Evaluation of hand and finger heat loss with a heated hand model.
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A heated full-scale hand model has been used to determine indirectly hand and finger heat losses of human subjects exposed to four ambient cold conditions (0, 4, 10 and 16 degrees C, air velocity approximately 0.3 m/s). Heat transfer coefficients determined with the hand model, were used to calculate heat flux based on measured skin to ambient temperature gradients. The responses of eight subjects from a previous study were used for the analysis. The measurements were carried out in a small climate chamber which was cooled by evaporating liquid carbon dioxide. The thermal hand was put into the chamber in a vertical position with the thumb up. The surface temperature of the thermal hand was controlled at 21, 25, 28, 31 and 34 degrees C under each of the four ambient cold conditions, in order to investigate possible temperature dependence of the calculated combined convective and radiate heat transfer coefficient (hCR). The value of hCR varied between approximately 9-13 W/m2 degree C for fingers and palm and back of hand, respectively. Calculated heat losses showed significant individual variation, corresponding to the maintained skin to ambient temperature gradient. Individual values from about 50 to more than 300 W/m2 were calculated. Several subjects showed CIVD and heat fluxes associated with this phenomenon were sometimes doubled. The measurement results showed realistic and comparable with literature date. The advantages of the thermal hand model can be counted as easy to use; directly measures the heat loss; highly reproducible and no interruption. It appears that a heated hand model provides a useful methods for analysis and quantification of hand heat loss. (+info)
BACKGROUND: Spontaneous tremor is relatively common in normothermic patients after operation and has been attributed to many causes. The hypothesis that nonthermoregulatory shivering-like tremor is facilitated by postoperative pain was tested. In addition, the effects of intravenous lidocaine on nonthermoregulatory tremor were evaluated. METHODS: Patients undergoing knee surgery were anesthetized with 2 microg/kg intravenous fentanyl and 0.2 mg/kg etomidate. Anesthesia was maintained with 1.7 +/- 0.8% (mean +/- SD) isoflurane. Intraoperative forced-air heating maintained normothermia The initial 44 patients were randomly allocated to receive an intra-articular injection of 20 ml saline (n = 23) or lidocaine, 1.5% (n = 21). The subsequent 30 patients were randomly allocated to receive an intravenous bolus of 250 microg/kg lidocaine followed by an infusion of 13 microg x kg(-1) x h(-1) lidocaine or an equivalent volume of saline when shivering was observed. Patient-controlled analgesia was provided for all patients: 3.5 mg piritramide, with a lockout interval of 5 min, for an unlimited total dose. Shivering was graded by a blinded investigator using a four-point scale. Pain was assessed by a 100-mm visual analog scale (0 = no pain and 100 = worst pain). The arteriovenous shunt status was evaluated with forearm-minus-fingertip skin-temperature gradients. RESULTS: Morphometric characteristics and hemodynamic responses were similar in the four groups. Core and mean skin temperature remained constant or increased slightly compared with preoperative values, and postoperative skin-temperature gradients were negative (indicating vasodilation) in nearly all patients. After intra-articular injection of saline, pain scores for the first postoperative hour averaged 46 +/- 32 mm (mean +/- SD), and 10 of the 23 (43%) patients shivered. In contrast, the pain scores of patients who received intra-articular lidocaine were significantly reduced to 5 +/- 9 mm and shivering was absent in this group (P < 0.05). In the second portion of the study, neither intravenous lidocaine nor saline reduced the magnitude or duration of nonthermoregulatory tremor or the patients' pain scores. CONCLUSIONS: Intra-articular, but not intravenous, lidocaine reduced surgical pain and prevented nonthermoregulatory shivering. Therefore, these data indicate that postoperative pain facilitates nonthermoregulatory shivering. (+info)
The biogenesis of mitochondria requires products of the nuclear and mitochondrial genomes. Recent studies of adaptive thermogenesis have shown how mitochondrial proliferation and respiratory activity in brown fat and skeletal muscle are directed by the transcriptional coactivator PGC-1. (+info)
Inhibitory effects of leptin-related synthetic peptide 116-130 on food intake and body weight gain in female C57BL/6J ob/ob mice may not be mediated by peptide activation of the long isoform of the leptin receptor.
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We recently reported that intraperitoneal administration of leptin-related synthetic peptide 116-130 [LEP-(116-130)] resulted in reduced food intake and significant weight loss in homozygous female C57BL/6J ob/ob mice. In this study, we used two in vitro bioassays to show that the interaction of LEP-(116-130) with the long form of the leptin receptor (OB-Rb), the receptor isoform that is predominantly expressed in the hypothalamus, is not required for the observed in vivo effects of the peptide on energy balance. LEP-(116-130) was unable to compete the binding of alkaline phosphatase-leptin fusion protein to OB-R. Moreover, LEP-(116-130) was unable to activate signal transduction by OB-Rb in vitro. In homozygous female C57BLKS/J-m db/db mice that do not express OB-Rb, intraperitoneal administration of LEP-(116-130) reduced body weight gain and blood glucose levels but not food intake, which further supports a mechanism of action that does not require peptide interaction with OB-Rb. (+info)
MEK1 protein kinase inhibition protects against damage resulting from focal cerebral ischemia.
