Central Thermoregulatory Control Research Articles

Abstract PR278

Background & Objectives: The MRI environment requires a cool ambient temperature between 20-22°C for proper magnet function which predisposes children to heat loss (1). However absorption of radiofrequency generated by the MRI scanner may also alter normal thermoregulation and partially offset heat loss. Most general anesthetics also impair central thermoregulatory control by inhibiting normal tonic thermoregulatory vasoconstriction. Ketamine, unique among anesthetics, increases plasma concentration of norepinephrine and peripheral arteriolar resistance (2). In contrast, propofol causes profound venodilatation than other anesthetics. However, insufficient data exist for temperature changes for both sedated and non-sedated children during MRI examinations in 3 Tesla (T) MRI systems. The purpose of this study was to evaluate temperature variance for non-sedated and propofol- or ketamine-sedated pediatric patients during MRI. Materials & Methods: ASA I-II, 103 children, undergoing brain MRI were randomly allocated into three groups. Group I (n=34) received no sedation, Group II (n=35) sedated with 0,1 mg/kg midazolam+2 mg/kg propofol and Group III (n=34) sedated with 0,1 mg/kg midazolam+1,5 mg/kg ketamine. Additional 1 mg/kg propofol in Group II and 0.5 mg/kg ketamine in Group III was provided and repeated to maintain sedation. Pre-scanning, post-scanning and 1 hour after MRI-scanning temperature were measured at the right tympanic site. Temperature changes, specific absorption rate (SAR), consumption of sedatives, total number of scans and duration of scans were also recorded. Results: Demographic data were comparable among three groups. Pre-scanning and post-scanning temperatures were similar between groups whereas measured temperatures 1 hour after MRI were significantly different between Group I and Group II (p=0.005). In Group I and III, post-scanning temperatures were significantly increased in comparison to pre-scanning values (p=0,001, p=0,002, respectively). The temperatures measured 1 hour after MRI were returned to pre-scanning values in Group I but significant temperature difference was continued in Group III (p=0.008). Specific absorption rate (SAR), consumption of sedatives, total number of scans and duration of scans were similar among groups. Conclusion: While confirming temperature rising effect of MRI in children, this study also report that propofol or ketamine has no clinically significant effect on body temperature during sedation for MRI scanning.

Central control of body temperature.

Central neural circuits orchestrate the behavioral and autonomic repertoire that maintains body temperature during environmental temperature challenges and alters body temperature during the inflammatory response and behavioral states and in response to declining energy homeostasis. This review summarizes the central nervous system circuit mechanisms controlling the principal thermoeffectors for body temperature regulation: cutaneous vasoconstriction regulating heat loss and shivering and brown adipose tissue for thermogenesis. The activation of these thermoeffectors is regulated by parallel but distinct efferent pathways within the central nervous system that share a common peripheral thermal sensory input. The model for the neural circuit mechanism underlying central thermoregulatory control provides a useful platform for further understanding of the functional organization of central thermoregulation, for elucidating the hypothalamic circuitry and neurotransmitters involved in body temperature regulation, and for the discovery of novel therapeutic approaches to modulating body temperature and energy homeostasis.

Central neural control of thermoregulation and brown adipose tissue.

Central neural circuits orchestrate the homeostatic repertoire that maintains body temperature during environmental temperature challenges and alters body temperature during the inflammatory response. This review summarizes the experimental underpinnings of our current model of the CNS pathways controlling the principal thermoeffectors for body temperature regulation: cutaneous vasoconstriction controlling heat loss, and shivering and brown adipose tissue for thermogenesis. The activation of these effectors is regulated by parallel but distinct, effector-specific, core efferent pathways within the CNS that share a common peripheral thermal sensory input. Via the lateral parabrachial nucleus, skin thermal afferent input reaches the hypothalamic preoptic area to inhibit warm-sensitive, inhibitory output neurons which control heat production by inhibiting thermogenesis-promoting neurons in the dorsomedial hypothalamus that project to thermogenesis-controlling premotor neurons in the rostral ventromedial medulla, including the raphe pallidus, that descend to provide the excitation of spinal circuits necessary to drive thermogenic thermal effectors. A distinct population of warm-sensitive preoptic neurons controls heat loss through an inhibitory input to raphe pallidus sympathetic premotor neurons controlling cutaneous vasoconstriction. The model proposed for central thermoregulatory control provides a useful platform for further understanding of the functional organization of central thermoregulation and elucidating the hypothalamic circuitry and neurotransmitters involved in body temperature regulation.

