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Orientador: Alberto Cliquet Junior Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas Resumo: A regulação autonôma da temperatura corporal (Tc) torna-se ineficiente em lesados medulares (LM). A temperatura da pele (Tpele) sofre influência do fluxo sanguíneo da pele, da microcirculação e da temperatura ambiente. Em função disso, nossa pesquisa visou três objetivos: a) elaboração de mapas da Tpele pelos dermátomos (C2 a S2) em LM e controle; b) verificação da existência e grau de pecilotermia em LM; c) aplicação da estimulação elétrica (EENM) em LM e o estudo da variação da Tpele. O dispositivo utilizado para as medidas da Tpele foi o termômetro infravermelho (TI). Na 1ª etapa, 20 tetraplégicos, 21 paraplégicos e 11 controles foram expostos à temperatura ambiente de 24ºC. Na comparação entre os mapas obtivemos os seguintes resultados: diferenças significativas da Tpele nos dermátomos C3, C7, T2, T3, T8, T9, L1, L2, L4 e S2 para controle versus LM; C5, C6, C8, T1, T10, L3 e S1 para controle versus tetraplégicos; C5, C6, C7 e T5 para tetraplégicos versus paraplégicos. Quanto ao nível de lesão, apenas L5 e S1 do grupo paraplégico, apresentaram diferenças significativas. Na 2ª etapa, 13 tetraplégicos, 14 paraplégicos e 8 controles foram expostos a temperaturas ambientes de 24ºC e 20ºC. As medidas das Tpele na testa e nos dermátomos C2, L2, L3, L5 e S2 obedeceram ao seguinte protocolo: a) Baseline 24ºC; b) após 20 minutos em 20ºC - t1 e c) após 40 minutos em 20ºC - t2. Na comparação entre os grupos as diferenças significativas foram: testa, C2 e L3 entre controle versus tetraplégicos; L2 e S2 entre controle versus tetraplégicos e paraplégicos. Na testa e no dermátomo C2 a Tpele no grupo controle diminuiu nos primeiros 20 minutos e depois estabilizou até o final dos 40 minutos, o que não aconteceu com os grupos de tetraplegia e paraplegia que continuaram diminuindo. Nos demais dermátomos o comportamento foi similar em todos os grupos que continuaram diminuindo suas Tpele. Na 3ª etapa, 36 tetraplégicos e 36 paraplégicos foram submetidos ao protocolo da EENM. A estimulação foi aplicada nos músculos quadríceps (QDs), tibial anterior (TA). As temperaturas foram medidas na testa e nos dermátomos C2, C3, T4, T6, T10, L2, L3, L4 e L5 e sob os eletrodos utilizados. As avaliações seguiram as seguintes ordens: a) antes da EENM-linha de base; b) logo após a EENM - t0; c) 10 minutos após o término da EENM - t10 e d) após 20 minutos do término da EENM - t20. A Tpele aumentou nos dermátomos estimulados e sob os eletrodos utilizados, apresentando diferenças significativas na maioria dos dermátomos, nos três tempos analisados (t0, t10 e t20). Já os dermátomos L3, L4, C2, C3, T4, T6 e T10 diminuiram a Tpele nos oito subgrupos analisados. A elaboração do mapa de Tpele pode fornecer uma nova ferramenta para avaliar os LM na prática clínica e sua função autonômica em diferentes protocolos utilizados na reabilitação. O estudo da Tpele em temperatura ambiente mais baixa (20ºC) revelou que os LM são pecilotérmicos moderados e podem ter um intervalo de ajuste de temperatura. Quanto à aplicação de EENM em LM, concluímos que além de benefícios na restauração muscular e bem-estar, poderá contribuir para o estudo do mecanismo termorregulador Abstract: Autonomic regulation of body temperature (Tc) is ineffective in individuals with spinal cord injured (SCI). The skin temperature (Tskin) is influenced by the skin's blood flow, microcirculation and ambient temperature. As a result, our research aimed at three objectives: a) elaboration maps of Tskin by dermatomes (C2 to S2) in SCI and able-bodied; b) verification of the existence and degree of poikilothermia in SCI; c) application of electrical stimulation (NMES) in SCI and the study of Tskin variation. The device used for measuring the Tskin was the infrared thermometer (IT). In the 1st stage, 20 tetraplegics, 21 paraplegics and 11 able-bodied were exposed to an ambient temperature of 24ºC. When comparing the maps, we obtained the following results: significant differences in the Tskin in dermatomes C3, C7, T2, T3, T8, T9, L1, L2, L4 and S2 for able-bodied versus SCI; C5, C6, C8, T1, T10, L3 and S1 for able-bodied versus tetraplegics; C5, C6, C7 and T5 for tetraplegics versus paraplegics. As for the level of injury, only L5 and S1 of the paraplegic group showed significant differences. In the 2nd stage, 13 tetraplegics, 14 paraplegics and 8 able-bodied were exposed to ambient temperatures of 24ºC and 20ºC. The measurements of the skin on the forehead and dermatomes C2, L2, L3, L5 and S2 followed the following protocol: a) Baseline 24ºC; b) after 20 minutes at 20ºC ¿ t1 and c) after 40 minutes at 20ºC - t2. Comparing between the groups, the significant differences were: forehead, C2 and L3 between control versus tetraplegics; L2 and S2 between control versus tetraplegics and paraplegics. On the forehead and on the C2 dermatome, the Tskin in the able-bodied group decreased in the first 20 minutes and then stabilized until the end of the 40 minutes, which did not happen with the tetraplegics and paraplegia groups that continued to decrease. In the other dermatomes, the behavior was similar in all groups that continued to decrease their Tskin. In the 3rd stage, 36 tetraplegics and 36 paraplegics were submitted to the NMES protocol. The stimulation was applied to the quadriceps (QDs), anterior tibialis (AT) muscles. Temperatures were measured on the forehead and C2, C3, T4, T6, T10, L2, L3, L4 and L5 dermatomes and under the electrodes used. The assessments followed the following orders: a) before the baseline NMES; b) right after NMES-t0; c) 10 minutes after the end of NMES-t10 and d) after 20 minutes the end of NMES-t20. Tskin increased in stimulated dermatomes and under the electrodes used, showing significant differences from Tskin in most dermatomes, in the three analyzed moments (t0, t10 and t20). Dermatomes L3, L4, C2, C3, T4, T6 and T10 decreased the Tskin in the eight subgroups analyzed. The elaboration of the Tskin map can provide a new tool to evaluate SCI in clinical practice and its autonomic function in different protocols used in rehabilitation. The study of Tskin at a lower ambient temperature (20ºC) revealed that the SCI are moderate poikilotermics and can have a temperature adjustment interval. As for the application of NMES in SCI, we conclude that in addition to benefits in muscle restoration and well-being, it may contribute to the study of the thermoregulatory mechanism Doutorado Fisiopatologia Cirúrgica Doutora em Ciências CNPQ 140215-2014-0 FAPESP 2016/50253-0

