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PubMed1998

A randomised placebo controlled trial of oral misoprostol in the third stage of labour.

OBJECTIVE: To compare oral misoprostol 400 microg with placebo in the routine management of the third stage of labour. DESIGN: A double-blind placebo controlled trial. Setting The labour ward of an academic hospital in Johannesburg, South Africa with 7000 deliveries per annum. PARTICIPANTS: Low-risk women expected to deliver vaginally. METHODS: Women in labour were randomly allocated to receive either misoprostol 400 microg orally or placebo after the birth. Conventional oxytocics were given immediately if blood loss was thought to be more than usual. Postpartum blood loss in the first hour was measured by collection in a special flat plastic bedpan. Side effects were recorded. MAIN OUTCOME MEASURES: Measured blood loss > or = 1000 ml within the first hour after birth. Use of additional oxytocics. RESULTS: The groups were well matched. Measured blood loss > or = 1000 ml occurred in 15/250 (6%) after misoprostol and 23/250 (9%) after placebo (relative risk 0.65; 95% confidence interval 0.35-1.22). The difference may have been reduced by the greater use of conventional oxytocics in the placebo group, which was statistically significant for intravenous oxytocin infusion (2.8% vs 8.4%, relative risk 0.33, 95% confidence interval 0.14-0.77). Shivering was more common in the misoprostol group (19% vs 5%, relative risk 3.69; 95% confidence interval 2.05-6.64). CONCLUSIONS: Shivering has been shown in this study to be a specific side effect of misoprostol administered orally in the puerperium. No serious side effects were noted. Misoprostol shows promise as a method of preventing postpartum haemorrhage. Because of the potential benefits for childbearing women, particularly those in developing countries, further research to determine its effects with greater certainty should be expedited.

Administration, Oral↗
PubMed2000

The misoprostol third stage of labour study: a randomised controlled comparison between orally administered misoprostol and standard management.

OBJECTIVE: To compare misoprostol with standard oxytocic regimens in the prevention of postpartum haemorrhage. DESIGN: Randomised controlled trial. SETTING: Obstetric unit in a large teaching hospital. METHODS: One thousand women randomised to 500 microg misoprostol given orally or to standard oxytocic regimens of oxytocin, oxytocin with ergometrine, or ergometrine. MAIN OUTCOME MEASURES: Incidence of postpartum haemorrhage and the incidence and severity of side effects. RESULTS: Postpartum haemorrhage occurred in 12% of women given misoprostol and in 11% of women given standard oxytocic drugs (relative risk (RR) 1.10, 95% confidence interval (CI) 0.79, 1.55). Blood loss of 1000 mL or more occurred in 2% of women in each group. Nausea, headache, dizziness and tiredness were less frequent with misoprostol (RR (95% CI) 0.71 (0.59, 0.84); 0.53 (0.38, 0.74); 0.73 (0.61, 0.87) and 0.88 (0.83, 0.94) respectively). The main side effects of misoprostol were shivering (RR 1.95, 95% CI 1.69, 2.25) and a rise in temperature (difference in mean rise 0.34 degrees C, 95% CI 0.26, 0.42). CONCLUSION: Oral misoprostol for the prevention of postpartum haemorrhage was comparable to standard oxytocics. Many side effects were less common with misoprostol but shivering and pyrexia were more common. Larger randomised trials are needed before establishing the equivalence between misoprostol and standard oxytocic drugs in the prevention of postpartum haemorrhage.

Administration, Oral↗
PubMed1987

Developmental expression of the myelin proteolipid protein and basic protein mRNAs in normal and dysmyelinating mutant mice.

