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PubMed1997

Lidocaine pharmacokinetics and toxicity in newborn pigs.

In newborn infants suffering from perinatal asphyxia seizures, lidocaine (LD) has proved to be an effective anticonvulsant. At high concentrations, however, LD can itself cause convulsions. The convulsive concentration of LD (LD(conv)) varies among species. The aim of this study was to describe LD pharmacokinetics and to define the LD(conv) in awake newborn pigs. Eighteen Land race newborn pigs aged 12-60 h, weight 1.0-2.5 kg, were enrolled. LD, 2 mg/kg intravenous (IV) bolus, (n = 11) was given to estimate pharmacokinetic variables. Continuous LD infusion 2 mg x kg(-1) x min(-1) IV (n = 5) and repeated bolus doses of 15 mg/kg (n = 4) were given until electroencephalogram-confirmed seizures appeared. After the bolus injection, the elimination half-life for LD was 0.87-5.44 h. Increasing plasma concentration (LD(pl)) during infusion resulted in sedation after 5-10 min and in shivering, nystagmus, neck extension, tonic-clonic seizures at LD(conv) of 40.6 +/- 12.7 mg/L (mean +/- SD). The unbound LD(pl) at seizures was 4.4 +/- 2.4 mg/L. Younger animals convulsed at higher LD(conv) (r2 = 0.85). LD pharmacokinetics in newborn pigs were found to be dose-dependent at high plasma concentrations. At lower plasma concentrations, LD pharmacokinetics appeared to be linear. The central nervous system is the primary target for the toxic effect of LD in awake newborn pigs. LD neurotoxicity is age-dependent, and younger pigs convulse at a higher LD(conv).

Age Factors↗
PubMed2002

The influence of active warming on signal quality of pulse oximetry in prehospital trauma care.

UNLABELLED: Victims of trauma such as contusions and simple fractures are usually transported by paramedics. Because many victims are intoxicated with alcohol or other drugs, they are vulnerable to some risk of inadequate respiration. Thus, their oxygenation is monitored by noninvasive pulse oximetry. We tested the hypothesis that active warming of the whole body during transport to the hospital can improve the reliability of arterial oxygen saturation (SpO(2)) monitoring. Twenty-four trauma patients transported to hospital were included in the study and randomly assigned to two groups: one group (n = 12) was covered with normal wool blankets, and the other group (n = 12) was treated with resistive heating blankets during transport. We recorded core temperature, shivering, skin temperature at the forearm and finger, SpO(2), and hemodynamic variables. Before randomization, both groups were comparable. On arrival at the hospital, the actively warmed patients had significantly warmer core (36.1 +/- 0.3 degrees C versus 35.5 +/- 0.3 degrees C; P < 0.001) and skin (34.1 +/- 1.5 degrees C versus 24.9 +/- 1.4 degrees C; P < 0.001) temperatures. In the actively warmed group, the pulse oximeter had significantly fewer alerts (31 versus 58) and a significantly less time of malfunction (146 +/- 42 s versus 420 +/- 256 s) and provided more constant measurements in the actively warmed group (P < 0.001). In this study we showed that active warming improves pulse oximeter monitoring quality in trauma patients during transport to the hospital. IMPLICATIONS: Clinical trials show that pulse oximeter signal quality is limited by hypothermia. In this study we show that active whole-body warming of trauma victims improves monitoring quality during transport to the hospital.

Aged↗
PubMed1995

Heat flow and distribution during epidural anesthesia.