The present study aimed to quantitate 15 perfluoroalkyl acids (PFAAs) in 125 adult American alligators at 12 sites across the southeastern United States. Of those 15 PFAAs, 9 were detected in 65% to 100% of samples: perfluorooctanoic acid, perfluorononanoic acid, perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnA), perfluorododecanoic acid, perfluorotridecanoic acid (PFTriA), perfluorotetradecanoic acid, perfluorohexanesulfonic acid (PFHxS), and perfluorooctane sulfonate (PFOS). Males (across all sites) showed significantly higher concentrations of 4 PFAAs: PFOS (p = 0.01), PFDA (p = 0.0003), PFUnA (p = 0.021), and PFTriA (p = 0.021). Concentrations of PFOS, PFHxS, and PFDA in plasma were significantly different among the sites in each sex. Alligators at both Merritt Island National Wildlife Refuge (FL, USA) and Kiawah Nature Conservancy (SC, USA) exhibited some of the highest PFOS concentrations (medians of 99.5 ng/g and 55.8 ng/g, respectively) in plasma measured to date in a crocodilian species. A number of positive correlations between PFAAs and snout-vent length were observed in both sexes, suggesting that PFAA body burdens increase with increasing size. In addition, several significant correlations among PFAAs in alligator plasma may suggest conserved sources of PFAAs at each site throughout the greater study area. The present study is the first to report PFAAs in American alligators, to reveal potential PFAA hot spots in Florida and South Carolina, and to provide a contaminant of concern when assessing anthropogenic impacts on ecosystem health. Environ Toxicol Chem 2017;36:917-925. Published 2016 Wiley Periodicals Inc. on behalf of SETAC. This article is a US government work and, as such, is in the public domain in the United States of America.