Recent advances in thermoregulation.

Thermoregulation is the maintenance of a relatively constant core body temperature. Humans normally maintain a body temperature at 37°C, and maintenance of this relatively high temperature is critical to human survival. This concept is so important that control of thermoregulation is often the principal example cited when teaching physiological homeostasis. A basic understanding of the processes underpinning temperature regulation is necessary for all undergraduate students studying biology and biology-related disciplines, and a thorough understanding is necessary for those students in clinical training. Our aim in this review is to broadly present the thermoregulatory process taking into account current advances in this area. First, we summarize the basic concepts of thermoregulation and subsequently assess the physiological responses to heat and cold stress, including vasodilation and vasoconstriction, sweating, nonshivering thermogenesis, piloerection, shivering, and altered behavior. Current research is presented concerning the body's detection of thermal challenge, peripheral and central thermoregulatory control mechanisms, including brown adipose tissue in adult humans and temperature transduction by the relatively recently discovered transient receptor potential channels. Finally, we present an updated understanding of the neuroanatomic circuitry supporting thermoregulation.

Niezamierzona śródoperacyjna hipotermia

Inadvertent perioperative hypothermia complicates a large percentage of surgical procedures and is related to multiple factors. Strictly regulated in normal conditions (± 0.2°C), the core body temperature of an anaesthetised patient may fall by as much as 6°C, while a 2°C decrease is very common. This is due to a combination of anaesthesia-related impairment of the central thermoregulatory control and a cool operating room temperature, which, when superimposed on insufficient insulation and a failure to actively warm the patient, may result in profound temperature disturbances. As a result, prolonged wound healing, increased risk of wound infection, a higher rate of cardiac morbidity, and greater intraoperative blood loss and postoperative blood transfusion requirements may occur. The reasons for this are said to include underlying changes in microcirculation, coagulation, immunology and an increase in the duration of action of most anaesthesia medications. As effective methods have been available for a number of years now, it is currently indicated to maintain intraoperative normothermia in order to minimise procedure-related risk and improve patient comfort.

Insulin-like Growth Factor 1-mediated Hyperthermia Involves Anterior Hypothalamic Insulin Receptors

The objective is to investigate the role of insulin-like growth factor 1 (IGF-1) in the regulation of core body temperature. Sequencing cDNA libraries from individual warm-sensitive neurons from the preoptic area (POA) of the hypothalamus, a region involved in the central control of thermoregulation, identified neurons that express both IGF-1 receptor (IGF-1R) and insulin receptor transcripts. The effects of administration of IGF-1 into the POA was measured by radiotelemetry monitoring of core temperature, brown adipose tissue (BAT) temperature, metabolic assessment, and imaging of BAT by positron emission tomography of 2-[(18)F]fluoro-2-deoxyglucose uptake combined with computed tomography. IGF-1 injection into the POA caused dose-dependent hyperthermia that could be blocked by pretreatment with the IGF-1R tyrosine kinase inhibitor, PQ401. The IGF-1-evoked hyperthermia involved activation of brown adipose tissue and was accompanied by a switch from glycolysis to fatty acid oxidation as a source of energy as shown by lowered respiratory exchange ratio. Transgenic mice that lack neuronal insulin receptor expression in the brain (NIRKO mice) were unable to mount the full hyperthermic response to IGF-1, suggesting that the IGF-1 mediated hyperthermia is partly dependent on expression of functional neuronal insulin receptors. These data indicate a novel thermoregulatory role for both IGF-1R and neuronal insulin receptors in IGF-1 activation of BAT and hyperthermia. These central effects of IGF-1 signaling may play a role in regulation of metabolic rate, aging, and the risk of developing type 2 diabetes.

