Colonic heating patterns and the variation of thermal resistance among rats

Wright, Gary L.; Knecht, Edwin A.; Wasserman, David H.

doi:10.1152/jappl.1977.43.1.59

Cited by 26 publications

(21 citation statements)

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“…Wide CTM values are reported for monkeys ($44.5 1C; Gathiram et al, 1987), dogs (37.7-41.1 1C; Drobatz and Macintire, 1996), sheep (43.7-44.0 1C; Hales et al, 1987), rats (40.4-45.4 1C;DuBose et al, 1983;Hubbard et al, 1976;Lord et al, 1984;Ohara et al, 1975;Wright et al, 1977), mice (42.7 1C and $44-45 1C; Leon et al, 2005;Wright, 1976), and salamanders ($33 1C; Hutchison and Murphy, 1985). Adolph (1947) determined the CTM in cats ($43.5 1C), dogs (41.7 1C), and rats (42.5 1C) and proposed differences in tissue susceptibility as responsible for CTM variability between species, although tissue injury was not measured in this study.…”

Section: The Hyperthermic Response To Heat Exposurementioning

confidence: 98%

“…Animal experimentation has typically relied on passive, rather than exertional heat exposure to study the role of cytokines (Adolph, 1947;Gathiram et al, 1987;Hall et al, 2001;Hubbard et al, 1976Hubbard et al, , 1977Lord et al, 1984;Romanovsky and Blatteis, 1996;Wilkinson et al, 1988;Wright, 1976;Wright et al, 1977). Elevated circulating concentrations of IL-1, IL-6, IL-8, IL-10, TNF and granulocyte colony stimulating factor have been observed following localized or whole body hyperthermia in primates (Bouchama et al, 2005), rabbits (Lin et al, 1994), mice (Neville and Sauder, 1988;Leon et al, in press) and rats (Chiu et al, 1995(Chiu et al, , 1996Haveman et al, 1996;Lin et al, 1997;Liu et al, 2000).…”

Section: Cytokines and Heat Strokementioning

confidence: 99%

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The thermoregulatory consequences of heat stroke: Are cytokines involved?

Leon

2006

Journal of Thermal Biology

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Section: The Hyperthermic Response To Heat Exposurementioning

confidence: 98%

Section: Cytokines and Heat Strokementioning

confidence: 99%

The thermoregulatory consequences of heat stroke: Are cytokines involved?

Leon

2006

Journal of Thermal Biology

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“…Three Tc patterns (Type I, uncompensable; Type II, compensable; Type III, triphasic) during heat exposure have been studied and identified [5]. Since investigations utilize different experimental designs each with its own methodological confounders, which can influence thermoregulatory responses and adaptations [3], a standardized heating procedure is warranted.…”

Section: Discussionmentioning

confidence: 99%

“…Three main types of Tc patterns have been identified: Type I (uncompensable), linear rise and sustained Tc; Type II (compensable), rapid rise then slower increase in Tc; Type III (triphasic), initial increase in Tc, followed by a plateau then a final increase in Tc [5]. Firm conclusions regarding the etiology of these temperature differences are difficult to draw since each investigation varies in their experimental design and have methodological confounders (e.g., chamber heating rates) that influences thermoregulatory profiles generated throughout heat stress [3].…”

mentioning

confidence: 99%

“…Specifically, the protocol involves 120 min of heat exposure, with the entire trial lasting approximately 180 min (including warm-up and cool-down); during the first 60 min, the environmental chamber is heating and reaches its preset temperature of 39.5˚C ± 0.2˚C [4]. According to the manufacturer of the Thermo Scientific Forma Environmental Chamber, Model 3961 [5], the heat chamber utilizes a directed airflow design that includes a positive pressure feed plenum and a negative pressure return plenum. This airflow mechanism, which is better suited than a top-to-bottom undirected airflow design, directs air across the surface of each solid shelf, with each shelf receiving a consistent flow of conditioned air for temperature uniformity and recovery [7].…”

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confidence: 99%

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Mice Heat Chamber Calibration

Poh¹,

Carus²,

Chen³

et al. 2014

JASMI

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Background: Firm conclusions regarding the etiology of heat exposure responses among animals are difficult to draw due to different experimental designs and methodological confounders, such as environmental chamber set-up and heating rates. The purpose of this investigation was to 1) validate the heat test protocol for mice models via cage location and orientation; and to 2) determine the maximum number of cages that can be used without compromising individual heating rates. Methods: A mice temperature transponder (G2 E-Mitter, Mini Meter, Respironics) was centrally positioned inside each mice cage set in the environmental chamber (Thermo Scientific Forma, Model 3961). Two cage orientations (adjacent, left-to-right and parallel, front-to-back) with 3 set-ups (top shelf, bottom shelf and both shelves) using 2 and 4 cages were examined in triplicate and averaged. Transponders equilibrated at 21.5˚C for 5 min, then exposed to 39.5˚C for a minimum of 60 min. Results: A major finding was that adjacent (L-R) top shelf set-up had the smallest temperature difference throughout the heat test (Δ = 0.43˚C vs. Δ = 2.2˚C) and at minute 60 (Δ = 0.2˚C vs. Δ = 1.8˚C). Both orientations for the bottom shelf set-up had a slower rise in temperature (0.04˚C·min −1 ) than other set-ups (0.3˚C·min −1 ). Using both shelves, top shelf cages were consistently warmer than bottom shelf cages (1.0˚C -3.6˚C) for both orientations. Conclusions: We strongly suggest using an adjacent (L-R) top shelf set-up since it enabled uniform chamber heating rates and standardized heat exposure. Bottom shelf is not recommended for use due to poor heating rate performance. Since an increased number of cages may obstruct heat flow patterns, a one shelf set-up with 2 cages should be used.

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Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

319

350

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Heat stroke is a life-threatening condition clinically diagnosed as a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic heat stroke primarily occurs in immunocompromised individuals during annual heat waves. Exertional heat stroke is observed in young fit individuals performing strenuous physical activity in hot or temperature environments. Long-term consequences of heat stroke are thought to be due to a systemic inflammatory response syndrome. This article provides a comprehensive review of recent advances in the identification of risk factors that predispose to heat stroke, the role of endotoxin and cytokines in mediation of multi-organ damage, the incidence of hypothermia and fever during heat stroke recovery, clinical biomarkers of organ damage severity, and protective cooling strategies. Risk factors include environmental factors, medications, drug use, compromised health status, and genetic conditions. The role of endotoxin and cytokines is discussed in the framework of research conducted over 30 years ago that requires reassessment to more clearly identify the role of these factors in the systemic inflammatory response syndrome. We challenge the notion that hypothalamic damage is responsible for thermoregulatory disturbances during heat stroke recovery and highlight recent advances in our understanding of the regulated nature of these responses. The need for more sensitive clinical biomarkers of organ damage is examined. Conventional and emerging cooling methods are discussed with reference to protection against peripheral organ damage and selective brain cooling.

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Colonic heating patterns and the variation of thermal resistance among rats

Cited by 26 publications

References 0 publications

The thermoregulatory consequences of heat stroke: Are cytokines involved?

The thermoregulatory consequences of heat stroke: Are cytokines involved?

Mice Heat Chamber Calibration

Heat Stroke

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