The typical core temperature (Tc) profile displayed during heatstroke (HS) recovery consists of initial hypothermia followed by delayed hyperthermia. Anecdotal observations led to the conclusion that these Tc responses represent thermoregulatory dysfunction as a result of brain damage. We hypothesized that these Tc responses are mediated by a change in the temperature setpoint. Tc (± 0.1°C; radiotelemetry) of male C57BL/6J mice was monitored while they were housed in a temperature gradient with ambient temperature (Ta) range of 20–39°C to monitor behaviorally selected Ta (Ts) or an indirect calorimeter (Ta = 25°C) to monitor metabolism (V̇o2) and calculate respiratory exchange ratio (RER). Responses to mild and severe HS (thermal area 249.6 ± 18.9 vs. 299.4 ± 19.3°C·min, respectively) were examined through 48 h of recovery. An initial hypothermia following mild HS was associated with warm Ts (∼32°C), ∼35% V̇o2 decrease, and RER ∼0.71 that indicated reliance on fatty acid oxidation. After 24 h, mild HS mice developed hyperthermia associated with warm Ts (∼32°C), ∼20% V̇o2 increase, and RER ∼0.85. Severe HS mice appeared poikilothermic-like in the temperature gradient with Tc similar to Ts (∼20°C), and these mice failed to recover from hypothermia and develop delayed hyperthermia. Cellular damage (hematoxylin and eosin staining) was undetectable in the hypothalamus or other brain regions in severe HS mice. Overall, decreases and increases in Tc were associated with behavioral and autonomic thermoeffectors that suggest HS elicits anapyrexia and fever, respectively. Taken together, Tc responses of mild and severe HS mice suggest a need for reinterpretation of the mechanisms of thermoregulatory control during recovery.

A 87-year-old woman was admitted with a rapidly progressive confusion, disorientation and myoclonus, all suggestive of sporadic Creutzfeldt-Jakob disease (sCJD). This diagnosis was initially strongly supported by the EEG, which showed slow background activity and triphasic waves, combined with the finding of an increased level of 14-3-3 protein in the cerebrospinal fluid. Remarkably, this patient had also developed hypothermia, which, after warming-up, resulted in alleviation of the mental disturbances and disappearance of myoclonus. Over time, the EEG abnormalities disappeared. She recovered clinically for which reason the diagnosis of sCJD had to be rejected; however, she kept the inability to maintain body temperature (poikilothermia). Therefore, in patients with the aforementioned symptoms body temperature should be measured and adequately managed. Our hypothesis is that she suffered from a misleading acquired encephalopathy with reversible EEG and laboratory features, mimicking sCJD. When laboratory findings suggest sCJD it remains very important to see whether or not these findings are compatible with the clinical observations.

Temperature regulation in humans is controlled by the hypothalamus. After death by neurological criteria, the hypothalamus ceases to function and poikilothermia ensues. Preservation of normothermia in those patients destined to become organ donors is an important part of maintaining the normal physiology of the organs and organ systems. Typical means of achieving normothermia include increasing the temperature of the ambient air, infrared warming lights, instillation of warmed intravenous fluids, and warm air or water blankets.In this prospective case series of five organ donors, we used an intravascular temperature modulation catheter (Alsius, Irvine, CA) to maintain normothermia in organ donors declared dead by neurological criteria. Data on accuracy of temperature maintenance at 37 degrees C and nursing ease of use were collected.This intravascular temperature modulation catheter provided an accurate method of temperature regulation in brain death donor and easier to use from a nursing workload perspective.Intravascular warming is a viable method for the maintenance of normothermia in organ donors. The experience here provides some insight into the ability of these devices to warm patients in other clinical situations.

The glutamate NMDA receptor has been suggested to be involved in thermoregulation. To further analyse its role, the thermoregulatory responses of rats treated with 0.5 mg·kg–1 of dizocilpine (MK801) were compared with those of control rats treated only with the same volume of saline during a 180-min exposure at one of the six different ambient temperatures, ranging from cold to heat. Colonic temperature (Tco) and tail skin temperature (Ttail) were measured throughout using Cu–Ct thermocouples. In the cold (2.4 and 12.3 °C), Tco decreased either sharply (MK801) or progressively (saline), reaching the same final value (2.4 °C) or a lower value in the MK801-treated rats (12.3 °C). At the same time, Ttail decreased in both groups. In the cool environment (20.7 °C), Tco and Ttail decreased in both groups, with lower final values in MK801-treated rats. At thermoneutrality (28.8 °C), the MK801-induced hyperthermia remained steady, while Ttail increased in both groups. In the heat (34.6 and 36.2 °C), Tco and Ttail increased in both groups, with higher final values in MK801-treated rats. Moreover, at 36.2 °C, only MK801-treated rats exhibited heatstroke. It is thus suggested that MK801-induced inhibition of NMDA receptors impairs thermoregulation, especially in the heat.Key words: thermoregulation, NMDA receptor, MK801, poikilothermia, rat.