BACKGROUND: Core hypothermia after induction of epidural anesthesia results from both an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors thus evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution. METHODS: Twelve minimally clothed male volunteers were evaluated in a approximately 22 degrees C environment for 2.5 control hours before induction of epidural anesthesia and for 3 subsequent hours. Epidural anesthesia produced a bilateral sympathetic block in only six volunteers, and only their results are reported. Shivering, when observed, was treated with intravenous meperidine. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in esophageal or tympanic membrane (core) temperatures, leaving the core hypothermia specifically resulting from redistribution. RESULTS: Arm heat content decreased approximately 5 kcal/h after induction of anesthesia, but leg heat content increased markedly. Most of the increase in leg heat content was in the lower legs and feet. Core temperature increased slightly during the control period but decreased 0.8 +/- 0.3 degrees C in the 1st hour of anesthesia. Redistribution, contributing 89% to this initial decrease, required a net transfer of 20 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 0.4 +/- 0.3 degrees C, with redistribution contributing 62%. Thus, only 7 kcal were redistributed during the 2nd and 3rd hours of anesthesia. Redistribution therefore contributed 80% to the entire 1.2 +/- 0.3 degrees C decrease in core temperature during the 3 h of anesthesia. CONCLUSIONS: Core hypothermia during the 1st hour after induction of epidural anesthesia resulted largely from redistribution of body heat from the core thermal compartment to the distal legs. Even after 3 h of anesthesia, redistribution remained the major cause of core hypothermia. Despite the greater fractional contribution of redistribution during epidural anesthesia, core temperature decreased only half as much as during general anesthesia because metabolic rate was maintained and the arms remained vasoconstricted.

Adjuvants, Anesthesia↗
PubMed1997

Dexmedetomidine as an anesthetic adjunct in coronary artery bypass grafting.

BACKGROUND: Alpha 2-adrenergic agonists decrease sympathetic tone with ensuing attenuation of neuroendocrine and hemodynamic responses to anesthesia and surgery. The effects of dexmedetomidine, a highly specific alpha 2-adrenergic agonist, on these responses have not been reported in patients undergoing coronary artery bypass grafting. METHODS: Eighty patients scheduled for elective coronary artery bypass grafting received, in a double-blind manner, either a saline placebo or a dexmedetomidine infusion, initially 50 ng.kg-1.min-1 for 30 min before induction of anesthesia with fentanyl, and then 7 ng.kg-1.min-1 unit the end of surgery. Filling pressures, blood pressure, and heart rate were controlled by intravenous fluid and by supplemental anesthetics and vasoactive drugs. RESULTS: Compared with placebo, dexmedetomidine decreased plasma norepinephrine concentrations by 90%, attenuated the increase of blood pressure during anesthesia (3 vs. 24 mmHg) and surgery (2 vs. 14 mmHg), but increased slightly the need for intravenous fluid challenge (29 vs. 20 patients) and induced more hypotension during cardiopulmonary bypass (9 vs. 0 patients). Dexmedetomidine decreased the incidence of intraoperative (2 vs. 13 patients) and postoperative (5 vs. 16 patients) tachycardia. Dexmedetomidine also decreased the need for additional doses of fentanyl (3.1 vs. 5.4), the increments of enflurane (4.4 vs. 5.6), the need for beta blockers (3 vs. 11 patients), and the incidence of fentanyl-induced muscle rigidity (15 vs. 33 patients) and postoperative shivering (13 vs. 23 patients). CONCLUSIONS: Intraoperative intravenous infusion of dexmedetomidine to patients undergoing coronary artery revascularization decreased intraoperative sympathetic tone and attenuated hyperdynamic responses to anesthesia and surgery but increased the propensity toward hypotension.

Adjuvants, Anesthesia↗
PubMed2003

Additional experience with dexmedetomidine in pediatric patients.

PURPOSE: This study evaluates the efficacy of dexmedetomidine in clinical scenarios other than sedation during mechanical ventilation. METHODS: We conducted a retrospective chart review and presentation of case series of children in the pediatric intensive care unit and the postanesthesia care unit who received dexmedetomidine. RESULTS: Dexmedetomidine was administered by continuous infusion to three patients and as a single bolus dose (0.5 microg/kg) to two patients. In the five clinical scenarios, dexmedetomidine provided effective sedation during spontaneous ventilation in two patients, reversed the clinical signs and symptoms of withdrawal from illicit substances in one patient, and was effective in the treatment of postanesthesia emergence delirium and shivering in two additional patients. CONCLUSION: These preliminary data suggest that dexmedetomidine may be an effective agent for sedation in spontaneously breathing patients, in the treatment of drug withdrawal, and in the treatment of two common postanesthesia problems.