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The MEK1 (MAP kinase/ERK kinase)/ERK (extracellular-signal-responsive kinase) pathway has been implicated in cell growth and differentiation [Seger, R. & Krebs, E. G. (1995) FASEB J. 9, 726-735]. Here we show that the MEK/ERK pathway is activated during focal cerebral ischemia and may play a role in inducing damage. Treatment of mice 30 min before ischemia with the MEK1-specific inhibitor PD98059 [Alessi, D. R., Cuenda, A., Cohen, P. , Dudley, D. T. & Saltiel, A. R. (1995) J. Biol. Chem. 270, 27489-27494] reduces focal infarct volume at 22 hr after ischemia by 55% after transient occlusion of the middle cerebral artery. This is accompanied by a reduction in phospho-ERK1/2 immunohistochemical staining. MEK1 inhibition also results in reduced brain damage 72 hr after ischemia, with focal infarct volume reduced by 36%. This study indicates that the MEK1/ERK pathway contributes to brain injury during focal cerebral ischemia and that PD98059, a MEK1-specific antagonist, is a potent neuroprotective agent. (+info)
Flight-muscle adenylate pool responses to flight demands and thermal constraints in individual Colias eurytheme (Lepidoptera, pieridae).
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We study here the connections among body temperature variation, flight performance and flight 'fuel' metabolism in Colias eurytheme butterflies, to begin re-examining the metabolic reasons for animal thermoregulation. Methods are presented for (a) stable extraction of adenylates (and other metabolites) from the flight muscles of individual Colias eurytheme, (b) automated separation and quantitative analysis of individual adenylate samples by high-pressure liquid chromatography and (c) reliable, low-variance assay of inorganic phosphate levels in the same extracts. Correlations among metabolite concentrations and two indices of muscle cytosol ATP maintenance occur as expected on general metabolic principles. [ATP] and [ATP]/[ADP] decline from resting levels to reach a plateau in the first minute of free, interrupted flight, while [AMP] increases at the same time; these concentrations do not vary further for up to 6 min total flight time. In an initial test of the alternative metabolic bases of the thermoregulation of Colias eurytheme, we find that [ATP]/[ADP] rises between a body temperature, T(b), of 31 and 35 degrees C, at the base of the behavioral thermal optimum for flight, but then decreases again at T(b)=39 degrees C, at the top of the behavioral thermal optimum and well short of damaging temperatures. This is not consistent with the view that metabolic effectiveness increases monotonically up to the lower limits of thermal damage to enzymes, but supports an alternative hypothesis that the narrowness of thermoregulation results from a system-based constraint on the breadth of temperature over which maximal energy processing is possible. (+info)
Effects of a neuronal nitric oxide synthase inhibitor on lipopolysaccharide-induced fever.
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It has been demonstrated that nitric oxide (NO) has a thermoregulatory action, but very little is known about the mechanisms involved. In the present study we determined the effect of neuronal nitric oxide synthase (nNOS) inhibition on thermoregulation. We used 7-nitroindazole (7-NI, 1, 10 and 30 mg/kg body weight), a selective nNOS inhibitor, injected intraperitoneally into normothermic Wistar rats (200-250 g) and rats with fever induced by lipopolysaccharide (LPS) (100 microg/kg body weight) administration. It has been demonstrated that the effects of 30 mg/kg of 7-NI given intraperitoneally may inhibit 60% of nNOS activity in rats. In all experiments the colonic temperature of awake unrestrained rats was measured over a period of 5 h at 15-min intervals after intraperitoneal injection of 7-NI. We observed that the injection of 30 mg/kg of 7-NI induced a 1.5 degrees C drop in body temperature, which was statistically significant 1 h after injection (P<0.02). The coinjection of LPS and 7-NI was followed by a significant (P<0.02) hypothermia about 0.5 degrees C below baseline. These findings show that an nNOS isoform is required for thermoregulation and participates in the production of fever in rats. (+info)
Direct cooling of the human brain by heat loss from the upper respiratory tract.
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This study is the first report on human intracranial temperature in conscious patients during and after an upper respiratory bypass. Temperatures were measured in four subjects subdurally between the frontal lobes and cribriform plate (T(cr)) and on the vault of the skull (T(sd)). Further measurements were taken in the esophagus (T(es)) and on the tympanic membrane. Reinstitution of airflow in the upper respiratory tract under conditions of mild hyperthermia gave a rapid drop in T(cr) of 0.4-0.8 degrees C. In three patients the intracranial temperature at the basal aspect of the frontal lobes fell below T(es). Thus local selective cooling of the brain surface below that of the trunk temperature was shown to occur. Intensive breathing by the patients after extubation for a 3-min period produced a cooling at the site of T(cr) measurement at a rate of up to 0.1 degrees C/min, and this response could be evoked on demand. The results support the view that cooling of the upper airway can directly influence human brain temperature. (+info)