Despite its proven clinical application for protection-preservation of the brain and heart during cardiac surgery, hypothermia research has fallen in and out of favor many times since its inception. Since the 1980s, there has been renewed research and clinical interest in therapeutic hypothermia for resuscitation of the brain after cardiac arrest or TBI and for preservation-resuscitation of extracerebral organs, particularly the abdominal viscera in low-flow states such as HS. Although some of the fears regarding the side effects of hypothermia are warranted, others are not. Without further laboratory and clinical studies, the significance of these effects cannot be determined and ways to overcome these problems cannot be developed. Currently, at the turn of the century, there are significant data demonstrating the benefit of mild-to-moderate hypothermia in animals and humans after cardiac arrest or TBI and in animals during and after HS. The clinical implications of uncontrolled versus controlled hypothermia in trauma patients and the best way to assure poikilothermia for cooling without shivering are still unclear. It is time to consider a prospective trial of therapeutic, controlled hypothermia for patients during traumatic HS and resuscitation. The authors believe that the new millennium will witness remarkable advantages of the use of controlled hypothermia in trauma. Starting in the prehospital phase, mild hypothermia will be induced in hypovolemic patients, which will not only decrease the immediate mortality rate but perhaps also will protect cells and reduce the likelihood of secondary inflammatory response syndrome, multiple organ failure, and late deaths. The most futuristic applications will be hypothermic strategies to achieve prolonged suspended animation for delayed resuscitation in traumatic exsanguination cardiac arrest.

Objective: To assess the effects of steady-state spontaneous hypothermia on multimodality evoked potentials and on peripheral nerve conduction in human poikilothermia. Design and Setting: Case series at a university hospital. Patients: Four patients (four women, aged 28 to 37 years) with acquired poikilothermia. Main Outcome Measures: Short-latency somatosensory, brain-stem auditory, and visual evoked potentials as well as motor and sensory peripheral nerve conduction velocity during steady-state spontaneous hypothermia and normothermia. Results: The marked latency prolongation of all evoked potentials and decreased peripheral nerve conduction velocity observed during steady-state spontaneous hypothermia (mean±SD core temperature, 33.5±0.3°C) compared with normothermia (36.9±0.4°C) agrees with previous findings during short-term induced hypothermia. Conclusions: The unequivocal effect of sustained mild spontaneous hypothermia on evoked potentials and peripheral nerve conduction velocity underlines the importance of meticulous attention to even small alterations in core temperature in interpreting neurophysiological investigations.

WOS: 000305226300018, PubMed ID: 22426665, A 21-year-old woman was admitted due to altered mental status and hypothermia. The patient had a diagnosis of neuromyelitis optica (NMO) for 12 years and she was positive for serum anti-aquaporin 4 antibody. On admission, physical examination revealed coma with decerebration rigidity and poikilothermia. Magnetic resonance images of the brain revealed widespread, gadolinium enhancing lesions in the periventricular areas and the diencephalic structures. Laboratory investigations revealed hyponatremia and hypothyroidism. The patient was treated with high dose steroids. Both symptomatic and asymptomatic brain lesions may develop in patients with NMO. However, poikilothermia has not been reported in patients with NMO before.

A Fabry patient with poikilothermia is described. Laboratory investigations, neuro-imaging and autonomic function tests did not disclose a cause. Assessment of intra-epidermal nerve fibre density and quantitative sensory testing revealed small fibre neuropathy with a highly impaired cold sensation. We speculate that the poikilothermia is either caused by a vascular lesion in the hypothalamus not visible on MRI or by small fibre neuropathy leading to disturbed body temperature perception and therefore impaired thermoregulation.