Adolescent↗
PubMed1979

Redistribution of body heat during anaesthesia. A comparison of halothane, fentanyl and epidural anaesthesia.

Epidural anaesthesia and high dose fentanyl (50 micrograms/kg) when used to supplement nitrous oxide and oxygen anaesthesia for a standard lower abdominal operation were associated with a mean fall in deep body temperature, as measured in the external auditory meatus, of 0.46 degrees C and 0.6 degrees C/hr respectively. This is significantly different from the mean values of 0.14 degrees C and 0.2 degrees C/hr which were recorded when moderate dose fentanyl (10 micrograms/kg) or 0.5% halothane were used to supplement anaesthesia. When mean skin temperature is combined with the core temperature to provide an estimate for total body heat, there is no difference between the groups. Redistribution of body heat occurs and this may be related to reduced adrenergic stimulation and altered regional blood flow. Where the facilities and environments are inadequate for the maintenance of normothermia, care should be taken in the choice of anaesthetic technique. In the recovery period mean body heat gain showed a wide scatter of results but those patients receiving epidural anaesthesia were slow to rewarm despite a high incidence of shivering in this group. The implications of this are discussed.

Adult↗
PubMed1969

Tremor induced by tetrabenazine.

1. Acute administration of tetrabenazine produced tremor in cats, in doses which caused sedation but not hypothermia.2. The pattern of movements resembled shivering rather than Parkinsonism, and warming the skin suppressed the tremor.3. The tremor was not influenced by hyoscine.4. Tremor produced by amylobarbitone was essentially similar to that induced by tetrabenazine.

Amobarbital↗
PubMed1972

The hyperglycaemic effect of morphine.

1. In the unanaesthetized cat, an injection of 0.75 mg of morphine into a lateral cerebral ventricle produced strong hyperglycaemia; on intravenous injection, 10 to 30 times larger doses were required. Other effects produced with both injections were shivering, pupillary dilatation, opening of the eyes, miaowing, periods of excitation, and analgesia. Between the periods of excitation the cat did not react to objects moving in front of its eyes and it had a vacant stare.2. Noradrenaline, adrenaline, and 5-hydroxytryptamine (5-HT) injected intraventricularly (250 mug, twice) depressed the hyperglycaemia due to intraventricular morphine, and noradrenaline also depressed the hyperglycaemia due to intravenous morphine. Adrenaline produced the strongest and 5-HT the weakest depression. 5-HT did not depress the other effects of morphine, but the catecholamines depressed most of them; only analgesia and the vacant stare appeared to be unaffected.3. Reserpine injected intraventricularly (0.5 mg, twice) greatly accentuated the hyperglycaemia as well as the other effects produced by intraventricular morphine, but pupillary dilatation and opening of the eyes no longer occurred; the protrusion of the nictitating membranes produced by the reserpine persisted.4. Pentobarbitone sodium injected intraperitoneally in an anaesthetizing dose practically abolished the morphine hyperglycaemia, but injected intraventricularly in a dose of a few milligrammes, it had a two fold effect: depression followed by enhancement of the morphine hyperglycaemia. The enhancement may be due to sensitization of the effect of the adrenaline released by morphine, since adrenaline hyperglycaemia was enhanced as well.5. Morphine did not seem to act on structures in the walls of either the lateral or third ventricle when producing its hyperglycaemic effect on intraventricular injection. The action may therefore be on more caudally situated parts of the neuro-axis, on the central grey, on structures in the floor of the fourth ventricle or of the lateral recesses, or even on structures near the ventral surface of the brain stem.

Analgesia↗
PubMed1968

The effect of intraventricular injections of noradrenaline, 5-hydroxytryptamine, acetylcholine and tranylcypromine on the ox (Bos taurus) at different environmental temperatures.

