Shiver suppression using focal hand warming in unanesthetized normal subjects. (17/200)

BACKGROUND: A decrease of 1 or 2 degrees C in core temperature may provide protection against cerebral ischemia. However, during corporeal cooling of unanesthetized patients, the initiation of involuntary motor activity (shiver) prevents the reduction of core temperature. The authors' laboratory previously showed that focal facial warming suppressed whole-body shiver. The aim of the current study was to determine whether the use of hand warming alone could suppress shiver in unanesthetized subjects and hence potentiate core cooling. METHODS: Subjects (n = 8; healthy men) were positioned supine on a circulating water mattress (8-15 degrees C) with a convective-air coverlet (14 degrees C) extending from their necks to their feet. A dynamic protocol was used in which focal hand warming was used to suppress involuntary motor activity, enabling noninvasive cooling to decrease core temperatures. The following parameters were monitored: (1) heart rate; (2) blood pressure; (3) core temperature (rectal, tympanic); (4) cutaneous temperature and heat flux; (5) subjective shiver level (SSL scale 0-10) and thermal comfort index (scale 0-10); (6) metabolic data (n = 6); and (7) electromyograms. RESULTS: During cooling without hand warming, involuntary motor activity increased until it was widespread. After subjects reported whole-body shiver (SSL > or = 7), applied hand warming, in all cases, reduced shiver levels (SSL < o r= 3), decreased electromyographic root mean square amplitudes, and allowed core temperature to decrease from 37.0 +/- 0.2 to 35.9 +/- 0.5 degrees C (measured rectally). CONCLUSIONS: Focal hand warming seems to be valuable in minimizing or eliminating the need to suppress involuntary motor activity pharmacologically when it is desired to induce or maintain mild hypothermia; it may be used in conjunction with facial warming or in cases in which facial warming is contraindicated.  (+info)

Awake microlaparoscopy with the Insuflow device. (18/200)

BACKGROUND AND OBJECTIVES: Patients undergoing laparoscopy often complain of shoulder pain, shivering, or both following laparoscopy. An increase in awake microlaparoscopic procedures has been reported. The objective of this study was to investigate the usefulness of heating and humidifying the carbon dioxide gas for the pneumoperitoneum with the Insuflow device (Lexion Medical, St. Paul, Minnesota) during awake microlaparoscopic procedures. METHODS: Awake microlaparoscopy was performed with the Insuflow device for heating and humidifying the carbon dioxide for the pneumoperitoneum. RESULTS: The incidence of transient shoulder pain in the Insuflow group was 5% compared with 40% in the dry carbon dioxide group. No patient in the Insuflow group complained of shivering, whereas 55% in the control group had shivering. Fogging of the microlaparoscope lens was decreased in the Insuflow group. CONCLUSIONS: Heating and humidifying the carbon dioxide gas produced fewer patient complaints of shoulder pain and shivering and decreased fogging of the microlaparoscope lens compared with procedures done with dry carbon dioxide during awake microlaparoscopic procedures.  (+info)

Meperidine exerts agonist activity at the alpha(2B)-adrenoceptor subtype. (19/200)

