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

Central body temperature, which usually is well controlled, typically decreases more than 1 degree C during the 1st h of general anesthesia. This hypothermia has been attributed partially to an anesthetic-induced peripheral vasodilation, which increases cutaneous heat loss to the environment. Based on the specific heat of humans, heat loss would have to increase more than 70 W for 1 h (in a 70-kg person) to explain hypothermia after induction of general anesthesia. However, during epidural anesthesia, sympathetic blockade increases heat loss only slightly. Furthermore, thermoregulatory vasoconstriction in unanesthetized humans decreases heat loss to the environment only 15 W. Therefore, we tested the hypothesis that the hypothermia that follows induction of general anesthesia does not result from increased cutaneous heat loss. Heat loss and skin-surface and tympanic membrane temperatures, before and after induction of isoflurane anesthesia, were measured in five minimally clothed volunteers. Peripheral skin blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Cutaneous heat losses in watts were summed from ten area-weighted thermal flux transducers. Tympanic membrane temperature, which was stable during the 30-min control period preceding induction, decreased 1.2 +/- 0.2 degrees C in the 50 min after induction. Isoflurane anesthesia decreased mean arterial blood pressure approximately 20%. Average skin-surface temperature increased over 15 min to 0.5 degree C above control. Heat loss from the trunk, head, arms, and legs decreased slightly, whereas loss from the hands and feet (10.5% of the body surface area) doubled (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isoflurane-induced vasodilation minimally increases cutaneous heat loss. 199 Aug 97

Neuroprotective agents may exert their effect by reducing cerebral oxygen demand (CMRO2), increasing cerebral oxygen delivery, or by altering ongoing pathological processes. Barbiturates provide neuroprotection by reducing the CMRO2 necessary for synaptic transmission while leaving the component necessary for cellular metabolism intact. Isoflurane may exert a neuroprotective effect by a similar mechanism but its efficacy is likely less than that of barbiturates due to adverse effects on cerebral blood flow. Lidocaine reduces CMRO2 by affecting both cellular metabolic processes and synaptic transmission and thus resembles hypothermia in its mechanism of action. Benzodiazepines reduce CMRO2 by reducing synaptic transmission and their use as neuroprotectants produces less haemodynamic compromise than barbiturates. The mechanism of protection by calcium entry blocking agents appears to be due to improved blood flow as opposed to altering abnormal Ca++ fluxes. In contrast, agents such as ketamine and MK-801 may prevent abnormal Ca++ fluxes through their competitive interaction with N-methyl-D-aspartate receptors. Phenytoin prevents K(+)-mediated ischaemic events from progressing. Agents worthy of further investigation include corticosteroids, free radical scavengers, prostaglandin inhibitors and iron chelators.
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PMID:Brain protection: physiological and pharmacological considerations. Part II: The pharmacology of brain protection. 222 93

Somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded over Erb's point (N10), neck (N13) and scalp (N20) of 17 neurologically normal patients during hypothermic cardiopulmonary bypass. Anesthesia was induced with fentanyl and 100% oxygen, and supplemented with isoflurane as necessary. All 3 SEPs were recorded at esophageal temperatures (Te) of down to 19.5 degrees C. The central conduction time (CCT, defined as N20-N13 interpeak interval) increased exponentially with decreasing temperature (CCTTe = 1.066(37)-Te X CCT37; r = -0.96). The spinal conduction time (SCT, defined as N13-N10 interpeak interval) also increased exponentially but less steeply than the CCT (SCTTe = 1.047(37)-Te X SCT37; r = -0.89), and the N10 peak latency increased exponentially and least steeply (N10Te = 1.033(37)-Te. N10(37); r = -0.87). Anesthetic doses of fentanyl (75 micrograms/kg) did not affect the SEPs. Isoflurane (inspired concentration, 0.25-2.0%) produced dose-dependent increases in CCT of up to 13% and decreased N20 amplitude. All patients had normal CTs after rewarming and none suffered postoperative neurological deficits. Differences in slopes of the latency-temperature functions indicate that cooling produces more conduction slowing in central than in peripheral segments of the pathway and can be accounted for by estimates of the effects of cooling on synaptic delay and axonal conduction between wrist and cortex. The consistency of SEPs between patients both during stable hypothermia and when temperature was changing suggests their potential as a sensitive monitor of cerebral status during hypothermic cardiopulmonary bypass.
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PMID:Central and spinal somatosensory conduction times during hypothermic cardiopulmonary bypass and some observations on the effects of fentanyl and isoflurane anesthesia. 241 46