1. 1.Heterocephalus glaber (the naked mole rat) is unique amongst mammals in that it is an endothermic poikilotherm. This unusual mode of thermoregulation leads one to question other thermoregulatory reactions such as the thermal response to pyrogens. 2. 2.The thermal component of the fever response of Heterocephalus glaber was investigated. Body temperature was measured following injections of a Gram-positive pyrogen (Staphylococcus aureus cell walls) and saline (n = 9). 3. 3.Injection with saline resulted in a 0.8 ± 0.2°C rise in temperature and a 4 h thermal response index of 1.5 ± 0.5°C · h. This is primarily attributed to handling stresses and was not different to the effects of handling without any injection. 4. 4.A significant monophasic fever developed 50min after S. aureus injection and was maintained until 190 min post-injection. Compared with pre-injection baseline measurements, the maximum change in temperature was 1.5 ± 0.2°C, and the 4 h thermal response index was 3.4 ± 0.5°C · h. After removing the apparent handling effects (as shown by the saline treatment) the pyrogen-induced elevation in body temperature was 0.7°C. 5. 5.This poikilothermic mammal can therefore endogenously elevate body temperature and shows a positive fever response to Gram-positive pyrogens.

The compositional properties of DNAs from 122 species of fishes and from 18 other cold-blooded vertebrates (amphibians and reptiles) were compared with those from 10 warm-blooded vertebrates (mammals and birds) and found to be substantially different. Indeed, DNAs from cold-blooded vertebrates are characterized by much lower intermolecular compositional heterogeneities and CsCl band asymmetries, by a much wider spectrum of modal buoyant densities in CsCl, by generally lower amounts of satellites, as well as by the fact that in no case do buoyant densities reach the high values found in the GC-richest components of DNAs from warm-blooded vertebrates. In the case of fish genomes, which were more extensively studied, different orders were generally characterized by modal buoyant densities that were different in average values as well as in their ranges. In contrast, different families within any given order were more often characterized by narrow ranges of modal buoyant densities, and no difference in modal buoyant density was found within any single genus (except for the genus Aphyosemion, which should be split into several genera). The compositional differences that were found among species belonging to different orders and to different families within the same order are indicative of compositional transitions, which were shown to be essentially due to directional base substitutions. These transitions were found to be independent of geological time. Moreover, the rates of directional base substitutions were found to be very variable and to reach, in some cases, extremely high values, that were even higher than those of silent substitutions in primates. The taxonomic and evolutionary implications of these findings are discussed.

A general functional relationship between body weight (10−11 to 108 g) and ingestion rate has been found to exist throughout the protistan and metazoan kingdoms. Results, based on a mathematical interpretation of standardized, quantitative data, indicate that ingestion rate is a log–log linear function (i.e., power function) of body weight (I = a W0.829 for cold-blooded forms and I = a W0.778 for warm-blooded forms, where I = ingestion rate and W = body weight). The slopes of the cold-blooded and warm-blooded regression lines are not significantly different from each other (i.e., they are parallel). This allows one to use the difference between the respective curves to estimate the weight-specific cost of warm-bloodedness. Such an analysis of the data indicates that a warm-blooded organism must ingest about ten times more food per unit body weight than cold-blooded forms. This functional relationship may be a manifestation of the physiological constraints placed on organisms by surface area to volume ratio phenomena, related to absorptive surfaces, mouth areas, and body volumes. The present analysis suggests that flexibility in functional design is limited by physical phenomena which affect phenotypic plasticity.