2010 Carl Ludwig Distinguished Lectureship of the APS Neural Control and Autonomic Regulation Section: Central neural pathways for thermoregulatory cold defense

Central neural circuits orchestrate the homeostatic repertoire to maintain body temperature during environmental temperature challenges and to alter body temperature during the inflammatory response. This review summarizes the research leading to a model representing our current understanding of the neural pathways through which cutaneous thermal receptors alter thermoregulatory effectors: the cutaneous circulation for control of heat loss, and brown adipose tissue, skeletal muscle, and the heart for thermogenesis. The activation of these effectors is regulated by parallel but distinct, effector-specific core efferent pathways within the central nervous system (CNS) that share a common peripheral thermal sensory input. The thermal afferent circuit from cutaneous thermal receptors includes neurons in the spinal dorsal horn projecting to lateral parabrachial nucleus neurons that project to the medial aspect of the preoptic area. Within the preoptic area, warm-sensitive, inhibitory output neurons control heat production by reducing the discharge of thermogenesis-promoting neurons in the dorsomedial hypothalamus. The rostral ventromedial medulla, including the raphe pallidus, receives projections form the dorsomedial hypothalamus and contains spinally projecting premotor neurons that provide the excitatory drive to spinal circuits controlling the activity of thermogenic effectors. A distinct population of warm-sensitive preoptic neurons controls heat loss through an inhibitory input to raphe pallidus sympathetic premotor neurons controlling cutaneous vasoconstriction. The model proposed for central thermoregulatory control provides a platform for further understanding of the functional organization of central thermoregulation.

Cold thermoregulatory responses following exertional fatigue

Participants in prolonged, physically demanding cold-weather activities are at risk for a condition called "thermoregulatory fatigue". During cold exposure, the increased gradient favoring body heat loss to the environment is opposed by physiological responses and clothing and behavioral strategies that conserve body heat stores to defend body temperature. The primary human physiological responses elicited by cold exposure are shivering and peripheral vasoconstriction. Shivering increases thermogenesis and replaces body heat losses, while peripheral vasoconstriction improves thermal insulation of the body and retards the rate of heat loss. A body of scientific literature supports the concept that prolonged and/or repeated cold exposure, fatigue induced by sustained physical exertion, or both together, can impair the shivering and vasoconstrictor responses to cold ("thermoregulatory fatigue"). The mechanisms accounting for this thermoregulatory impairment are not clear, but there is evidence to suggest that changes in central thermoregulatory control or peripheral sympathetic responsiveness to cold lead to thermoregulatory fatigue and increased susceptibility to hypothermia.

Reply to Mahe, Rousseau, Saumet, and Abraham

LETTERS TO THE EDITORReply to Mahe, Rousseau, Saumet, and AbrahamLacy A. Holowatz and W. Larry KenneyLacy A. Holowatz and W. Larry KenneyPublished Online:01 Apr 2009https://doi.org/10.1152/japplphysiol.00038.2009MoreSectionsPDF (30 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations to the editor: We thank Dr. Mahe and colleagues (2) for their letter commenting on our recent findings that chronic low-dose aspirin therapy (81 mg) consistently and significantly attenuates reflex-mediated cutaneous vasodilation during heat stress (1). Daily low-dose aspirin (81 mg) is the gold standard antiplatelet therapy for primary and secondary prevention of atherothrombotic disease. Furthermore, the number of individuals engaging in medically supervised and unsupervised aspirin therapy is increasing because of the proven and substantiated cardiovascular benefits (3).Our recent findings provide the initial observation that reflex vasodilation in aged humans engaging in aspirin therapy is attenuated. However, before we make recommendations for altering antiplatelet drug therapy during environmental heat exposure, additional research is needed to determine 1) whether low-dose aspirin is effecting central thermoregulatory control, in which case sweating responses may also be diminished, 2) whether other antiplatelet drugs have similar effects on reflex vasodilation, and 3) whether lower doses (<81 mg) of aspirin provide sufficient antiplatelet effects without impairing reflex cutaneous vasodilation. This research into these basic mechanisms is necessary to provide evidenced-based recommendations and potential interventions for vulnerable clinical populations during heat exposure.REFERENCES1 Holowatz LA, Kenney WL. Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilation in middle-aged humans. J Appl Physiol 106: 500–505, 2009.Link | ISI | Google Scholar2 Mahe G, Rousseau P, Saumet JL, Abraham. About “Chronic low-dose aspirin therapy attenuates reflex cutaneous vasodilatation in middle-aged humans.” J Appl Physiol; doi:10.1152/japplphysiol.91653.2008.Link | ISI | Google Scholar3 Patrono C, Rocca B. Aspirin: promise and resistance in the new millennium. Arterioscler Thromb Vasc Biol 28: s25–32, 2008.Crossref | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: L. A. Holowatz, 204 Noll Lab, Penn State, Univ. Park, PA 16802 (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 106Issue 4April 2009Pages 1472-1472 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00038.2009History Published online 1 April 2009 Published in print 1 April 2009 Metrics