Isoflurane (1.5 to 3.0 vol% in oxygen) was used to control intraoperative hypertension in 10 patients undergoing hypothermic cardiopulmonary bypass surgery. Isoflurane was administered through the membrane oxygenator of the bypass pump and yielded plateau concentrations in arterial blood ranging from 36.6 to 84.4 micrograms/ml (0.5 and 1.16 vol%, respectively). Isoflurane dosing resulted in prolonged periods (21 to 63 minutes) of EEG burst suppression and isoelectric activity in nine patients. Burst suppression was not a result of hypothermia. There was a close temporal relationship between isoflurane concentration and the onset of burst suppression (mean onset time: 27.3 +/- 4.56 minutes after isoflurane begun). The mean arterial isoflurane concentration at the onset of burst suppression was 46.5 +/- 10.7 micrograms/ml; the nasopharyngeal temperature was 26.0 degrees +/- 0.61 degrees C. Isoflurane was eliminated rapidly from blood with a mean apparent t1/2 of 18.8 +/- 5.46 minutes.
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PMID:Arterial isoflurane concentration and EEG burst suppression during cardiopulmonary bypass. 374 35

It is important to know the effects of anaesthetics on cerebral blood flow and cerebral metabolism to enable appropriate selection of agents for the brain injured patient. Thiopental possesses favourable cerebrovascular and metabolic properties but has not been shown to improve outcome in head injured patients. Propofol has properties similar to thiopental. Its rapid metabolism as well as its ability to reduce intracranial pressure and its antiemetic properties render it a very favourable drug. Despite controversies surrounding the effects of short-acting narcotics on intracranial pressure, they continue to be used because they provide stable haemodynamic conditions when used with care. Isoflurane is currently advocated as the best inhalational agent for neuroanaesthesia because of its lesser effects on cerebral blood flow and intracranial pressure. The effects of nitrous oxide on cerebral blood flow and intracranial pressure appear to vary according to the background anaesthetic used. Nitrous oxide is still widely used in most neuroanaesthetic practices, as its effects can be blunted by barbiturates, narcotics and/or hypocapnia. There is no convincing human study on the cerebral protective properties of anaesthetic agents although mild hypothermia has been shown experimentally to offer significant protection against global and focal ischaemia.
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PMID:Cerebrovascular and cerebral metabolic effects of commonly used anaesthetics. 771 Feb 26

Hypothermia and isoflurane alone increase the potencies of steroidal muscle relaxants (MRs). We studied the combined influence of isoflurane and hypothermia on MR potency. Phrenic nerve-hemidiaphragm preparations of rats were mounted in modified Krebs' solution and aerated with 5% CO2-95% O2 gas mixture at 37 degrees C and 4% CO2 at 27 degrees C to maintain the CO2 content constant. Phrenic nerves were stimulated with 0.1 Hz supramaximal impulses and elicited tension of the diaphragm was recorded. Isoflurane 1% was added after stabilization of twitch tension and MR was added 60 min later. Twitch tension was reduced by 20% +/- 2.5% at 37 degrees C and 3.5% +/- 0.7% at 27 degrees C from control with only isoflurane. The IC50 (inhibitory concentration, 50%) values of the MRs decreased significantly (P < 0.05) with isoflurane at both temperatures. The ratios of the IC50 values without and with isoflurane of the benzylisoquinolinium MRs were significantly more at both temperatures (P < 0.05) indicating the enhancement of potentiation of their action by isoflurane over steroidal MRs. When the soluble concentration of isoflurane at 27 degrees C was kept similar to that of at 37 degrees C, the ratios of all the MRs were reduced significantly from the ratios at 37 degrees C, indicating a reduction of potentiation. When the partial pressure of isoflurane was kept constant at 37 degrees C and 27 degrees C, the potentiating action of the MRs by isoflurane was similar. But when the partial pressure was decreased to keep the concentration of isoflurane constant, the potentiation was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of isoflurane and temperature on the actions of muscle relaxants in rat in vitro. 776 49

Perioperative thermal manipulations are usually directed at the skin surface because methods of directly warming the core are invasive or ineffective. However, inadequate heat flow between peripheral and core compartments will decrease the rate at which core temperature changes. We therefore determined whether core hypothermia is delayed after initiation of surface cooling. Six volunteers were anesthetized with propofol and midazolam, and maintained under three layers of passive insulation for 2.5-4 h. Subsequently, the skin surface was cooled using forced air, 1000 L/min, at 10 degrees C. Isoflurane was added as necessary to maintain arteriovenous shunt vasodilation. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Average arm and leg (peripheral) tissue temperatures were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. Overall body heat content decreased approximately 234 kcal during 2.5 h of active cooling. Core temperature, which was nearly constant before active cooling, decreased approximately 1.3 degrees C/h. There was no delay between initiation of active cooling and the decrease in core temperature. Furthermore, peripheral (arm and leg) and core (trunk and head) tissue heat contents decreased at virtually the same rates: approximately 50 kcal/h and approximately 47 kcal/h, respectively. These data indicate that there is little restriction of heat flow between peripheral and core tissues in vasodilated, anesthetized subjects.
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PMID:Rapid core-to-peripheral tissue heat transfer during cutaneous cooling. 861 Sep