International audience; ObjectiveA large spectrum of surgical techniques can be proposed to young patients presenting with hypothalamic hamartomas (HH) associated with severe epilepsy. The aim of this report is to point on some clinical and anatomical parameters supposed to influence the choice of the surgical approach and to emphasize the specific role of radiosurgery.Materials and methodsWe reviewed both our experience and the recent literature based on a Pubmed search. Lateral pterional, midline frontal through the lamina terminalis, transcallosal interforniceal approaches, endoscopic treatment through the foramen of Monro, disconnecting surgery, radiofrequency ablation, brachytherapy and gamma knife surgery (GKS) were all considered. Mortality, morbidity, and efficacy of each of these techniques were compared. Specific limits, difficulties, and constraints were taken into account. Our experience of radiosurgery is based on a prospective trial which enrolled 60 patients with HH and associated severe epilepsy between October 1999 and December 2005.ResultsSeveral surgical techniques can lead to a real reversal of the epileptic encephalopathy. The main factors for the decision-making process are the age, the size of the lesion and its anatomical type (according to our original classification), the severity of the epilepsy, and the severity of the cognitive/psychiatric comorbidity. In our prospective trial (GKS), 27 patients have a follow-up superior to 3 years. Among those, 59.2% have an excellent result with a dramatic behavioral and cognitive improvement and are completely seizure-free (37%) or have only rare non-disabling seizures (22.2%). No permanent neurological complication has been observed so far; three patients have presented a transient poïkilothermia. GKS is clearly the safer approach for these difficult patients. Young patients with severe epilepsy and comorbidity must be operated on using a curative approach as early as possible. Very large type VI or mixed type with a large component above the floor of the third ventricle must be disconnected and then the upper remnant can be ideally treated by GKS (staged surgery). Type V (rarely epileptic) and IV are frequently operable by disconnection. Type I HH deeply embedded in the hypothalamus are operated on by GKS efficiently and safely. Type II HH can be operated on either endoscopically or transcallosally or by GKS depending on the parents’ choice and severity of epilepsy. In small type III HH, GKS is a safer procedure, due to the very close relationship to the fornix and mammillary bodies. In very large type III HH, transcallosal interforniceal approach is proposed but with significant risks especially concerning short-term memory. When the lesion is sufficiently small, GKS is globally offering the patient a rate of seizure cessation comparable to microsurgery with, however, a much lower risk (no neurological deficit reported till now).ConclusionOur first results indicate that GKS is as effective as microsurgical resection and very much safer. GKS also allows avoiding the vascular risk related to radiofrequency lesioning or stimulation. The disadvantage of radiosurgery is its delayed action. Longer follow-up is mandatory for a reliable evaluation of the role of GKS. The early effect on subclinical discharges turns out to play a major role in the dramatic improvement of sleep quality, behavior, and developmental learning acceleration at school.

Both whole-body heat exposure and intraperitoneal heating (IPH) result in a body temperature (T(b)) fall that occurs once heating is abated ("hyperthermia-induced hypothermia"). This phenomenon involves a decrease in the threshold T(b) (T(b-thresh)) for activation of metabolic heat production (cold defense). Whether the T(b-thresh) for ear skin vasodilation (heat defense) also changes during hyperthermia-induced hypothermia remains unknown. In experiment 1, we applied IPH to guinea pigs by perfusing water through a preimplanted intraperitoneal thermode and delivered the total heat load of either approximately 1.5 kJ ("short" IPH; perfusion duration: 14 min) or approximately 3.0 kJ ("long" IPH; 40 min). Short IPH caused skin vasodilation and a 1.1 degrees C rise in T(b); no hypothermia occurred when IPH ceased. Long IPH caused vasodilation and hyperthermia of a comparable magnitude (1.4 degrees C) that were followed by a T(b) fall to 1.9 degrees C below the preheating value. In experiment 2, the Tb-thresh for skin vasodilation was measured twice: at the beginning of long IPH and at the nadir of the post-IPH hypothermia. The two T(b-thresh) values were 39.0 (SEM 0.1)degrees C and 39.2 (SEM 0.2)degrees C respectively. In the controls, the T(b-thresh) was measured at the beginning and after short IPH; both control values were 39.0 (SEM 0.2)degrees C. We conclude that the hyperthermia-induced hypothermia, although previously shown to be coupled with a decrease in the T(b-thresh) for cold defense, occurs without any substantial change in the T(b-thresh) for heat defense. We speculate that postheating thermoregulatory disorders are associated with threshold dissociation, thus representing the poikilothermic (wide dead-band) type of T(b) control.

Poikilothermia syndrome is a rare cause of intrinsic thermoregulatory failure. Patients with this syndrome regulate body temperature poorly, if at all. Recently, a patient was referred to us who had clinical evidence of poikilothermia syndrome, as well as long-standing multiple sclerosis. Computerized tomography and magnetic resonance scanning failed to identify a hypothalamic lesion. The patient was gradually warmed to sweating, and then cooled to vasoconstriction and shivering. The core-temperature thresholds triggering each defence were calculated, after compensating for the changes in skin temperature. The calculated sweating threshold was 38.3 degrees C (normal: 37.0 +/- 0.3 degrees C). The vasoconstriction threshold was 34.4 degrees C (normal: 36.4 +/- 0.3 degrees C). The sweating-to-vasoconstriction interthreshold range was thus approximately 4 degrees C, which is between 10 and 20 times the normal value. The shivering threshold was 31.8 degrees C (normal: 35.6 +/- 0.3 degrees C). The vasoconstriction-to-shivering range was thus approximately 2.5 degrees C which is more than twice the normal value. The pattern of thermoregulatory failure in this patient resembled that resulting from general anaesthesia.

