Evaluation and improvement of the thermoregulatory system for the two-node bioheat model

2021 ◽  
pp. 111235
Author(s):  
L. Ji ◽  
A. Laouadi ◽  
C. Shu ◽  
L. Wang ◽  
M.A. Lacasse
1979 ◽  
Vol 237 (1) ◽  
pp. R80-R88 ◽  
Author(s):  
S. Sakaguchi ◽  
S. F. Glotzbach ◽  
H. C. Heller

Unanesthetized, unrestrained kangaroo rats (Dipodomys) were studied to examine the changes in the frequency and duration of sleep states caused by long-term manipulations of hypothalamic temperature (Thy) at a thermoneutral (30 degrees C) and a low (20 degrees C) ambient temperature (Ta). A cold stimulus present in either the hypothalamus or the skin decreased both the total sleep time (TST) and the ratio of paradoxical sleep (PS) to TST. At a low Ta, TST, but not the PS-to-TST ratio, was increased by raising Thy, indicating that a cold peripheral stimulus could differentially inhibit PS. At a thermoneutral Ta, cooling Thy decreased both TST and the PS/TST. Changes in the amount of PS were due largely to changes in the frequency, but not the duration, of individual episodes of PS, suggesting that the transition to PS is partially dependent on the thermoregulatory conditions existing during slow-wave sleep (SWS). These results are consistent with the recent findings that the thermoregulatory system is functional during SWS but is inhibited or inactivated during PS.


1988 ◽  
pp. 145-158 ◽  
Author(s):  
H. Craig Heller ◽  
Steven Glotzbach ◽  
Dennis Grahn ◽  
Carolyn Radeke

2007 ◽  
Vol 292 (1) ◽  
pp. R37-R46 ◽  
Author(s):  
Andrej A. Romanovsky

While summarizing the current understanding of how body temperature (Tb) is regulated, this review discusses the recent progress in the following areas: central and peripheral thermosensitivity and temperature-activated transient receptor potential (TRP) channels; afferent neuronal pathways from peripheral thermosensors; and efferent thermoeffector pathways. It is proposed that activation of temperature-sensitive TRP channels is a mechanism of peripheral thermosensitivity. Special attention is paid to the functional architecture of the thermoregulatory system. The notion that deep Tb is regulated by a unified system with a single controller is rejected. It is proposed that Tb is regulated by independent thermoeffector loops, each having its own afferent and efferent branches. The activity of each thermoeffector is triggered by a unique combination of shell and core Tbs. Temperature-dependent phase transitions in thermosensory neurons cause sequential activation of all neurons of the corresponding thermoeffector loop and eventually a thermoeffector response. No computation of an integrated Tb or its comparison with an obvious or hidden set point of a unified system is necessary. Coordination between thermoeffectors is achieved through their common controlled variable, Tb. The described model incorporates Kobayashi’s views, but Kobayashi’s proposal to eliminate the term sensor is rejected. A case against the term set point is also made. Because this term is historically associated with a unified control system, it is more misleading than informative. The term balance point is proposed to designate the regulated level of Tb and to attract attention to the multiple feedback, feedforward, and open-loop components that contribute to thermal balance.


Author(s):  
Radostina A. Angelova

The thermophysiological comfort is one of the aspects of the human comfort. It is related to the thermoregulatory system of the body and its reactions to the temperature of the surrounding air, activity and clothing. The aim of the chapter is to present the state of the art in the wearable technologies for helping the human thermophysiological comfort. The basic processes of body's thermoregulatory system, the role of the hypothalamus, the reactions of the body in hot and cold environment, together with the related injuries, are described. In the second part of the chapter smart and intelligent clothing, textiles and accessories are presented together with wearable devices for body's heating/cooling.


Obesity ◽  
2019 ◽  
Vol 27 (6) ◽  
pp. 963-970
Author(s):  
Borja Martinez‐Tellez ◽  
Mireia Adelantado‐Renau ◽  
Francisco M. Acosta ◽  
Guillermo Sanchez‐Delgado ◽  
Antonio Martinez‐Nicolas ◽  
...  

1983 ◽  
Vol 245 (3) ◽  
pp. R379-R385
Author(s):  
A. V. Ferguson ◽  
L. Bauce ◽  
W. L. Veale ◽  
K. E. Cooper

The febrile response of the New Zealand White rabbit in animals less than 1 yr old was compared with that in 3-yr-old animals. A reduced febrile response to both endotoxin and live bacteria injected intravenously was observed in the older group of animals. Peripheral vasoconstriction was observed, suggesting the drive to increase body temperature remained. Plasma catecholamines increased significantly in both groups of animals during fever. However, significantly greater increases in plasma epinephrine were observed in the older animals. A significant deficit in catecholamine-induced thermogenesis was observed in the older group of rabbits. This deficit alone does not explain the reduced febrile response, as beta-adrenergic blockade does not suppress the febrile response of young animals. Thus it is suggested that the primary deficit resulting in a reduced febrile response in the 3-yr-old rabbits is due to other age-related changes in the thermoregulatory system.


1982 ◽  
Vol 52 (2) ◽  
pp. 410-415 ◽  
Author(s):  
F. Furuyama

The survival times of unanesthetized rats in 42.5 degree C. 48% rh were studied in 12 different strains. In males, Sprague-Dawley rats (P less than 0.01) and Fisher 344/MK (P less than 0.05) showed significantly higher heat tolerance than the other 9 strains. Among Sprague-Dawley rats, females tolerated heat longer than males (P less than 0.05). There was no difference in lethal body temperature according to strains and exposure temperatures (38.5–48.5 degree C). Maximum survivable body temperature was 43.1 degree C in males and 43.3 degree C in females. The body weight loss in heat was greater in Sprague-Dawley, Fisher 344/MK, and JCL:Wistar strains. The degree of saliva spreading during the equilibrium period just below the maximum survivable body temperature correlated significantly with heat tolerance and was found to be the index of strain difference in heat tolerance. These findings demonstrated that the thermoregulatory system of rats is controlled genetically, though survival times of individuals in different strains sometimes overlap.


1977 ◽  
Vol 42 (1) ◽  
pp. 74-79 ◽  
Author(s):  
C. A. Fuller ◽  
J. M. Horowitz ◽  
B. A. Horwitz

Upon exposure of rats to 2 G environments (achieved by centrifugation), there occurred a rapid decrease in colonic temperature (Tco) followed, after about 50 min, by a slow recovery toward precentrifugation levels. The initial drop in Tco was accompanied by decreases in hypothalamic and spinal cord temperatures and increases in tail temperature (Tta). In contrast to this anomalous response (i.e., increased heat loss (manifested by increased Tta) despite decreasing temperature at spinal and hypothalamic thermoreceptor areas) the return toward normal Tco appeared to involve appropriate thermoregulatory responses. The initial fall in Tco was decreased in magnitude by inverting the rat during acceleration, thereby suggesting that mechanical forces acting on the brain may underlie this temperature decrease. Exposure to cold during centrifugation allowed further examination of the thermoregulatory system. Unlike the initial acceleration-induced changes, the cold-evoked fall in Tco was not accompanied by increasing Tta and was modified by the environmental conditioning of the rats. These results are consistent with the view that exposure to 2 G adversely affects the thermoregulatory ability of rats challenged by cold.


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