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

Hypothermia and shivering are common during epidural anesthesia for cesarean delivery but are not always accompanied by a sensation of coldness. To test the hypothesis that central temperature changes are not perceived during epidural anesthesia, we measured central and skin temperatures and thermal perception in 30 patients undergoing cesarean delivery with epidural anesthesia. Central temperature decreased 1.0 +/- 0.6 degrees C from control values during anesthesia and surgery, but thermal perception scores did not reflect central temperatures (P = 0.56) or changes in central temperature (P = 0.63). A feeling of warmth was significantly correlated with increased mean skin temperature (P = 0.02) and increased upper body skin temperature (P = 0.03). We conclude that central temperature is poorly perceived and is less important than skin temperature in determining thermal perception during high levels of epidural anesthesia.
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PMID:Central temperature changes are poorly perceived during epidural anesthesia. 160 82

The general pharmacological properties of (-)-(S)-9-fluoro-2,3-dihydro-3- methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido[1,2,3-de][1,4] benzoxazine-6-carboxylic acid hemihydrate (levofloxacin, DR-3355, CAS 100986-85-4), an optically active isomer of ofloxacin, were examined. 1. Central nervous system (CNS): DR-3355 at 200-600 mg/kg p.o. showed depressant activity on the CNS, as was indicated by the depressant syndrome (mice), decreased spontaneous motor activity (mice) and hypothermia (mice and rabbits). In the cat behavior and EEG experiments, it had both stimulant and depressant effects at 30-100 mg/kg i.p., and caused transient slow waves followed by seizures at 20-30 mg/kg i.v. DR-3355 had no effect on convulsion, hexobarbital anesthesia, pain reaction to a tail pinch, or conditioned avoidance response, except that it showed mild analgesic activity in acetic acid writhing at 600 mg/kg p.o. 2. Respiratory and cardiovascular system: DR-3355 produced a hypotensive and a bradycardiac effect after the rapid i.v. injection of 6 mg/kg or more in anesthetized dogs, accompanied by an increase in plasma histamine concentration. Both changes were markedly reduced when the test drug was administered by continuous i.v. infusion. 3. Autonomic nervous system: DR-3355 inhibited nictitating membrane contraction induced by both pre- and post-ganglionic stimulation, and inhibited the depressor response to acetylcholine at 20 mg/kg i.v. It had no influence on pupil size or on pressor response to norepinephrine. 4. Gastrointestinal system: DR-3355 at 600 mg/kg p.o. inhibited gastric secretion. Dog gastrointestinal motility was slightly inhibited, and was then stimulated over the dose range of 2-20 mg/kg i.v. It had no influence on gastrointestinal propulsion, the gastric emptying rate or the gastric mucosa. 5. Isolated smooth muscle: At a concentration of 5 x 10(-4) g/ml, DR-3355 was devoid of spasmogenic or smasmolytic activity, except for showing a slight relaxation effect (trachea), inhibition of nicotine-induced contraction (ileum) and spontaneous or oxytocin-induced motility (pregnant uterus). 6. Miscellaneous: DR-3355 inhibited the urine output and carrageenin-induced paw edema at 600 mg/kg p.o. It had no effect on skeletal muscle contraction or the corneal reflex.
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PMID:General pharmacology of the new quinolone antibacterial agent levofloxacin. 162 43

Postoperative neurological deficit may result from ischaemic or hypoxic hypoxaemia. Postural cerebral hypoperfusion may ensue when a pre-existing asymptomatic vascular anomaly in combination with rotation of the head for surgical positioning compromises cerebral blood flow. CASE REPORT. A 30-year-old man was referred for recraniotomy for glioblastoma. Following uneventful induction of anaesthesia, increased diuresis and progressive hypothermia were observed. The postoperative period was complicated by a seizure, followed by apnoea requiring reintubation of the trachea. A CAT scan revealed global cerebral oedema with subtotal compression of the third ventricle. Intracranial pressure was 60 mm Hg as measured by an epidural probe. On the 1st postoperative day clinical and electroneurophysical signs of brain death were observed; the patient underwent organ explantation the next day. PATHOLOGY. Pathological examination revealed pronounced global hypoxaemic lesions and an S-shaped internal carotid artery with intimal proliferation (Fig. 1). The diagnostic conclusion was cerebral ischaemia following carotid occlusion caused by carotid kinking and completed by surgical positioning (rotation of the head). CONCLUSION. Carotid kinking is a rare abnormality, and patients at risk may not be identified preoperatively. Though it is questionable whether this disaster could have been prevented at all, electroneurophysiological monitoring would have been the only early monitoring system capable of detecting diminishing cerebral blood flow. Although a request for routine intraoperative neurophysiological monitoring seems unrealistic at present, it has to be acknowledged that only such monitoring could have provided the information needed to save this patient.
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PMID:[A fatal intraoperative cerebral ischemia following kinking of the internal carotid artery?]. 163 22