BACKGROUND: The opioid agonist meperidine has actions, such as antishivering, that are more pronounced than those of other opioid agonists and that are not blocked with nonselective opioid antagonists. Agonists at the alpha(2) adrenoceptors, such as clonidine, are very effective antishivering drugs. Preliminary evidence also indicates that meperidine interacts with alpha(2) adrenoceptors. The authors therefore studied the ability of meperidine to bind and activate each of the alpha(2)-adrenoceptor subtypes in a transfected cell system. METHODS: The ability of meperidine to bind to and inhibit forskolin-stimulated cyclic adenosine monophosphate formation as mediated by the three alpha(2)-adrenoceptor subtypes transiently transfected into COS-7 cells has been tested. The ability of the opioid antagonist naloxone and the alpha(2)-adrenoceptor antagonists yohimbine and RX821002 to block the analgesic action of meperidine in the hot-plate test was also assessed. The ability of meperidine to fit into the alpha(2B) adrenoceptor was assessed using molecular modeling techniques. RESULTS: Meperidine bound to all alpha2-adrenoceptor subtypes, with alpha(2B) having the highest affinity (alpha(2B), 8.6 +/- 0.3 microm; alpha(2C), 13.6 +/- 1.5 microm, P < 0.05; alpha(2A), 38.6 +/- 0.7 microm). Morphine was ineffective at binding to any of the receptor subtypes. Meperidine inhibited the production of forskolin-stimulated cyclic adenosine monophosphate mediated by all receptor subtypes but was most effective at the alpha(2B) adrenoceptor (alpha(2B), 0.6 microm; alpha(2A), 1.3 mm; alpha(2C), 0.3 mm), reaching the same level of inhibition (approximately 70%) as achieved with the alpha2-adrenoceptor agonist dexmedetomidine. The analgesic action of meperidine was blocked by naloxone but not by the alpha 2-adrenoceptor antagonists yohimbine and RX821002. The modeling studies demonstrated that meperidine can fit into the alpha(2B)-adrenoceptor subtype. CONCLUSION: Meperidine is a potent agonist at the alpha2 adrenoceptors at its clinically relevant concentrations, especially at the alpha(2B)-adrenoceptor subtype. Activation of the alpha(2B) receptor does not contribute significantly to the analgesic action of meperidine. This raises the possibility that some of its actions, such as antishivering, are transduced by this mechanism.  (+info)

Endothermic heat production in honeybee winter clusters. (20/200)

In order to survive cold northern winters, honeybees crowd tightly together in a winter cluster. Present models of winter cluster thermoregulation consider the insulation by the tightly packed mantle bees as the decisive factor for survival at low temperatures, mostly ignoring the possibility of endothermic heat production. We provide here direct evidence of endothermic heat production by 'shivering' thermogenesis. The abundance of endothermic bees is highest in the core and decreases towards the surface. This shows that core bees play an active role in thermal control of winter clusters. We conclude that regulation of both the insulation by the mantle bees and endothermic heat production by the inner bees is necessary to achieve thermal stability in a winter cluster.  (+info)

Nitrous oxide decreases shivering threshold in rabbits less than isoflurane. (21/200)

BACKGROUND: Comparable minimum alveolar concentration (MAC) fractions of volatile anaesthetics produce similar thermoregulatory impairment. Nitrous oxide, however, decreases the vasoconstriction threshold less than sevoflurane or isoflurane. We tested the hypothesis that nitrous oxide also decreases shivering threshold less than isoflurane alone or in combination. METHODS: Twenty-four rabbits were assigned randomly to one of three 0.3 MAC anaesthetic regimens: (i) nitrous oxide 69%; (ii) nitrous oxide 35% and isoflurane 0.3%; or (iii) isoflurane 0.6%. Body temperature was lowered by perfusing 10 degrees C water through a U-shaped thermode positioned in the colon. Shivering was evaluated by inspection. RESULTS: The rabbits anaesthetized with nitrous oxide alone shivered at 37.0 (0.5) degrees C (P<0.01 vs other groups). In those given the nitrous oxide and isoflurane combination, the shivering threshold was 36.4 (0.5) degrees C and that in the isoflurane group was 35.9 (0.4) degrees C. CONCLUSION: This study indicates that nitrous oxide reduces the shivering threshold less than isoflurane.  (+info)

Interaction between the effects of spinal heating and cooling and of injections into a lateral cerebral ventricle of noradrenaline, 5-hydroxytryptamine and carbachol on thermoregulation in sheep. (22/200)

1. A study has been made of the interactions of the thermoregulatory effects of spinal cord heating and cooling and of the injections into the cerebral ventricle of noradrenaline, 5-hydroxytryptamine (5-HT) and carbamylcholine in sheep. 2. The interactions of spinal cord heating and the injections into the cerebral ventricle of noradrenaline, 5-HT and carbamylcholine were very similar to those of hypothalamic heating or of high ambient temperature and the injections into the cerebral ventricle of these substances. These results are interpreted as evidence of the synaptic convergence of the pathways from peripheral, spinal cord and hypothalamic warm-sensors at or before the points of action of these synaptically active substances. 3. The only definite thermoregulatory effect of spinal cooling was the onset of shivering which could be due to a purely spinal effect of cold. No substantial evidence was obtained of an interaction between spinal cooling and an injection of noradrenaline, 5-HT or carbamylcholine into the cerebral ventricle. Thus there was no clear indication of centripetal pathways from spinal cold sensors converging with those from the skin and the hypothalamus for which evidence of convergence was obtained in an earlier study. 4. The results of this study are expressed in terms of the neuronal model of Bligh, Cottle & Maskrey (1971) and Maskrey & Bligh (1971), appropriately modified.  (+info)