In the present series of experiments we tested whether ethanol decreases body temperature by impairing thermal regulation (poikilothermia) or by shifting the set point downwards. The central temperature of rats kept in a thermocline and the selected ambient temperature were recorded by telemetry. After an IP injection of 2 g/kg of ethanol the rats selected an ambient temperature 7 degrees C lower than the one they selected before the ethanol injection and 8 degrees C lower than the one selected by the same rats after saline injection. At the same time the central temperature decreased by 2.5 degrees C. After about 40 min the rats preferred warmer ambient temperatures and 10 min later the central temperature began to rise. When, after ethanol, the rats were kept at 30 degrees C the central temperature remained at the normal level. At 35-36 degrees C the central temperature of normal rats without ethanol rose, in 1 h, from 37 degrees C to 39.75 degrees C. The results suggest that ethanol hypothermia is due to a downward shift of the set point and, in fact, is an anapyrexia, a condition inverse to fever.

Involvement of cholesterol in thermally induced restructuring of biological membranes was investigated in several tissues of rainbow trout (Oncorhynchus mykiss). Cholesterol-rich plasma membranes (PM) were isolated from erythrocytes, liver, kidney, and gill of fish acclimated to 5 and 20 degrees C. Mean PM cholesterol-to-phospholipid molar ratios (C/P) from warm-acclimated animals were significantly higher than those of cold-acclimated fish in liver (0.26 vs. 0.18; P < 0.01), kidney (0.49 vs. 0.40; P < 0.02), and gill (0.66 vs. 0.60; P < 0.05); erythrocyte C/P did not differ significantly with acclimation temperature (0.28 vs. 0.25; P = 0.25). In light of the ordering effects of cholesterol on fluid-phase membranes, these results are consistent with a role for cholesterol in the homeoviscous response of some poikilotherm PMs. Tissue differences in both PM cholesterol levels and the magnitude of thermally evoked cholesterol changes may reflect tissue-specific membrane functions. Lower PM C/P of trout tissues relative to corresponding data available for homeotherms also support a possible evolutionary relationship between cholesterol content and thermal adaptation of the PM.

Poikilothermia, the inability to maintain a constant core temperature independent of ambient temperature, markedly influences both the mental and physical function of affected patients; furthermore, prolonged hypothermia can induce numerous complications. To establish the pathophysiology of thermoregulation underlying poikilothermia in man, we compared 4 women with acquired poikilothermia, with 9 female control subjects. The activity of the main thermoregulatory effector mechanisms was assessed in a thermoneutral environment, and during subsequent cold stress and heat exposure. At thermoneutrality the patients had a significantly lower rectal temperature and resting metabolic rate compared with the controls; no patient showed peripheral vasoconstriction or shivering. Cooling revealed markedly reduced peripheral vasoconstriction in 3 patients and failure of the metabolic response in 2 patients; unlike controls, no patient exhibited shivering. Heat challenge revealed severely reduced capacity for heat dissipation in all patients. We conclude that in patients with poikilothermia, the mechanisms for both heat conservation and heat dissipation are seriously attenuated. Careful monitoring of the core temperature and adequate measures to maintain normothermia are of great importance in patients with poikilothermia in order to provide adequate treatment, improve the quality of life, and prevent serious complications.

An account is given of the three major techniques of estimating daily accumulated heat units from maximum-minimum temperatures: daily mean temperature, triangulation, and sine curve. Each of these techniques is also modified for partial correction of errors due to geographical bias. The efficiencies of the techniques in estimating heating units for the development of a soil insect are compared with actual measurements of heating units taken from field temperature data with a planimeter. The daily mean temperature technique with modification is the best estimator of heating units.