1. Noradrenaline, 5-hydroxytryptamine (5-HT), acetylcholine and tranylcypromine were injected or infused into the lateral ventricle of the ox. The effects of these drugs on heart and respiration rates, heat production, rectal, skin and hypothalamic temperatures and skin evaporative loss were measured when the animal was exposed to environmental temperatures ranging from -1 degrees C to +30 degrees C.2. Acetylcholine (0.001-2 mg) had no detectable effect on temperature regulation at 20 degrees C.3. In small doses (0.005-0.05 mg) 5-HT had no detectable effect. Larger doses (2-5 mg) given in a cold environment (-1 degrees C) also had no effect but the same doses given in warm environments (15-30 degrees C) caused increases in skin temperatures, skin evaporative loss and respiratory rate, and decreases in rectal and hypothalamic temperatures.4. Infusion of tranylcypromine (0.107 ml./min of a 1 in 50 solution) in a warm environment (20 degrees C) also caused a decrease in rectal temperature after a delay of 1-1(1/2) hr during which no effects were apparent.5. Noradrenaline (2 mg) had no effect on temperature regulation when injected into animals in a warm environment (30 degrees C). When injected (1 mg) into animals in a cold environment (-1 degrees C) shivering stopped and heat production and rectal and hypothalamic temperatures were decreased.6. It is concluded that intraventricular 5-HT and noradrenaline both cause a decrease in body temperature, and it is unlikely that central temperature regulation in the ox is mediated only by these two substances.

Acetylcholine↗
PubMed1969

Control of body temperature in the unanaesthetized monkey by cholinergic and aminergic systems in the hypothalamus.

1. In the unanaesthetized rhesus monkey, 5-hydroxytryptamine (5-HT), catecholamines, acetylcholine or carbachol were micro-injected in a volume of 1.0 mul. or less through chronically implanted cannulae at eighty-six sites in the hypothalamus.2. 5-HT in doses of 2-10 mug caused a long-lasting elevation in temperature which was dose-dependent. An anatomical ;mapping' of the hypothalamus revealed that the hyperthermic action of 5-HT was localized to the anterior, pre-optic area directly ventral to the anterior commissure.3. Noradrenaline in doses of 1-12 mug produced a dose-dependent fall in temperature of short duration. An anatomical ;mapping' showed that the hypothermic action of this and other catecholamines was again localized to the anterior, pre-optic region.4. Acetylcholine, alone or in a mixture with eserine, or carbachol caused a dose-dependent hyperthermia which was characterized by an intense rise of short duration and vigorous shivering. A ;mapping' of this response revealed a diffuse patterning of sites throughout the hypothalamus which were sensitive to the application of acetylcholine and carbachol. However, in one circumscribed region at the junction between the posterior hypothalamus and mesencephalon, the two cholinomimetic substances caused a marked fall in temperature.5. We conclude that 5-HT activates a cholinergic heat production pathway which projects from the anterior to posterior hypothalamus. Noradrenaline, on the other hand, blocks the hyperthermic action of 5-HT rather than activates the heat loss system. A chemically mediated heat loss pathway apparently does not exist in the hypothalamus.

Acetylcholine↗
PubMed1971

The role of sodium and calcium ions in the hypothalamus in the control of body temperature of the unanaesthetized cat.

1. Isolated regions of the anterior, posterior and other areas of the hypothalamus of the unanaesthetized cat were perfused by means of push-pull cannulae lowered through permanently implanted guide tubes. Each site was perfused for a 30 min interval at a rate of 50 mul./min. Concentrations of sodium, calcium, potassium and magnesium ions in the perfusate were altered selectively.2. Sodium ions in a concentration which varied from 13.6 to 68.0 mM in excess of the level in extracellular fluid caused a steep rise in the temperature of the cat when the solution was perfused at sites located within the posterior hypothalamic area. Shivering, vasoconstriction, and piloerection accompanied the increase in temperature. When the chloride was replaced in the perfusate by the toluene-p-sulphonate salt of sodium, the hyperthermia was equally intense. Solutions containing excess sodium ions perfused within the anterior and other hypothalamic areas produced either a slight fall or rise in temperature as well as other physiological changes.3. Calcium ions in a concentration which varied from 2.6 to 10.4 mM in excess of the physiological level perfused at the same sites within the posterior region of the hypothalamus produced a sharp fall in body temperature, which was accompanied by vasodilatation and a decrease in the activity of the cat. When solutions containing excess calcium were perfused in the anterior and other hypothalamic areas, no consistent change in temperature occurred.4. Potassium or magnesium ions in concentrations which varied from two to ten times the level in extracellular fluid had virtually no effect on the temperature of the cat when they were perfused in the anterior, posterior or other areas of the hypothalamus.5. We conclude that the constancy in the ratio between sodium and calcium ions in the posterior hypothalamus may be the inherent mechanism by which the set-point for body temperature is determined.