Expression of the myelin proteolipid protein (PLP) was examined in the nuclei and polysomes of 12-27-day-old quaking, jimpy, and shiverer mouse brains and in 2-27-day-old normal brains and compared with expression of the myelin basic proteins (MBPs). Northern blots showed the presence of multiple mouse PLP RNAs, the developmental expression of which coincided with myelination. Two major mouse PLP RNAs, 3.5 and 2.6 kilobases in length, were observed in both cytoplasmic polyribosomes and nuclei, and, in addition, a larger 4.6-kilobase PLP RNA was observed in nuclei. Quantitative measurements with slot blot analyses showed that the levels of PLP and MBP RNAs peaked simultaneously at 18 days in nuclei but that maximal levels of PLP RNA lagged behind MBP RNA by several days in the polysomes. The developmental expression of both major classes of myelin protein mRNAs was affected in all three mutants. In shiverer brains, the levels of PLP mRNA in polysomes and nuclei were only 30-55% of control levels after 15 days. Thus, the deletion of a portion of the MBP gene appeared to have a major effect on the expression of the PLP gene in this mutant. In jimpy mice, where the mutation has been shown to involve the PLP gene, expression of MBP mRNA was also severely reduced, to less than 25% of control values. In quaking brains, the expression of each gene followed its own developmental course, different from each other and different from the normal mouse. The extent to which the expression of PLP and MBP was affected by the quaking mutation depended on the age at which it was examined.

Animals↗
PubMed1993

Expression of myelin protein genes and other myelin components in an oligodendrocytic cell line conditionally immortalized with a temperature-sensitive retrovirus.

We have conditionally immortalized oligodendrocytes isolated from normal and shiverer primary mouse brain cultures through the use of the retroviral vector ZIPSVtsA58. This vector encodes an immortalizing thermolabile simian virus 40 large T antigen (Tag) and allows for clonal selection by conferring neomycin (G418) resistance. We isolated 14 shiverer and 10 normal lines that expressed the early oligodendrocyte marker 2',3'-cyclic nucleotide 3'-phosphodiesterase mRNA. These cell lines grew continuously at the permissive temperature (34 degrees C) and displayed Tag nuclear immunostaining. On shifting to nonpermissive temperatures (39 degrees C), the cells showed rapid arrested cell growth and loss of Tag staining. One line (N20.1) engineered from normal oligodendrocytes also expressed myelin basic protein (MBP) and proteolipid protein (PLP) mRNAs, genes normally expressed by mature, differentiated oligodendrocytes. No differences in any of the myelin-specific protein mRNA levels were observed in N20.1 cells grown at 39 degrees C for > 9 days compared with cells maintained at 34 degrees C. Immunocytochemical staining revealed N20.1 cells to be positive for the oligodendrocyte surface markers--galactocerebroside, A007, and A2B5. However, MBP and PLP polypeptides could not be detected by western blot or immunocytochemical staining at either the permissive or nonpermissive temperature. Cell-free protein synthesis experiments indicated that the MBP mRNAs isolated from N20.1 cells were translatable and directed the synthesis of the 17-, 18.5-, and 21.5-kDa MBP isoforms. Analysis of the PLP/DM20 gene splice products by polymerase chain reaction indicated that the expression of DM20 mRNA predominated over that of PLP mRNA in this cell line. Because the cell line expressed the MBP and PLP genes, it represents a "mature" oligodendrocyte, but the splicing patterns of these genes indicate that it is at an early stage of "maturation." This cell line has now been passaged > 40 times with fidelity of phenotype and genotype.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1970

Central effects of picrotoxin when acting from the liquor spaces in anaesthetized cats.

1. Picrotoxin was perfused through different parts of the cerebral ventricles in cats anaesthetized with chloralose, and applied topically to the upper cervical cord in cats anaesthetized with intraperitoneal pentobarbitone sodium. With both methods, picrotoxin produced effects similar to those produced by tubocurarine; but it was active in weaker concentrations.2. Perfused through the third ventricle, picrotoxin caused shivering resulting in a rise of rectal temperature, increased motor excitability, muscle jerks, tachypnoea, mydriasis, and withdrawal of the nictitating membranes. The effects were due to an action on structures in the walls of the ventral half of the ventricle, because they occurred only on perfusion of tubocurarine through this half and not on its perfusion through the dorsal half of the third ventricle. Noradrenaline perfused through the third ventricle abolished the shivering and the rise in temperature, but did not affect the motor hyperexcitability or the muscle jerks, whereas pentobarbitone sodium similarly perfused abolished these effects as well.3. Perfused through the inferior horn of a lateral ventricle, picrotoxin caused excitation of the hippocampus. This resulted in a rhythmic discharge of high voltage negative spikes in the electrocorticogram taken from the occipital cortices. The spikes developed after-positivity with after-discharges and were interrupted from time to time by bursts of fast activity termed episodes. This abnormal discharge was recorded also from the perfusion cannula which was inserted into the inferior horn and acted as a lead from the surface of the hippocampus.4. Perfused through the anterior horn of a lateral ventricle picrotoxin caused a rhythmic discharge of negative spikes which was recorded from the anterior horn cannula and resulted from excitation of the grey matter in the anterior limbic area which forms part of the medial wall of the horn.5. Applied to the surface of the upper cervical cord, picrotoxin produced scratching movements.

