo while the control rats received only placebo gas exposures. Chronic tolerance developed to N2O hypothermia over these repeated administrations. A test for Pavlovian drug conditioning found no evidence that conditioned temperature effects contributed to chronic tolerance development. In a second experiment, naive rats were given a 380-min exposure to 60% N2O and a 380-min exposure to placebo gas in a counterbalanced order. Acute tolerance did develop to N2O hypothermia, with the recovery of temperature beginning after a mean of 141 min of gas administration. Hence, both acute and chronic tolerance develop to N2O's hypothermic effects in rats.
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PMID:Nitrous oxide-induced hypothermia in the rat: acute and chronic tolerance. 997 63

On average, the hypothermia exhibited by rats receiving 60% nitrous oxide (N2O) eventually abates despite the continued inhalation of the drug (i.e., acute tolerance develops). However, large individual differences occur in both the magnitude of hypothermia achieved and the degree of acute tolerance that develops. To determine whether the degree of temperature loss and subsequent recovery during N2O administration are reliable characteristics of an individual, we measured intraperitoneal temperature via telemetry in 77 Long-Evans rats that each received 60% N2O for 5 h during two sessions separated by 14 days. Good intersession reliability (Pearson's r) was observed for simple change and adjusted change scores for both initial N2O temperature sensitivity (.61 < or = r < or = .62), and acute tolerance development (.46 < or = r < or = .52). In a separate experiment, three groups of rats were selected based on their individual body temperature patterns during an initial N2O administration: (1) insensitive to N2O hypothermia (n = 8); (2) marked hypothermia followed by acute tolerance development (n = 6); and (3) marked hypothermia followed by little acute tolerance development (n = 6). When retested 10 days later, each group exhibited a body temperature profile similar to that observed during the initial N2O exposure. Thus, the temperature profile observed during a rat's initial exposure to 60% N2O reflects a reproducible response for that animal.
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PMID:Reliability of individual differences in initial sensitivity and acute tolerance to nitrous oxide hypothermia. 1152 66

Although accumulating evidence suggests that increased extracellular glutamate concentrations may play an important role in hypoxic-ischemic brain injury, dopamine and other catecholamines also seem to be involved. The N-methyl-D-aspartate receptor antagonist MK 801 and moderate hypothermia (32-34 degrees C) are each known to be neuroprotective, but their combined effect on the release and metabolism of neurotransmitters is unknown. Seven-day-old pups (n: 150) underwent right common carotid artery ligation to induce hemispheric ischemia, and were later subjected to 120 minutes of hypoxia with 8% O2 and 92% N2O. Half the rats (Group I, n: 74) were subjected to normothermic conditions throughout the hypoxic period. Moderate hypothermia (30-32 degrees C) was induced in the other pups (Group II, n: 76) immediately after artery occlusion, and was maintained throughout the hypoxic period. Prior to inducing hypoxia, half of the rats in each group (Groups IA and IIA) received vehicle solution (0.9% NaCI) and the other rats (Groups IB and IIB) received MK 801 (0.5 mg/kg) subcutaneously at 45 and 120 minutes after occlusion. Intracerebral temperature was recorded every 15 minutes after occlusion. Infarct area (n: 40) was calculated after staining with 2% 2,3,5 triphenyltetrazolium chloride. Neuronal damage (n: 42) was assessed by quantifying CA1-CA3 neuronal loss at five hippocampal levels. The amount of damage to the monoamine system of the corpus striatum was determined based on the dopamine and 3,4 dihydroxyphenylacetic acid levels in the corpus striatum in both hemispheres (n: 46), as measured by high-pressure liquid chromatography and compared with normal control pups' values (n: 10). The normothermia/saline-treated pups had significantly larger infarct areas than the MK 801 only, hypothermia only, or MK 801/hypothermia combination groups. Neuropathological examination and striatal tissue monoamine data also confirmed marked neuronal damage in this group. Although MK 801 treatment alone resulted in significantly smaller infarct area and less tissue damage than was observed in the normothermia/saline-treated group, the moderate hypothermia and the MK 801/hypothermia combination treatment groups both exhibited better neuronal protection, especially in the corpus striatum. The rats that received combined treatment also had a significantly lower mortality rate.
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PMID:Neuroprotective effects of MK 801 and hypothermia used alone and in combination in hypoxic-ischemic brain injury in neonatal rats. 1178 Jul 74


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