Both cold and warm ischemia occur during liver transplantation. Hypothermia and Wisconsin solution preserve adenine nucleotide energy status, which is crucial to hepatic function and viability. The volatile anesthetic isoflurane has been shown to preserve energy status in anoxic isolated hepatocytes in warm Krebs solution. The present study examined isoflurane effects on energy status during incubation also in Wisconsin or Krebs-plus-adenosine solution at 37 degrees or 4 degrees. Hepatocytes were isolated from rat liver after perfusion with Krebs + collagenase. In 25-mL flasks, 12.5 million cells in 2.5 mL of Krebs, Krebs plus 5 mmol/L adenosine, or Wisconsin solution were incubated under an atmosphere of O2/CO2 or N2/CO2 (19:1) +/- isoflurane (3 volumes% = 2ED50), for 30 minutes at 37 degrees C or 4 degrees C. Adenine nucleotides were measured by high-performance liquid chromatography (HPLC), lactate enzymatically. During warm (37 degrees) anoxia, Wisconsin solution preserved energy status; Krebs plus adenosine did not. Isoflurane further protected energy status in all three solutions. Hypothermia (4 degrees) alone greatly decreased anoxic loss of energy status in all solutions. In Wisconsin solution only, energy status tended to be higher in anoxic than in oxygenated cells and was further enhanced by isoflurane, with corresponding increases in lactate. During 30 minutes of either warm or cold anoxia, isoflurane and Wisconsin solution each helped preserve adenine nucleotide energy status in isolated hepatocytes, at least in part through enhanced glycolysis.
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PMID:Energy status in anoxic rat hepatocytes: effects of isoflurane, solution composition, and hypothermia. 934 69

It is known that hypothermia can improve outcome when induced during ischemia. We evaluated whether hypothermia can decrease ischemic injury if it is induced after incomplete ischemia. Rats were anesthetized with 1.4% inspired isoflurane, and ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Hypothermia (31 degrees C) was induced or normothermia (37 degrees C) was maintained for 1 h after completion of the ischemic challenge. Isoflurane anesthesia was maintained during this period. Five of 15 normothermic rats and 3 of 15 hypothermic rats died of stroke after ischemia. For all rats tested, hypothermic-treated animals had a significantly better neurologic outcome than normothermic rats (p less than 0.05). Histopathology showed a correlation of r = 0.67 (p less than 0.05) with neurologic outcome, and neuronal damage was significantly worse in normothermic compared with hypothermic rats (p less than 0.05). These results show that postischemic hypothermia will decrease neuronal injury and improve neurologic outcome associated with incomplete ischemia.
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PMID:Postischemic treatment with hypothermia improves outcome from incomplete cerebral ischemia in rats. 1581 76

Isoflurane is one of the safest and most accepted anesthetic agents for reptiles, birds, and mammals. It has also been used in terrestrial amphibians. The use of inhalation agents in an entirely aquatic frog presents a new dilemma for delivery in contrast to terrestrial species. The African Clawed Frog respires by using both transcutaneous gas exchange and air breathing. These frogs remain submerged for long periods of time, thus making standard inhalation techniques impractical. We tested five methods for delivering isoflurane: 1) bubbling isoflurane and oxygen in the water, 2) intracoelomic injection, 3) subcutaneous injection, 4) intramuscular injection, and 5) topical application. For the topical application, we developed a simple technique by using an absorptive pad with a vapor-barrier backing, saturating the pad with the liquid isoflurane, and placing the pad on the back of the frog while it was confined in a plastic bowl. Although two of the three injectable routes induced anesthesia, only the topical route produced rapid induction with consistent, safe recovery. Bubbling isoflurane with oxygen into water was unsuccessful. Topical application of isoflurane was most successful and appears to be a safe and practical method that can be used as an alternative to tricaine methylsulphonate, hypothermia, or other methods for anesthetizing African Clawed Frogs.
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PMID:Isoflurane anesthesia in the African clawed frog (Xenopus laevis). 1148 51


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