Action Potentials↗
PubMed1978

Hyperthermic responses to central and peripheral injections of morphine sulphate in the cat.

1 The effect of morphine on body temperature was studied in conscious, unrestrained cats provided with implanted third or lateral cerebral ventricular cannulae, jugular venous catheters and retroperitoneal thermocouples.2 Intraventricular injections of 2.5-50 mug and intravenous injections of 1-10 mg/kg morphine sulphate produced dose-related hyperthermic responses. Similar mean increases in body temperature after administration of a given dose were elicited in cats which had not previously received morphine and, provided that tolerance was avoided by spacing injections at least 72 h apart, in cats which received a series of injections of morphine. Morphine was at least 850 times more potent when injected into the third ventricle than when given intravenously. Increasing the dose of morphine sulphate injected into the third ventricle to 1250 mug only prolonged the hyperthermia. Morphine did not produce hypothermia at any dose tested.3 Injection of 10 mug morphine sulphate into the third ventricle produced similar hyperthermias at ambient temperatures (tas) of 4-6, 21-23 and 33-36 degrees C. The increase in body temperature was associated with shivering at the lower tas. At the highest ta, shivering was not evoked, but respiratory rate decreased after morphine if it was initially elevated. These results suggest that morphine increased the level at which body temperature was regulated.4 Neither metiamide nor indomethacin antagonized morphine so histamine and prostaglandins were apparently not required for the hyperthermic effect.

Animals↗
PubMed1978

Recovery from anaesthesia in ponies: a comparative study of the effects of isoflurane, enflurane, methoxyflurane and halothane.

The duration and quality of recovery after separate 2 hour anaesthetic periods with equipotent alveolar concentrations of isoflurane, enflurane, halothane and methoxyflurane were evaluated in experimental ponies. Recovery was shortest after isoflurane anaesthesia, followed by enflurane, halothane and finally methoxyflurane, although standing was achieved more rapidly after enflurane than after isoflurane. This sequence of recovery times was compatible with the respective solubilities of the 4 agents. The smoothest recovery was obtained after isoflurane anaesthesia, followed by methoxyflurane, halothane and then enflurane. The isoflurane recovery was characterized by very quiet and prolonged sternal recumbency with excellent coordination upon standing. The chief difficulties with halothane recovery were shivering and delayed coordination upon standing. Enflurane anaesthesia was followed by a very brief period of sternal recumbency but there was considerable shivering and incoordination upon standing. This may have been due to central nervous stimulation during anaesthesia producing a residual excitatory effect. On the basis of this investigation, isoflurane was considered to be the most satisfactory volatile anaesthetic for the horse.

Anesthesia, Inhalation↗
PubMed1995

Environmental effects on thermoregulation and breathing patterns during early postnatal development in hand-reared lambs.