Selective blockade of 5-HT2A receptors attenuates the increased temperature response in brown adipose tissue to restraint stress in rats

Previous studies have demonstrated that 5-HT2A receptors may be involved in the central control of thermoregulation and of the cardiovascular system. Our aim was to test whether these receptors mediate thermogenic and tachycardiac responses induced by acute psychological stress. Three groups of adult male Hooded Wistar rats were instrumented with: (i) a thermistor in the interscapular area (for recording brown adipose tissue temperature) and an ultrasound Doppler probe (to record tail blood flow); (ii) temperature dataloggers to record core body temperature; (iii) ECG electrodes. On the day of the experiment, rats were subjected to a 30-min restraint stress preceded by s.c. injection of either vehicle or SR-46349B (a serotonin 2A receptor antagonist) at doses of 0.01, 0.1 and 1.0 mg/kg. The restraint stress caused a rise in brown adipose tissue temperature (from, mean ± s.e.m., 36.6 ± 0.2 to 38.0 ± 0.2°C), transient cutaneous vasoconstriction (tail blood flow decreased from 12 ± 2 to 5 ± 1 cm/s), increase in heart rate (from 303 ± 15 to 453 ± 15 bpm at the peak, then reduced to 393 ± 12 bpm at the steady state), and defaecation (6 ± 1 pellets per restraint session). The core body temperature was not affected by the restraint. Blockade of 5-HT2A receptors attenuated the increase in brown adipose tissue temperature and transient cutaneous vasoconstriction, but not tachycardia and defaecation elicited by restraint stress. These results indicate that psychological stress causes activation of 5-HT2A receptors in neural pathways that control thermogenesis in the brown adipose tissue and facilitate cutaneous vasoconstriction.

Heat Illness and Heat Stroke

1. David S. Jardine, MD* 1. *Children's Hospital, Seattle, Wash After completing this article, readers should be able to: 1. Describe the laboratory abnormalities that accompany heat stroke. 2. Understand the relationship between core temperature and injury. 3. Discuss strategies to reduce the risk of heat stroke during athletic events. 4. Describe the physical findings of patients suffering from heat stroke. 5. List the most common sequelae of heat stroke. 6. Identify the body temperature above which heat injury begins to occur. 7. Explain the differences between malignant hyperthermia and heat stroke. 8. Discuss the differences between heat stress, heat exhaustion, and heat stroke. Heat illness is caused by an inability to maintain normal body temperature because of excess heat production or decreased heat transfer to the environment. Heat stroke arises when cellular injury is caused by excess body temperature. If the core temperature rises above 105.8°F (41°C) for more than a short time, thermal injury results. Proteins are denatured, and injured cells undergo apoptosis (programmed cell death) or necrosis. Even before injury takes place, an individual may suffer transient mental and physical impairment, which is called heat exhaustion. Heat stroke is a medical emergency that is associated with a mortality of approximately 12% in adult patients. Treatment requires aggressive supportive care to minimize mortality. It is important to recognize the difference between fever and heat stroke. Fever is a normal response, during which the core temperature remains under the control of the central thermoregulatory centers that reside in the hypothalamus and brainstem. When a pyrogenic stimulus is received, core temperature is elevated rapidly to a new set point that is regulated by normal mechanisms. Maximum febrile temperatures rarely exceed 105.8°F (41°C). (1) In contrast, during heat illness, normal heat transfer mechanisms are overwhelmed and central thermoregulatory control is ineffective. Consequently, the core temperature can rise quickly to injurious levels. ### Heat Stress Before heat stroke occurs, lesser degrees of dysfunction …

