Der Mechanismus der Wärmeregulation

Thauer, Rudolf K.

doi:10.1007/bf02322414

Cited by 130 publications

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“…The mice that died usually failed to eat; this was probably not a primary cause of death, but a consequence of an already existing morbid state. A sudden decline in the temperature of the skin causes sympathetic stimulation [Thauer, 1939]. Ordinarily this probably leads to an increase in heat production [Hsieh and Carlson, 1957], presumably through shivering or at least increased muscular metabolism [Hart, 1958].…”

Section: Discussionmentioning

confidence: 99%

Mortality, Growth and Liver Glycogen in Young Mice Exposed to Cold

1960

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Mice of four strains were reared at 21°C. and then transferred to ‐3°C., in individual cages with nesting material. Controls were kept in similar conditions at 21°C. Many of the mice of two A strains died when stressed by cold at the age of 3 weeks, but none at 5 or 12 weeks. Many C57BL and GFF mice died when stressed at 5 weeks. Death usually occurred during the first 3 days, often on the first day. All stressed mice lost weight, especially in the first 2 days; if they survived, they made up the lost weight but they grew more slowly than the controls at all stages. Mice reared at ‐3°C. and stressed in that temperature when 3 weeks old had a lower mortality than those transferred from 21°C., and survivors did not lose weight. Mice reared at ‐3°C. and transferred to 21°C. at 3 weeks, although initially lighter, grew quickly and after 1 week were as heavy as the controls. Three‐week‐old mice stressed at ‐3°C. lost liver glycogen quickly whether they had been reared at 21°C. or ‐3°C. This was not due to a failure to eat, and there was no evidence that death resulted from inability to mobilize carbohydrate reserves.

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Section: Discussionmentioning

confidence: 99%

Mortality, Growth and Liver Glycogen in Young Mice Exposed to Cold

1960

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History of the National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury

Guttmann¹

1967

Spinal Cord

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It has never been unequivocally established whether or not the spinal cord, chronically isolated from the brain above the thoracic sympathetic outflow, plays any part in temperature regulation. Animals, kept in rooms at an air temperature of 800 F (26.50 C), after chronic traumatic lesions of the spinal cord, behave essentially as poikilotherms (Pfluiger, 1878;Pembrey, 1897; Freund & Strassmann, 1912;Sherrington, 1924), but if they are kept at 60-700 F (15.6-21.1l C) they appear to regain some measure of temperature regulation against cold (Thauer, 1939;Clark, 1940). Studies on man are equivocal. Some authors claim that patients with acute traumatic lesions in the lower cervical segments are, initially, hyperthermic but later regain an ability to sweat (Foerster, 1936). Others state that they are hypothermic (Holmes, 1915).The experimental studies reported in this paper were made on human male patients, who, with one exception, had complete lesions due to injuries at various levels in the spinal cord, in order to study further the nature of the thermo-regulatory processes in spinal man. The subjects comprised one normal man, four patients with lesions at segmental levels between C6 and T1, one with a lesion below T 4 and one with a lesion below T 8. In all patients many months had elapsed since their injuries to the spinal cord. These subjects were exposed at rest and naked for 1-2 hr at air temperatures of 18-20, 28 and 35370 C. These temperatures and the design of the experiments were chosen to effect a comparison with the data of Hardy & du Bois (1938, 1941) and so to bring out any alteration in the thermoregulatory processes due to the cord lesions. METHODSThe patients were all in good physical condition. None had bedsores nor urinary infection of any consequence. The cervical lesion patients and theT4 patientwere bed-ridden and subject,therefore. to a smaller range of fluctuation in environmental temperatures than the other men. The wards THERMOREGULATION IN SPINAL MAN 407 of this hospital were neither centrally heated nor air-conditioned, and hence the microclimate of these patients probably shows a considerable variation between winter and summer. Their physical characteristics are given in Table 1.The same experimental procedure was adopted in each study. The subjects were stripped and rested nude for 1 hr on hospital beds at an environmental temperature of 270 C. Thereafter they were transferred either to an environmental temperature of 18-20 or 35-37O C for 1i-2 hr. The cold temperature conditions were obtained in a room open to the outside air, but shielded from direct and most reflected radiation from the sun on the colder days of the summers of 1954 and 1956. Air in the room was circulated slowly by means of a small electric fan to avoid gradients.The study at 35-37°C was made in a specially constructed 'hot box' (Guttmann, 1947). The heat source was a series of infra-red electric heaters in the roof of the box, but the patient was shielded from direct radiation. The air heated in this way was circ...

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Interaction of Body Temperatures in Control of Thermoregulatory Effector Mechanisms

Jessen

1996

Comprehensive Physiology

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Der Mechanismus der Wärmeregulation

Cited by 130 publications

References 425 publications

Mortality, Growth and Liver Glycogen in Young Mice Exposed to Cold

Mortality, Growth and Liver Glycogen in Young Mice Exposed to Cold

History of the National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury

Interaction of Body Temperatures in Control of Thermoregulatory Effector Mechanisms

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