In order to compare the effects of blood-gas management on cerebral blood flow, metabolism and neurological outcome after hypothermic cardiopulmonary bypass (CPB) we have studied 65 patients undergoing aorto-coronary bypass surgery allocated randomly to either a pH-stat (temperature-corrected blood-gas management) or an alpha-stat (temperature-uncorrected blood-gas management) group. All patients were examined neurologically on the day before and the 7th day after operation. In 20 patients of the pH-stat group and in 15 patients of the alpha-stat group we measured cerebral blood flow (CBF), using the argon washin technique, and also cerebral oxygen (CMRO2) and glucose (CMRg) uptake. Measurements were performed in awake patients, after induction of anaesthesia with fentanyl, midazolam and pancuronium under normothermic conditions, during CPB at a venous blood temperature of 26 degrees C and at the end of surgery. Compared with postinduction values, hypothermia was associated with an 18% reduction in CBF and decreases in CMRO2 and CMRg of 61% and 60%, respectively, in the alpha-stat group. In the pH-stat group, CMRO2 and CMRg decreased also, by 58% and 74%, respectively, whereas CBF increased by 191%, indicating uncoupling of flow and metabolism. As there were no statistically significant differences between the metabolic variables in both groups, we conclude that acid-base management did not affect cerebral metabolism, despite its influence on blood flow. After rewarming, CBF and cerebral metabolism normalized independently of acid-base management during hypothermia. Nevertheless, neurological dysfunction occurred more often in the pH-stat group (P = 0.036).
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PMID:Acid-base management during hypothermic cardiopulmonary bypass does not affect cerebral metabolism but does affect blood flow and neurological outcome. 163 3

In order to re-evaluate the role of two putative waking systems, we injected a neural cell body toxin, ibotenic acid (IA) (45 micrograms/microliters), into the mesencephalic reticular formation (MRF) and/or the posterior hypothalamus (PH). On the one hand, when the cell body destruction was only restricted to the MRF, the IA microinjection was followed by a temporary high voltage and slow neocortical electroencephalogram (EEG) during the first 24 postoperative hours and by a subsequent long term increase in waking which lasted 8-12 h. After the first postoperative day, there were no motor disturbances, no aphagia nor adypsia, no alteration of cortical activation and no modification of thermoregulation or of the sleep-waking cycle. On the other hand, the IA microinjection into the PH induced a hypothermia during the first postoperative night and a dramatic transient hypersomnia immediately after the disappearance of the anesthesia (14-24 h after the IA injection). On the third day, all cats recovered control level of paradoxical sleep (PS), slow wave sleep (SWS) and cerebral temperature. They presented normal motor behavior but they were not able to eat by themselves during the first postoperative week. Finally, when the lesions of the MRF and the PH were realized in one single operation, the cats were first motionless in a comatose state for 2-3 days. This state was accompanied by a transitory hypothermia and the suppression of a spontaneous or evoked cortical low voltage fast activity. However, from the 2nd postoperative week, both behavioral and EEG waking re-occurred. By contrast, the two successive operations (MRF followed by PH) did not induce a comatose state. We did not observe any deficit in motor behavior, and the sleep-waking cycle was quite normal as from the second postlesion day. In the MRF-PH-lesioned cats, the injection of alpha-methyl-p-tyrosine (150 mg/kg) induced a large decrease in waking and a moderate increase in PS. In the MRF-lesioned cats, IA produced a large area of cell body loss, centered in the MRF, that extended from levels A2 to A6 of stereotaxic planes and sometimes encroached upon the red nucleus and the substantia nigra. In the PH-lesioned cats, the histological analysis revealed a great loss of cell bodies in the PH extended from levels A8 to A12.5. The damage included the lateral and posterior hypothalamic areas and sometimes the tuberomamillary nucleus. In MRF- and PH-lesioned cats, the cell body loss extended from levels A2 to A12.5.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotoxic lesion of the mesencephalic reticular formation and/or the posterior hypothalamus does not alter waking in the cat. 167 7