Ondansetron does not reduce the shivering threshold in healthy volunteers

Ondansetron, a serotonin-3 receptor antagonist, reduces postoperative shivering. Drugs that reduce shivering usually impair central thermoregulatory control, and may thus be useful for preventing shivering during induction of therapeutic hypothermia. We determined, therefore, whether ondansetron reduces the major autonomic thermoregulatory response thresholds (triggering core temperatures) in humans. Control (placebo) and ondansetron infusions at the target plasma concentration of 250 ng ml(-1) were studied in healthy volunteers on two different days. Each day, skin and core temperatures were increased to provoke sweating; then reduced to elicit peripheral vasoconstriction and shivering. We determined the core-temperature sweating, vasoconstriction and shivering thresholds after compensating for changes in mean-skin temperature. Data were analysed using t-tests and presented as means (sds); P<0.05 was taken as significant. Ondensetron plasma concentrations were 278 (57), 234 (55) and 243 (58) ng ml(-1) at the sweating, vasoconstriction and shivering thresholds, respectively; these corresponded to approximately 50 mg of ondansetron which is approximately 10 times the dose used for postoperative nausea and vomiting. Ondansetron did not change the sweating (control 37.4 (0.4) degrees C, ondansetron 37.6 (0.3) degrees C, P=0.16), vasoconstriction (37.0 (0.5) degrees C vs 37.1 (0.3) degrees C; P=0.70), or shivering threshold (36.3 (0.5) degrees C vs 36.3 (0.6) degrees C; P=0.76). No sedation was observed on either study day. /b>. Ondansetron appears to have little potential for facilitating induction of therapeutic hypothermia.

The central melanocortin system and fever.

Fever is a phylogenetically ancient response that is mounted upon exposure of the host to pathogens or inflammatory agents. Melanocortin agonists act centrally to inhibit fever by acting at receptors, including the melanocortin-4 receptor, which is prominently expressed in key hypothalamic thermoregulatory centers. Furthermore, endogenous melanocortins act centrally as physiological modulators of fever, recruited during the febrile response to restrain its intensity. Functionally, these actions lie at the interface between the anti-inflammatory effects of melanocortins, which involve suppression of the synthesis and actions of proinflammatory cytokines, and the central control of thermoregulation. Considering the extensive neuroanatomic and functional overlaps between central pathways and peripheral effectors involved in thermoregulation and energy balance, it is not surprising that melanocortins have been found to influence the metabolic economy profoundly in pathological as well as normal states. For example, despite suppressing endotoxin-induced fever, endogenous melanocortins appear to mediate the associated anorexia, a classic component of the "illness syndrome" accompanying acute infections, and promote a negative energy balance. The thermoregulatory actions of melanocortins are in several respects functionally opposed, and are remarkably dependent on physiological state, indicating that responsiveness to melanocortins is a physiologically modulated variable. Elucidating the anti-inflammatory and thermoregulatory roles of central melanocortin receptors during inflammatory states may lead to novel pharmacotherapeutic targets based on selective targeting of melanocortin receptor subtypes, for clinical benefit in human disease states involving neuroinflammatory components and metabolic wasting.

Perioperative shivering: physiology and pharmacology.