This study examines the effect of hand-rearing developing lambs in a warm (WR; 25 degrees C) or cool (CR; 10-15 degrees C) ambient temperature on the control of thermoregulation and breathing patterns, when maintained at a fixed level of nutrition over the first month of postnatal life. Measurements were made during non-rapid eye movement sleep whilst lambs were maintained for at least 1 h at warm (28-19 degrees C) and cold (14-5 degrees C) ambient temperatures at 1, 7, 14 and 30 days of age. All lambs were able to maintain normal body temperature, but oxygen consumption was higher in CR lambs at 14 and 30 days of age. At 1 day of age shivering was rarely observed in any lambs, but at 7 and 14 days of age more WR than CR lambs responded to cold exposure via shivering. Plasma concentrations of triiodothyronine were higher at 7 and 14 days of age in CR lambs. Breathing frequencies were similar in WR and CR lambs, and from 7 days of age the incidence of expiratory laryngeal braking was higher in warm compared with cold study temperatures. By 30 days of age the recruitment of this mechanism was greater in CR lambs. Mean growth rate was slower over the first week of postnatal life in CR compared with WR lambs. This difference decreased over the first month of life, as growth rate increased from 83 to 130 g day-1 in the CR group but remained constant at approximately 150 g day-1 in the WR lambs. Total weight of the lungs and heart, but not the liver, were lower at 1 month but not at 1 week of postnatal life in CR lambs. It is concluded that a modest decrease in the ambient temperature in which postnatal lambs are reared, when on a fixed feed intake, alters lung size, the recruitment of laryngeal braking and the control of body temperature.

Animals↗
PubMed1997

Influence of feeding and ambient temperature on thermoregulation in newborn lambs.

This study examined the effect of ambient temperature and feeding on brown adipose tissue (BAT) function and thermoregulation in lambs born either vaginally at term or by Caesarean section close to term. Immediately after birth lambs were placed in a warm (30 degrees C) or cool (15 degrees C) ambient temperature and measurements of colonic temperature and heat production recorded for 6 h. Lambs were fed 50 ml of colostrum when 5 h old. The amount of uncoupling protein and level of guanosine 5'diphosphate (GDP) binding in BAT was higher in vaginally delivered lambs than in lambs delivered by Caesarean section. For each delivery group, GDP binding was greater in lambs maintained at 30 degrees C than in lambs maintained at 15 degrees C. O2 consumption, CO2 production and colonic temperature only increased after feeding in lambs born by Caesarean section and maintained at 30 degrees C, a response that was accompanied by a decreased incidence of shivering. Irrespective of delivery temperature, plasma thyroid hormone concentrations and noradrenaline content of BAT were lower in lambs born by Caesarean section than in those born vaginally. Plasma cortisol concentrations were higher in lambs delivered by Caesarean section, as was adrenaline content of BAT in these lambs maintained at 30 degrees C. It is concluded that the thermoregulatory response to feeding in terms of changes in both recruitment of shivering and colonic temperature were observed only in lambs delivered by Caesarean section.

Adipose Tissue, Brown↗
PubMed1967

Temperature effects produced in dogs and monkeys by injections of monoamines and related substances into the third ventricle.

1. In dogs the effects on rectal temperature of noradrenaline, adrenaline, 5-hydroxytryptamine (5-HT) and of the monoamine oxidase inhibitor tranylcypromine were studied following their injection into the third ventricle through a chronically implanted cannula. Tranylcypromine was given also by the intraperitoneal route.2. The hypothermic effect of the catecholamines and the hyperthermic effect of 5-HT previously demonstrated in anaesthetized dogs were obtained also in an unanaesthetized dog, but 5-HT was effective only in doses under 20 mug.3. Tranylcypromine (1 mg) injected into the third ventricle of dogs anaesthetized with pentobarbitone sodium produced shivering and a rise in temperature.4. Tranylcypromine (10 mg/kg) injected intraperitoneally caused a rise in temperature in the unanaesthetized dog. For a time shivering and panting, two effects which produce opposite change in temperature, were observed together. When injected shortly before an intraperitoneal injection of an anaesthetizing dose of pentobarbitone sodium, tranylcypromine not only prevented the fall in temperature which is normally produced by the anaesthetic but caused a greater and longer lasting rise than when given alone.5. The intraperitoneal injections of tranylcypromine produced profuse salivation, a peripheral effect which persisted after acute denervation and which was not abolished by atropine or tolazoline.6. In rhesus monkeys anaesthetized with intraperitoneal pentobarbitone sodium, noradrenaline, adrenaline, 5-HT and 5-hydroxytryptophan (5-HTP) were injected into the cannulated third ventricle. The catecholamines caused a fall in rectal temperature. No evidence was obtained that the fall resulted from a rise in hypothalamic temperature. The injections of 5-HT or of its precursor 5-HTP raised rectal temperature. Monkeys thus respond to the monoamines injected intraventricularly, in the same way as cats and dogs, and unlike rabbits, sheep, goats, oxen and rats.

