ASSESSMENT OF POULTRY DEEP BODY TEMPERATURE RESPONSES TO AMBIENT TEMPERATURE AND RELATIVE HUMIDITY USING AN ON-LINE TELEMETRY SYSTEM

2000 ◽  
Vol 43 (3) ◽  
pp. 717-721 ◽  
Author(s):  
B. Lacey ◽  
T. K. Hamrita ◽  
M. P. Lacy ◽  
G. L. Van Wicklen
Rangifer ◽  
1986 ◽  
Vol 6 (2) ◽  
pp. 81 ◽  
Author(s):  
L. Christine Cuyler ◽  
Nils A. Øritsland

Deep body temperature was recorded in two female Svalbard reindeer during summer and winter. The reindeer were subjected to naturally occurring weather, photoperiod and stimuli in outdoor pens on Svalbard. A telemetry system was employed using transmitters ingested into the rumen. Mean deep body temperature was 0.3°C higher in winter and while the animals were lying down. This suggests a different strategy for thermoregulation than that employed by other reindeer subspecies.


1987 ◽  
Vol 63 (6) ◽  
pp. 2189-2194 ◽  
Author(s):  
M. J. Pollard ◽  
D. Megirian ◽  
J. H. Sherrey

We studied the effect of different levels of hypoxia (10, 12 or 13, 15, and 18% O2) on the sleep-waking pattern (SWP) and the maximum-minimum core temperature of warm-acclimated (WA) and cold-acclimated (CA) rats at their neutral temperature, 29 degrees C. Whereas the SWP of WA rats showed a trend toward increasing disruption as the degree of hypoxia increased, CA rats exhibited no such trend. The effect was chiefly on the frequency of state changes and less on epoch durations. The SWP of WA rats was more vulnerable to hypoxia than that of CA rats. Maximum and minimum body temperatures of WA and CA rats were not significantly affected by O2 lack down to 10% inspired O2. We conclude that in the rat 1) hypoxia primarily affects the neural mechanism that governs the frequency of changes in sleep-waking states; 2) the extent of alterations in SWP's depends on the ambient temperature to which the rats are acclimated; and 3) hypoxia does not significantly affect deep body temperature at the animal's neutral temperature.


2000 ◽  
Vol 9 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Britt Lacey ◽  
Takoi K. Hamrita ◽  
Michael P. Lacy ◽  
Garrett V. Van Wicklen ◽  
Mike Czarick

1977 ◽  
Vol 9 (4) ◽  
pp. 334-336 ◽  
Author(s):  
William C. Gordon ◽  
Kerry L. Coburn ◽  
Zita M. Wenzel

1983 ◽  
Vol 244 (5) ◽  
pp. R621-R628 ◽  
Author(s):  
M. Cabanac ◽  
J. Leblanc

Six male human subjects were placed in a situation of physiological conflict, fatigue vs. cold discomfort. Dressed in swim suits and shoes they walked at 3 km X h-1 on a treadmill placed in a climatic chamber. The slope of the treadmill was varied from 0 to 24% and the ambient temperature (Ta) from 25 to 5 degrees C. The subjects could choose Ta when slope was imposed or the converse. They rated pleasure and displeasure of Ta and exercise. Deep body temperature and heart rate were monitored. The results show that the subjects adjusted their behavior to maintain approximatively steady deep body temperature and to limit heart rate below 120 beats X min-1. The physiological compromise was thus correlated to the drive for maximal pleasure-minimal displeasure in the two sensory dimensions fatigue and discomfort.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Kazuyuki Miyamoto ◽  
Keisuke Suzuki ◽  
Hirokazu Ohtaki ◽  
Motoyasu Nakamura ◽  
Hiroki Yamaga ◽  
...  

Abstract Background Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure. Methods Mildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS. Results The survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage. Conclusions We developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.


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