IN homeothermic species, a thermoregulatory system coordinates defenses against cold and heat to maintain internal body temperature within a narrow range, thus optimizing normal physiologic and metabolic function. The combination of anesthetic-induced thermoregulatory impairment and exposure to a cool environment makes most unwarmed surgical patients hypothermic. Although shivering is but one consequence of perioperative hypothermia, and rarely the most serious, it occurs frequently (i.e., 40–60% after volatile anesthetics), and it remains poorly understood. While coldinduced thermoregulatory shivering remains an obvious etiology, the phenomenon has also been attributed to numerous other causes. Our first goal is to review the organization of the thermoregulatory system, and particularly the physiology of postanesthetic shivering. We then discuss the pharmacology of thermoregulation and review the putative mechanisms and sites of action of various antishivering drugs.

Less Core Hypothermia when Anesthesia Is Induced with Inhaled Sevoflurane Than with Intravenous Propofol

Hypothermia after the induction of anesthesia results initially from core-to-peripheral redistribution of body heat. Sevoflurane and propofol both inhibit central thermoregulatory control, thus causing vasodilation. Propofol differs from sevoflurane in producing substantial peripheral vasodilation. This vasodilation is likely to facilitate core-to-peripheral redistribution of heat. Once heat is dissipated from the core, it cannot be recovered. We therefore tested the hypothesis that the induction of anesthesia with IV propofol causes more core hypothermia than induction with inhaled sevoflurane. We studied patients undergoing minor oral surgery randomly assigned to anesthetic induction with either 2.5 mg/kg propofol (n = 10) or inhalation of 5% sevoflurane (n = 10). Anesthesia in both groups was subsequently maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe skin temperature gradients <0[degree sign]C were considered indicative of significant vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Patients in both groups were vasodilated throughout most of the surgery. Nonetheless, core temperatures in patients who received propofol were significantly lower than those in patients who received inhaled sevoflurane. These data support our hypothesis that even a brief period of vasodilation causes substantial redistribution hypothermia that persists throughout surgery. Implications: Core temperatures in patients who received IV propofol were consistently lower than those in patients who received inhaled sevoflurane, although anesthesia was subsequently maintained with sevoflurane in nitrous oxide in both groups. This suggests that even a brief period of propofol-induced vasodilation during anesthetic induction causes substantial redistribution hypothermia that persists throughout surgery. (Anesth Analg 1999;88:921-4)

Epidural anesthesia impairs both central and peripheral thermoregulatory control during general anesthesia

Epidural anesthesia impairs both central and peripheral thermoregulatory control during general anesthesia

Reduction in the Shivering Threshold Is Proportional to Spinal Block Height

Hypothermia is nearly as common, and may be as severe, during spinal and epidural anesthesia as during general anesthesia. The authors have proposed that thermoregulatory failure results when regional anesthesia increases apparent leg skin temperature to a level far exceeding actual leg skin temperature. Extensive dermatomal blocks will alter thermal input to the hypothalamus from a greater skin-surface area more than less extensive ones and thus might be expected to impair central thermoregulatory control more. Accordingly, they tested the hypothesis that reduction in the shivering threshold is directly related to the number of dermatomes blocked during spinal anesthesia. Eleven men, aged 62 +/- 6 yr (mean +/- SD), undergoing urologic surgery were studied. Ice-cold lactated Ringer's solution was administered intravenously before spinal blockade and the shivering threshold (triggering core temperature) was established. Spinal anesthesia then was induced using a randomly assigned dose of 0.5% bupivacaine (2-4 ml). Again, sufficient cold lactated Ringer's solution was given to induce shivering. Tympanic membrane, ambient and skin temperatures were measured, and extent of block was defined by loss of temperature discrimination. Presence of shivering was evaluated by a blinded observer. Mean upper-body skin and ambient temperatures, cooling rates and intravenous fluid volumes at the two thresholds were compared using paired, two-tailed t tests (P < 0.05). Linear regression defined the relationship between reduction in shivering threshold and the number of dermatomes blocked. There were no significant differences between mean upper-body skin and ambient temperatures, cooling rates or intravenous fluid volumes at the control and spinal shivering thresholds. Spinal anesthesia reduced the shivering threshold in direct relation to the number of dermatomes blocked: delta threshold = 0.74 - 0.06 (dermatomes blocked); r2 = 0.58, P < 0.006. Extensive spinal blockade impairs central thermoregulatory control more than less extensive blockade. Clinicians can thus anticipate more core hypothermia during extensive than during restricted spinal blockade.