Animals↗
PubMed1971

Effects on body temperature of prostaglandins of the A, E and F series on injection into the third ventricle of unanaesthetized cats and rabbits.

1. Prostaglandins were injected into the third ventricle of unanaesthetized cats and rabbits whilst rectal temperature was recorded.2. In cats prostaglandin E(1) and E(2) (PGE(1) and PGE(2)) produced hyperthermia which mostly began within a minute of injection and lasted 1 or more hours. With PGE(1) the hyperthermia was shown to be dose dependent between 10 ng and 10 mug (2.8 x 10(-11) and 2.8 x 10(-8)M). The hyperthermia was associated with vigorous shivering, skin vasoconstriction and piloerection. In several experiments a secondary rise in temperature occurred a few hours after the injection but such an effect was sometimes observed with control injections of 0.9% NaCl solution as well.3. None of the other prostaglandins (A(1), F(1alpha), F(2alpha)) examined in cats had an immediate or strong effect on temperature comparable to the hyperthermia produced by PGE(1) and PGE(2).4. In rabbits PGE(1) (2 mug) also caused hyperthermia which began shortly after the injection and lasted for hours. PGF(2alpha) and PGA(1), did not affect temperature.5. In cats it was seen that an intraperitoneal injection of 4-acetamidophenol (paracetamol 50 mg/kg) did not affect the initial strong hyperthermia produced by PGE(1) and PGE(2) but abolished the secondary rise.6. The possibility is discussed that PGE(1) plays a role as a central transmitter or modulator in temperature regulation.

Acetaminophen↗
PubMed1972

Habituation and acclimatization of sheep to cold following exposures of varying length and severity.

1. Male and female Scottish Blackface sheep were shorn and exposed for 2 weeks either to a thermoneutral temperature (+30 degrees C), to chronic cold (+8 degrees C) or to +30 degrees C interrupted by daily short cold shocks (-10 degrees C). During and at the end of these conditioning treatments, the sheep also received two acute cold exposures (-20 degrees C, 4 m.p.h. wind for 2-8 hr) 1 week apart. Some of these sheep and a fourth (control) group, were subsequently re-shorn and slowly cooled to +8 degrees C.2. Resting metabolism and the metabolic response to cooling (both inferred from heart rates) were increased by previous chronic cold treatment. Resistance to body cooling (measured during acute cold exposure) was generally increased by both chronic and acute cold, and non-shivering thermogenesis was probably induced in the female sheep. These effects were defined as acclimatization.3. In contrast, cold shocks reduced the subsequent metabolic response to cold and encouraged facultative body cooling. This pattern of response (defined as habituation) therefore caused greater thermolability.4. Habituation and acclimatization were antagonistic. Habituation was removed by acute cold exposure and, conversely, acclimatization was inhibited by short cold shocks.5. There were sex differences in response but these were confounded by probable differences in insulation and in body condition (males thinner).6. It was concluded that the induction of different forms of adaptation depended on the length, severity and frequency of cold exposures. Habituation to whole body cold exposure apparently involved central nervous system centres normally receiving peripheral cold stimuli.

Acclimatization↗
PubMed1973

Failure of thermoregulation in the cold during hypoglycaemia induced by exercise and ethanol.

1. After young men had exercised for approximately 2 hr at 70% maximum O(2) uptake, and taken 28 ml. ethanol by mouth, their mean blood glucose fell to 2.17 mM. It fell further to 1.77 mM during a 30 min exposure to air at 14.5 degrees C. Plasma lactate, glycerol, beta-hydroxybutyrate and free fatty acid concentrations increased.2. Rectal temperature fell to reach a mean level of 34.49 degrees C by the end of the cold exposure; oesophageal temperature fell to as low as 33.00 degrees C in one case.3. Virtually no increase in metabolic rate and no visible shivering occurred during the cold exposure.4. Administration of glucose (mean 60.4 g) prevented the falls in temperature, and restored metabolic response to the cold to the size found in control experiments without exercise or ethanol.5. Neither exercise without ethanol or ethanol without exercise significantly lowered the blood glucose or impaired the maintenance of body temperature in the cold.6. One obese subject showed almost as great a fall in blood glucose and depression of metabolic response to cold as the thinner men, but no fall in body temperature.