Preserving the optimal function of donor organs must be the primary goal of physicians caring for patients who have been certified brain dead and from whom organs will be transplanted. During the hours before organ removal, several significant medical challenges may emerge. These challenges include restoration and maintenance of intravascular volume and cardiac output to assure adequate oxygen delivery to donor tissue; re suscitation of the patient from spontaneous cardiac ar rest ; evaluation and reversal of polyuria; management of poikilothermia and the effects of hypothermia; and treat ment of hypopituitarism and other possible changes in circulating hormones. Individual organ function and the interdependency among donor organs must be carefully monitored and balanced to assure that the recipient re ceives organs that have the best opportunity for optimal primary function. Care of the multiorgan brain dead pa tient and his or her family requires a multidisciplinary team skilled not only in the medical and surgical aspects of transplantation but also in the care of families who have suffered loss. A new focus for patient care is appropriate after the decision has been made that a patient is brain dead and will become an organ donor. Because preser vation of brain function is no longer possible, treat ment priorities should shift to maximize perfusion and function of the donor organs. Through careful management of the donor patient, the recipient will receive organs that are less likely to undergo pri mary failure. This discussion will review the physio logical support necessary to sustain brain dead pa tients and to optimize donor organ function until organ removal is completed. It is assumed that indi vidual organs will be assessed and accepted or re jected for donation using criteria established by lo cal organ procurement teams. Such criteria will not be discussed here. The brain dead organ donor presents a variety of management challenges (Table 1) that may extend over many hours while members of transplant teams and organ recipients are assembled and tis sue testing is completed. The responsibility for care may remain with the admitting physician or critical care medicine specialists, or it may be transferred to the transplant service. Coordination, however, remains the key to a successful outcome. The avail ability and interest of a knowledgeable physician to supervise the donor patient's care continues to be crucial because a variety of problems, each capable of rendering donor organs useless, may develop in the hours between brain death and organ removal.

In order to elucidate the relationship between the lateral hypothalamus, involving the occipito-mesencephalic and quinto-frontal tracts, and body temperature, electric destruction was carried out in various areas of the lateral hypothalamus in 35 chickens. Lesions extending from the anterior commissure to about 480μm rostral to it brought about transient hyperthemia to birds. On the other hand, destructions of all the lateral hypothalamus reaching from about 1.000μm caudal to the anterior commissure to the infundibulum and of the occipito-mesencephalic tract alone induced poikilothermia immediately after operation, which manifested severer symptoms than the former birds. In addition to these facts, the responses of the operated birds to a quick rise and fall of environmental temperature suggest that the area causing poikilothermia may work as a thermal regulator, and that the territory causing transient hyperthermia may be concerned with heat loss only.

A series of five experiments was undertaken in order to characterize the pharmacological effects of alcohol on the body temperature of the unrestrained rat. After a thermistor probe was fixed within the colon of each animal and its body temperature had stabilized, physiological saline. 2.0 g/kg or 4.0 g/kg of ethyl alcohol was given by intragastric gavage. A constant concentration of 20% was utilized with doses determined volumetrically according to the individual weight of the animal. The following observations were made: (1) At a laboratory room temperature of 22 degrees C, alcohol produced a dose-dependent decline in colonic temperature. This fall was enhanced when the rat was placed in a chamber with an ambient temperature of 8 degrees C, but reversed into a hyperthermic response when the ambient temperature of the rat was elevated to 36 degrees C. (2) If the rat was exposed for one hour to either a warm (36 degrees C) or cold (8 degrees C) ambient temperature beginning at the time of the intragastric gavage with alcohol, the body temperature of the animal correspondingly decreased or increased, respectively. The magnitude of the shift in the animal's colonic temperature depended solely on the dose of alcohol given, i.e., thermolability was enhanced to a greater extent by the r.0 g/kg dose than the 2.0 g/kg dose. Exposure of the rat to a high or low ambient temperature prior to intragastric gavage with alcohol also affected the body temperature displacement as well as the direction of change. (3) Following the 4.0 g/kg alcohol dose, the animal's colonic temperature could be controlled precisely by varying the ambient temperatures in the 26 degrees C--32 degrees C range of thermoneutrality; in fact, within limits, the rat's temperature could be held constant at any predetermined level. (4) Pretreatment of the animal with 6.0 ml of a 50% solution of glucose given subcutaneously failed to attenuate the poikilothermic effect of intragastric alcohol administered in a dose of 4.0 g/kg. (5) Comparisons of the effect on body temperature of equipotent doses of sodium pentobarbital (25 mg/kg), administered intraperitoneally, and alcohol (4.0 g/kg) given by gavage showed that either a high or low ambient temperature elevated or lowered the colonic temperature of the rat at an identical rate and magnitude. It is concluded that alcohol acts acutely as any other anesthetic agent to abolish all thermoregulatory control functions. Thus, the physiological mechanisms for the dissipation of body heat as well as those for heat production are incapacitated by the drug. Clearly, alcohol is a poikilothermic agent, and thus, the decline in body temperature observed in the animal typically kept at a laboratory room temperature of 20 degrees C--24 degrees C represents the result of a cold challenge and is not due to a postulated "hypothermic" effect of alcohol.