Heat balance precedes stabilization of body temperatures during cold water immersion. (23/200)

Certain previous studies suggest, as hypothesized herein, that heat balance (i.e., when heat loss is matched by heat production) is attained before stabilization of body temperatures during cold exposure. This phenomenon is explained through a theoretical analysis of heat distribution in the body applied to an experiment involving cold water immersion. Six healthy and fit men (mean +/- SD of age = 37.5 +/- 6.5 yr, height = 1.79 +/- 0.07 m, mass = 81.8 +/- 9.5 kg, body fat = 17.3 +/- 4.2%, maximal O2 uptake = 46.9 +/- 5.5 l/min) were immersed in water ranging from 16.4 to 24.1 degrees C for up to 10 h. Core temperature (Tco) underwent an insignificant transient rise during the first hour of immersion, then declined steadily for several hours, although no subject's Tco reached 35 degrees C. Despite the continued decrease in Tco, shivering had reached a steady state of approximately 2 x resting metabolism. Heat debt peaked at 932 +/- 334 kJ after 2 h of immersion, indicating the attainment of heat balance, but unexpectedly proceeded to decline at approximately 48 kJ/h, indicating a recovery of mean body temperature. These observations were rationalized by introducing a third compartment of the body, comprising fat, connective tissue, muscle, and bone, between the core (viscera and vessels) and skin. Temperature change in this "mid region" can account for the incongruity between the body's heat debt and the changes in only the core and skin temperatures. The mid region temperature decreased by 3.7 +/- 1.1 degrees C at maximal heat debt and increased slowly thereafter. The reversal in heat debt might help explain why shivering drive failed to respond to a continued decrease in Tco, as shivering drive might be modulated by changes in body heat content.  (+info)

Dexmedetomidine and meperidine additively reduce the shivering threshold in humans. (24/200)

BACKGROUND AND PURPOSE: Hypothermia might prove to be therapeutically beneficial in stroke victims; however, even mild hypothermia provokes vigorous shivering. Meperidine and dexmedetomidine each linearly reduce the shivering threshold (triggering core temperature) with minimal sedation. We tested the hypothesis that meperidine and dexmedetomidine synergistically reduce the shivering threshold without producing substantial sedation or respiratory depression. METHODS: We studied 10 healthy male volunteers (18 to 40 years) on 4 days: (1) control (no drug); (2) meperidine (target plasma level 0.3 microg/mL); (3) dexmedetomidine (target plasma level 0.4 ng/mL); and (4) meperidine plus dexmedetomidine (target plasma levels of 0.3 microg/mL and 0.4 ng/mL, respectively). Lactated Ringer's solution (approximately 4 degrees C) was infused through a central venous catheter to decrease tympanic membrane temperature by approximately 2.5 degrees C/h; mean skin temperature was maintained at 31 degrees C. An increase in oxygen consumption >25% of baseline identified the shivering threshold. Sedation was evaluated by using the Observer's Assessment of Sedation/Alertness scale. Two-way repeated-measures ANOVA was used to identify interactions between drugs. Data are presented as mean+/-SD; P<0.05 was statistically significant. RESULTS: The shivering thresholds on the study days were as follows: control, 36.7+/-0.3 degrees C; dexmedetomidine, 36.0+/-0.5 degrees C (P<0.001 from control); meperidine, 35.5+/-0.6 degrees C (P<0.001); and meperidine plus dexmedetomidine, 34.7+/-0.6 degrees C (P<0.001). Although meperidine and dexmedetomidine each reduced the shivering threshold, their interaction was not synergistic but additive (P=0.19). There was trivial sedation with either drug alone or in combination. Respiratory rate and end-tidal Pco2 were well preserved on all days. CONCLUSIONS: Dexmedetomidine and meperidine additively reduce the shivering threshold; in the small doses tested, the combination produced only mild sedation and no respiratory toxicity.  (+info)