Adult↗
PubMed1973

Effects of thermal stimulation of medulla oblongata and spinal cord on decerebrate rabbits.

1. Changes of rectal and ear temperatures, and respiratory and heart rates, during external thermal stress and during thermal displacement of the medulla oblongata and spinal cord have been investigated in rabbits, before and after decerebration, with ether inhalation only during the operation.2. Abrupt exposure of the intact animals to heat (35 degrees C) or cold (5 degrees C) produced appropriate thermoregulatory adjustments such as vasodilatation or vasoconstriction of the ear skin, and increase or decrease of respiratory frequency with little change in rectal temperature. After decerebration, these responses to heat and cold were reduced and rectal temperature was moderately altered.3. In intact animals, heating (42-43 degrees C) and cooling (32-33 degrees C) the medulla and spinal cord also produced appropriate thermoregulatory vasomotor and respiratory responses, although these were smaller than those caused by ambient heating and cooling. Heating these structures also produced bradycardia and cooling tachycardia. In addition, shivering-like movements over extremities and trunks or jaws were elicited, respectively, during spinal or medullary cooling. None of these responses was altered after decerebration.4. These results suggest that while the hypothalamus may be the principal site of thermoregulation, some independent but less powerful thermoregulatory structures exist in the medulla oblongata and spinal cord. Thermal responses to stimulating the latter structures are not results of afferent activation of the hypothalamic mechanism.

Animals↗
PubMed1976

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.

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.

Animals↗
PubMed1977

Thermoregulatory responses as a function of core temperature in humans.

1. Six healthy humans were immersed sequentially in baths maintained at a steady temperature of either 28 +/- 1 or 38-8 +/- 1 degree C. 2. Metabolic heat production was calculated by respiratory gas analysis. A ventilated capsule was placed on the forehead and sweat secretion was calculated from psychrometric recordings. Convective heat loss from one hand to water-perfused glove provided a continuous measurement of vasomotor response. 3. Heat production, sweating, and vasomotor heat loss were proportional to core temperature. 4. Sweating and vasomotor response were parallel. Vasoconstriction was complete, before the onset of shivering. 5. The thresholds for heat loss and heat production were superimposed, without a 'dead band' core temperature.

Body Temperature↗
PubMed1986

Multilocular adipocytes from muscovy ducklings differentiated in response to cold acclimation.

Morphological and functional aspects of adipose tissue from 6-week-old cold-acclimated muscovy ducklings reared at 4 degrees C ambient temperature (Ta) from the age of 1 week were examined for the occurrence of brown adipose tissue (b.a.t.) in order to explain non-shivering thermogenesis (n.s.t.) observed at this age. Metabolic rate and integrated muscle electrical activity (e.m.g.) were measured at different Ta (from -10 to +28 degrees C) in cold-acclimated and in control ducklings reared at thermoneutrality. The results confirm the existence of n.s.t. in 6-week-old cold-acclimated muscovy ducklings. In cold-acclimated ducklings, typical multilocular adipocytes were found in subcutaneous adipose deposits instead of the unilocular white adipocytes as in control ducklings. Mitochondria isolated from this differentiated tissue were less abundant than in b.a.t. of mammals. Their respiration rate was similar to the respiration rate of white adipose tissue mitochondria from control rats and much lower than the b.a.t. mitochondria rate from cold-acclimated rats. It is therefore unlikely that this differentiated adipose tissue contributes to the n.s.t. observed, an n.s.t. whose capacity reached 5.26 W/kg (+73.5% above resting metabolic rate) in cold-acclimated ducklings. The role of this differentiated adipose tissue in the metabolic adaptation to cold is discussed.

Acclimatization↗