Animals↗
PubMed1972

Effects of heating and cooling the spinal cord and medulla oblongata on thermoregulation in monkeys.

1. In the unanaesthetized monkey (Macaca cyclopis), heating the spinal cord or the medulla oblongata from 38 to 42-43 degrees C produced subcutaneous vasodilatation, respiratory acceleration (frequently interrupted with a period of apnoea in the medullary experiment), bradycardia and hypotension. The animal became drowsy and had a slight decrease of body temperature. Heating the medulla oblongata often induced retching and/or emesis.2. Cooling the spinal cord or medulla oblongata from 38 to 32-33 degrees C produced subcutaneous vasoconstriction, slower respiration, tachycardia and hypertension. The animal became restless and had a slight increase of body temperature. Cooling the spinal cord induced shivering of the four limbs, while cooling the medulla oblongata induced only shivering of the jaws.3. The effects of heating or cooling of the spinal cord or the medulla oblongata were antagonized by simultaneous application of temperature displacement of the opposite nature in the same areas or vice versa.4. The data suggest that some thermosensitive elements possibly responsible for thermoregulation reside in the spinal cord and the medulla oblongata.

Animals↗
PubMed1976

Effects of atropine, injected into a lateral cerebral ventricle of the rabbit, on fevers due to intravenous leucocyte pyrogen and hypothalamic and intraventricular injections of prostaglandin E1.

1. Cholinergic synapses in the hypothalamus may transmit information in those thermoregulatory pathways which function to raise body temperature. The effect of atropine, administered intracranially, on the febrile response to intravenous leucocyte pyrogen or intracranial prostaglandin E1 was therefore examined in conscious rabbits. 2. In rabbits exposed to a thermoneutral environment, micro-injections of PGE1, into the anterior hypothalamus, intraventricular injections of PGE1, and intravenous injection so leucocyte pyrogen all caused fever accompanied by vasoconstriction in the ears and reduced respiratory rate. Intraventricular injection of 200 mug atropine during such fevers attenuated their development. This was due to the activation of heat loss mechanisms through vasodilatation in the ears and an increase in the frequency of respiration. This suggests a similarity in the pattern of neuronal activity evoked by PGE1 and leucocyte pyrogen, at least at the site(s) where atropine directly or indirectly exerted its effect and in the efferent pathways from this site. 3. In rabbits exposed to a cold environment, intraventricular injection of PGE1 caused fever through the activation of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shievering and a decrease in O2 consumption so that temperature ceased to rise and returned to normal. 4. During fever, reversal by atropine of the increased heat conservation of rabbits in a neutral environment, and of their increased heat production in a cold environment adds further support to the concept that cholinergic synapses provide an important link in central temperature-rasising pathways.

Animals↗
PubMed1976

The effect of noradrenaline and 5-hydroxytryptamine injected into a lateral cerebral ventricle, on thermoregulation in the new-born lamb.

1. Respiratory frequency, shivering, ear skin temperatures and rectal temperatures were observed following intraventricular injections of noradrenaline (NA), 5-hydroxytryptamine (5-HT) and saline (NaCl) into new-born lambs exposed to ambient temperatures of 4, 21, or 30 degrees C. 2. Intraventricular NA caused respiratory rate to decrease and body temperature to increase in the 30 degrees C environment. At 21 degrees C, it increased ear skin temperature but did not significantly affect rectal temperature. At 4 degrees C, NA decreased shivering and rectal temperature fell. 3. 5-HT elevated respiratory rate in the 30 degrees C environment and increased ear skin temperature in the 21 and 4 degrees C environments. In the 4 degrees C environment rectal temperature decreased. 4. In general, the change in rectal temperature was related to the dosage of drug administered. Control injections of NaCl had no significant effect on any of the variables measured. 5. The monoaminergic pathways involved in thermoregulation in the new-born lamb appear to be organized in a manner similar to that of the adult sheep and are functional at birth.