Thermoregulation: pathology, pharmacology, and therapy

Section headings Temperature Regulation and Drugs: An Introduction. Mechanisms of Fever, R. Hellon et al . Antipyretics, C. G. Van Arman. Cardiac Output and its Distribution During Exercise and Heat Stress, A. W. Bell & J. R. S. ales. Drug-Related Heatstroke, W .G. Clark & J. M. Lip on. Malignant Hyperthermia: A Review, B. A. Britt. Local, Regional and Systemic Hyperthermia: Potentiation of Radiotherapy and Chemotherapy in Cancer Treatment, J. L. Meyer et al . Hydrotherapy: Mechanisms and Indications, P. Franchimont et al . Temperature Regulation and Anesthesia, H. M. Chinyanga. Surgical Hypothermia, C. A. Taylor. Accidental Hypothermia, B. C. Paton. Water and Electrolyte Exchange During Exposure to Cold, M. J. Fregly. Opioids and Opioid Receptors in Thermoregulation, T. F. Burks. Brain and Pituitary Peptides in Thermoregulation, W. G. Clark & J. M. Lip on. Effects of Ethanol on Thermoregulation, H. Kalant & A. D. Le. Capsaicin and Central Control of Thermoregulation, T. Hori. Index. 3167 lit. refs. appro.,x 88 illus.

Lateral distribution of hypothalamic signals controlling thermoregulatory vasomotor activity and shivering in rats

The present study explored the laterality of central nervous thermoregulatory control in anesthetized rats by measuring paw skin vasomotor activity and cold-induced shivering in hind leg muscles during unilateral preoptic area and anterior hypothalamus (POAH) warming and electrical stimulation or during unilateral thermal stimulation of abdominal skin. Unilateral POAH warming produced vasodilation on both sides of the body, but vasodilation on the ipsilateral side always either occurred at a lower threshold hypothalamic temperature or was stronger than on the contralateral side. In a cold environment (5 degrees C), shivering was suppressed simultaneously in both hind legs when one side of the POAH was warmed, and shivering reappeared simultaneously on both sides when POAH warming stopped. These results suggest that different thermoregulatory effectors are regulated in a different way by each side of the POAH. Unilateral thermal stimulation of the abdominal skin, on the other hand, affected vasomotor activity and shivering equally on both sides of the body, as previously reported for its influence on salivary secretion. Skin thermal signals from both sides of the body therefore seem to converge before they act on different thermoregulatory effector systems.

Ontogenetic development of the ophthalmic rete in relation to brain cooling in chickens and pigeons

The brain cooling capacity of the altricial pigeon increases during posthatching growth at a higher rate than that of the precocial duck and chicken. To determine if this difference between the altricial and the precocial modes of development can be related to growth rates of the vascular heat exchanger involved in brain cooling (the ophthalmic rete), we performed a morphometric analysis of this structure during the post-hatching maturation of the three species. The number of vascular units in the rete did not change during development but differed significantly among species. The retia continued to grow in length and diameter in an exponential relation with body mass at similar rates in all species. The surface area of the retial arteries, which reflects the area available for countercurrent heat exchange, also increased exponentially with body mass, but without significant differences among the three species. However, the effectiveness of the rete in brain cooling, as indicated by the degree of brain cooling per unit of heat-exchange area in the rete, was higher in the altricial pigeon than in the precocial chicken and duck. It is concluded that the posthatching morphometric changes in the ophthalmic rete (rete ophthalmicum) are important for the development of brain cooling capacity, but cannot solely explain differences in brain cooling between growing altricial and precocial birds. These differences are most likely related to differences in the maturation of the central thermoregulatory control system and the peripheral effector mechanisms among the two groups of birds.