Seven healthy patients were investigated during midazolam-fentanyl nitrous oxide-oxygen anaesthesia. The mechanical twitch response of the adductor pollicis muscle was recorded simultaneously during bilateral supramaximal train-of-four (TOF) stimulation of the ulnar nerves at the wrist. Intense neuromuscular block was evaluated using the post-tetanic count (PTC) method. Core temperature and the peripheral skin temperature of one arm were kept normal and stable. Following cooling of the other arm to a peripheral hand skin temperature of 27 degrees C, vecuronium was administered in a bolus dose of 0.05 mg.kg-1 followed by maintenance doses of 0.02 mg.kg-1. In the hypothermic and the normothermic arm the onset time following the bolus dose was 180 +/- 40 (mean +/- s.d.) seconds and 140 +/- 30 s, respectively, the duration of action was 26.4 +/- 4.5 and 16.5 +/- 4.0 min and the recovery time was 265 +/- 90 and 130 +/- 60 s (P less than 0.01). The time course of action following maintenance doses showed a similar marked difference between the hypothermic and the normothermic arm. In the normothermic arm a close correlation was found between the number of post-tetanic twitches and the time to first response to TOF stimulation. In contrast, in the hypothermic arm the number of post-tetanic twitches showed great variation with a poor correlation to the duration of intense neuromuscular block. It is concluded that the time course of action of a vecuronium-induced neuromuscular block is markedly prolonged during peripheral hypothermia and intense neuromuscular block cannot reliably be assessed using the PTC method at low peripheral temperature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of peripheral hypothermia on a vecuronium-induced neuromuscular block. 167 93

Two experiments were conducted to determine the effects of hypothermia and pentobarbital anesthesia, alone and in combination, on the brain-stem auditory evoked responses (BAERs) of rats. In experiment I, unanesthetized rats were cooled to colonic temperatures 0.5 and 1.0 degrees C below normal. In experiment II, 2 groups of rats were cooled and tested at 37.5, 36.0, 34.5 and 31.5 degrees C. One group was anesthetized during testing and the other group was awake. The rat BAER was sensitive to cooling of 1 degree C or less. Peak latencies were prolonged and peak-to-peak amplitudes were increased by hypothermia alone. The effect on amplitude may be related to the time course of temperature change or to stimulus level. Pentobarbital significantly affected both latencies and amplitudes over and above the effects of cooling. The specific effects of pentobarbital differed by BAER peak and by temperature. The findings point up the importance of the potential confound of anesthetic drugs in most of the evoked potential literature on hypothermia and, for the first time, quantify the complex interactions between pentobarbital and temperature which affect the BAER wave form.
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PMID:Differential impact of hypothermia and pentobarbital on brain-stem auditory evoked responses. 171 67

Acquisition of conditioned taste aversion (CTA) in rats is not prevented by functional decortication, anesthesia or hypothermia applied after intake of the flavored fluid and maintained throughout the action of the poison but is disrupted by bilateral application of 10 ng tetrodotoxin (TTX) into the parabrachial nuclei. The blockade is directly proportional to TTX dosage, indirectly proportional to distance of the injection site from parabrachial nuclei and equally affects CTAs using different CS (saccharin, NaCl) and different US (LiCl, carbachol, amphetamine, cycloheximide). CTA is disrupted by TTX applied up to 4 but not 8 days after a single CS-US pairing. TTX fails to disrupt overtrained CTA and elicits only a weak anterograde amnesia when applied 1 but 2 or more days before CTA acquisition. It is concluded that the parabrachial nuclei and the adjacent reticular formation probably represent the neural substrate of the permanent CTA engram the protracted consolidation of which is disrupted by prolonged cessation of impulse which is disrupted by prolonged cessation of impulse activity in the information storing network.
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PMID:Brain stem mechanisms of conditioned taste aversion learning in rats. 172 Jun 86

The increased metabolic and respiratory demand during naloxone recovery from opioid-based anesthesia could be related to the return of thermoregulation in hypothermic patients and thus be avoided by preventing intraoperative hypothermia. In this study, we measured O2 uptake (VO2) during naloxone-induced recovery in two groups of patients to determine the effect of intraoperative heat loss on postoperative VO2 changes. In seven patients, intraoperative hypothermia was prevented (normothermic group), whereas hypothermia was allowed to develop in seven other patients (hypothermic group). Core and skin temperatures were measured throughout the study to calculate changes in body heat content. Before naloxone antagonism of fentanyl-supplemented anesthesia, core temperature (mean +/- SEM) was 36.8 +/- 0.1 degrees C in the normothermic group and 34.2 +/- 0.2 degrees C in the hypothermic group (P less than 0.001). After titrated administration of naloxone during recovery, VO2 and minute ventilation (VE) increased in the hypothermic group, by 114 +/- 37% and 97 +/- 52% respectively (P less than 0.05), with a three-fold increase in four patients. In the normothermic group, VO2 increased significantly less (25 +/- 5%), without any significant change in VE. The change in VO2 and VE was significantly greater in patients who were hypothermic. VO2 was integrated throughout the recovery period to calculate recovery energy expenditure. Recovery energy expenditure and intraoperative heat loss were highly correlated (r = 0.88; P less than 0.01). This study demonstrates that the metabolic and respiratory stresses associated with naloxone-induced recovery from opioid-based anesthesia depend on the intraoperative heat loss and can therefore be reduced by preventing intraoperative hypothermia.
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PMID:Oxygen uptake during recovery following naloxone. Relationship with intraoperative heat loss. 172 37

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
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PMID:Acute postoperative hypertension in the hypertensive patient. 173 70


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