Animals↗
PubMed1980

Thermoregulatory noradrenergic and serotonergic pathways to hypothalamic units.

1. In guinea-pigs hypothalamic single units were extracellularly tested for their response to thermal stimulation of the skin and to electrical stimulation of two different pontine areas, the nucleus raphé magnus and the dorsomedial reticular formation. Furthermore, thermoregulatory control actions were measured during the stimulations.2. Electrical stimulation of those reticular formation areas containing noradrenaline cells caused an increase of oxygen uptake, electrical muscle activity and body temperature, while stimulation of the nucleus raphé magnus, known to contain serotonin cells, brought about inhibition or had no effect.3. The recorded units could be subdivided into three groups. Cell type a. Neurones on the boundary of preoptic and anterior hypothalamic regions which increased their firing rate when the skin was cooled and decreased it when the nucleus raphé magnus was stimulated. Cell type b. Neurones in the anterior hypothalamus which did not respond to brain-stem stimulation. Cell type c. More posterior neurones which increased their firing rate when the skin was warmed or when the nucleus raphé magnus was stimulated and decreased their firing rate when the reticular formation was stimulated.4. Cell type a seems to represent interneurones which are connected to the ascending serotonergic thermoregulatory pathway. As for cell type c, it is inferred that it could represent interneurones which control the threshold for shivering and non-shivering thermogenesis.

Action Potentials↗
PubMed1980

Thermoregulatory characteristics of neurogenic hyperthermia in the rat.

1. The thermoregulatory characteristics of the neurogenic hyperthermia produced in rats by unilateral mechanical destruction of the rostral hypothalamic/preoptic region were studied. 2. The investigational methods employed included (a) observing the thermoregulatory effector activities which were responsible for generation of hyperthermia, (b) observing the thermoregulatory reactions elicited by forcefully elevating or lowering core temperature during neurogenic hyperthermia and (c) observing the effect of ambient temperature on hyperthermia magnitude. 3. At 26 degrees C, hyperthermia was effected by a transient increase in shivering thermogenesis and a concomitant minimization of heat loss through the tail. 4. At 26 degrees C, perturbations of core temperature during the plateau phase of hyperthermia were induced by internal or external heating and cooling. The disturbances elicited compensatory changes in shivering activity and in tail vasomotor tonus, and core temperature was rapidly and precisely returned to its pre-perturbation level. 5. The magnitudes of hyperthermias experienced by rats lesioned at 10, 15, 26 and 32 degrees C, as measured by the change in colonic temperature and by the area under the fever curve, were not significantly different. At 36 degrees C, rats were hyperthermic prior to lesioning, and the magnitude of the lesion-induced hyperthermia was significantly attenuated. 6. The results indicate that the neurogenic hyperthermia produced by unilateral hypothalamic puncture in the rat is generated by a coordinated modulation of thermogenic and heat retentive effectors and that the plateau level of hyperthermia is well regulated. These characteristics are compatible with the hypothesis that neurogenic hyperthermia is mediated by prostaglandins released from injured tissue and acting on surviving rostral hypothalamic tissue.

Animals↗
PubMed1981

Independent clamps of peripheral and central temperatures and their effects on heat production in the goat.

1. Experiments were performed to study the interaction of skin and core temperatures in the control of heat production. Shorn goats with intravascular heat exchangers to control core temperature were immersed to the neck in a circulating water bath to clamp skin temperature. With bath temperature kept constant at levels between 32 and 42 degrees C, core temperature was varied between 40 and 36 degrees C, and the changes in heat production were measured. 2. With falling core temperature shivering occurred at all bath temperatures, and heat production rose. The threshold of core temperature below which heat production increased varied inversely to the level of skin temperature. Even at a bath temperature of 42 degrees C the slope at which heat production rose exceeded -5 W. kg-1 . C-1. The results show that in the goat even very high skin temperatures do not abolish the central impulse to shiver which is caused by low core temperature. 3. It is concluded that in the control of heat production, skin temperature and core temperature provide linear and independent inputs which do not replicate any known relationship between temperature and discharge frequency of thermoreceptors.

Animals↗
PubMed1982

The thermoregulatory effects of noradrenaline, serotonin and carbachol injected into the rat spinal subarachnoid space.

1. We have examined the effects on thermoregulation in the rat of noradrenaline bitartrate (NA), 5-hydroxytryptamine hydrochloride (5-HT) and carbamylcholine chloride (CCh) injected into the lumbar spinal subarachnoid space via a chronic indwelling catheter.2. Intrathecal injections of the monoamines and CCh reproducibly affected thermoregulation, whereas injections of control solutions had no effect.3. Intrathecal injections of NA (0.01-0.30 mumol) produced a dose-dependent hypothermia associated with a decrease in tail skin vasomotor tone. Shivering activity was not depressed during the hypothermia and sometimes increased. Intrathecal administration of the alpha-adrenergic agonist clonidine (0.0175-0.070 mumol) elicited changes in T(c) and T(sk) similar to those induced by intrathecal NA.4. Intrathecal 5-HT (0.030-0.90 mumol) elicited a dose-dependent hyperthermia accompanied by increased tail skin vasomotor tone and increased shivering.5. CCh injected intrathecally (0.001-0.06 mumol) evoked a dose-dependent hyperthermia. During the period when core temperature was rising, tail skin vasomotor tone increased and shivering-like activity was present. Once the maximum core temperature had been reached, tail skin vasodilatation occurred. Vasodilatation persisted until core temperature had returned to normal.6. Intravenous injections of 5-HT (0.30 and 0.90 mumol) or CCh (0.006 and 0.03 mumol) caused no thermoregulatory effect. The effects of these agents injected intrathecally were therefore not due to an action in the periphery.7. Intravenous infusions of NA (0.06 and 0.10 mumol) produced hypothermia and transient tail skin vasodilatation. We suggest that an action at peripheral sites may have contributed to the effects produced by intrathecal injection of this monamine.8. These findings suggest that spinal noradrenergic, serotonergic and cholinergic synapses may be importantly involved in the control of body temperature in the rat. The possible functional roles of these synapses and the putative spinal sites of action of the injected substances are discussed.

Animals↗
PubMed2003

Thermogenesis elicited by skin cooling in anaesthetized rats: lack of contribution of the cerebral cortex.

Non-noxious cooling stimuli were delivered to the shaved back of urethane-chloralose-anaesthetized, artificially ventilated rats using a plastic bag containing water at 24-40 degrees C. Cooling of the skin by 2-6 degrees C increased the rate of whole body oxygen consumption (.V(O(2)) and triggered electromyographic (EMG) activity recorded from the neck or femoral muscles. The cooling-induced (.V(O(2)) responses did not depend on core (colonic) temperature and followed skin temperature in a graded manner. Pretreatment with the beta-blocker propranolol (10 mg kg(-1), i.v.) greatly attenuated the (.V(O(2)) response but did not affect the EMG response. On the other hand, pretreatment with the muscle relaxant pancuronium bromide (2 mg kg(-1), i.v.) affected the (.V(O(2)) response very slightly but completely abolished the EMG activity. Accordingly, the cooling stimulus activated mainly non-shivering thermogenesis. Next, the contribution of the cerebral cortex to the cooling-induced thermogenesis was examined. Power spectral analysis of the electroencephalogram (EEG) showed that the cooling stimulus largely inhibited delta (0.5-3 Hz) waves, enhanced theta (3-8 Hz) waves, and slightly increased frequencies higher than 8 Hz. Pinching the hindpaw elicited changes in EEG similar to those elicited by skin cooling but did not increase the (.V(O(2)). Therefore, there was no relationship between changes in the EEG and the magnitude of thermogenesis. Finally, skin cooling increased the (.V(O(2)) of decorticated rats but did not increase that of decerebrated rats. The results suggest that the subcortical forebrain structure, but not cortical activation, is indispensable for non-shivering thermogenesis elicited by cooling stimulation of the skin.

Adrenergic beta-Antagonists↗