Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

2007 ◽  
Vol 292 (1) ◽  
pp. R186-R194 ◽  
Author(s):  
Chin Leong Lim ◽  
Gary Wilson ◽  
Lindsay Brown ◽  
Jeff S. Coombes ◽  
Laurel T. Mackinnon
Keyword(s):  
Heat Stress ◽  
Heat Tolerance ◽  
Tissue Damage ◽  
Wistar Rats ◽  
Heat Stroke ◽  
Heat Exposure ◽  
The Core ◽  
Male Wistar Rats ◽  
Inflammatory State ◽  
Severe Heat Stress

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (Tc) was 42°C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment ( baseline I), after 2 h of passive rest ( baseline II), at Tc 40°C (T40), and 15 min after achieving Tc 42°C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats ( P < 0.05). The duration of survival at T42°C was shortest in the TD+HE rats (9.9 ± 6.2 min) ( P < 0.01), followed by the T+HE (11.3 ± 6.1 min) and the HE (12.2 ± 4 min) ( P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats ( P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.

scholarly journals Effect of Heat Stress on Behavior, Physiological and Blood Parameters of Goat

2013 ◽  
Vol 22 (1-2) ◽  
pp. 37-45 ◽  
Author(s):  
MM Alam ◽  
MA Hashem ◽  
MM Rahman ◽  
MM Hossain ◽  
MR Haque ◽  
...  
Keyword(s):  
Heat Stress ◽  
Heat Exposure ◽  
Blood Parameters ◽  
Experimental Animals ◽  
Treatment Groups ◽  
Exposure Temperature ◽  
Heat Treated ◽  
Significant Difference ◽  
Humidity Index ◽  
Severe Heat Stress

The research was conducted to study the effect of heat stress on behavior, some physiological and blood parameters with nine goats of almost similar in age, sex and weight into three groups. Three groups were divided as zero hour (T0), four hours (T4) and eight hours (T8) heat exposure. Temperature–humidity index (THI) value was calculated as 28.17 which indicate the experimental animals were in extreme severe heat stress. Skin and rectal temperature had no significant differences among the treatment groups but respiration/panting and pulse rate were increased with the increased of heat stress from T0 to T8 group (P<0.01).  Significant difference was found in standing time and lying time (P<0.01) in experimental groups. There were significant changes (P<0.01) in number of urination and defecation per hour but no significant changes was found in duration per urination in heat treated groups. The amount of RBC, PCV%, Hb%, WBC were increased with the increased of heat stress (P<0.01). Neutrophil, eosinophil, lymphocyte and monocyte numbers increased significantly (P<0.01) in heat treated groups.  It can be concluded that heat stress had significant changes on some behavioral, physiological and blood parameters of goat.DOI: http://dx.doi.org/10.3329/pa.v22i1-2.16465 Progress. Agric. 22(1 & 2): 37 - 45, 2011  

A Single Heat Exposure Improves Heat Tolerance in a Mouse Exertional Heat Stroke Model

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Jermaine Allen Ward ◽  
Shauna Dineen ◽  
Mark Plamper ◽  
Thomas Mayer ◽  
Lisa Leon
Keyword(s):  
Heat Tolerance ◽  
Heat Stroke ◽  
Heat Exposure ◽  
Stroke Model ◽  
Exertional Heat Stroke

Chronic low-sodium diet in rats: responses to severe heat exposure

1985 ◽  
Vol 58 (1) ◽  
pp. 152-156 ◽  
Author(s):  
R. P. Francesconi ◽  
R. W. Hubbard
Keyword(s):  
Heat Stress ◽  
Thermal Sensitivity ◽  
Heat Exposure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Male Rats ◽  
Control Group ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Severe Heat Stress

To determine the effects of sodium (Na+) deficiency on the responses to severe heat stress (35.5 degrees C), immature (mean wt 150.4 g) male rats (n = 21) were fed a low-Na+ diet for 71 days. Rates of weight gain and food consumption were significantly (P less than 0.001) reduced in the low-Na+ group, whereas water consumption was unaffected. Prior to heat exposure circulating Na+ levels were unaffected by dietary Na+ restriction, but both circulating potassium (K+) and hematocrit levels were significantly (P less than 0.001) increased. After 24-h exposure to severe heat stress, circulating Na+ levels did manifest a significant (P less than 0.001) decrement in the low-Na+ group. K+ levels increased significantly (P less than 0.01) in the control group after 6 h of heat exposure but remained depressed in comparison with the low-Na+ group after 48 and 72 h. Although plasma renin activity (PRA) was not increased by chronic consumption of the low-Na+ diet or by severe heat exposure in the control group, severe heat stress in the low-Na+ group did elicit significant (P less than 0.005) increments in PRA after 24 h of exposure. Alternatively, plasma aldosterone levels were significantly (P less than 0.001) elevated by both the low-Na+ diet and heat stress. We concluded from these studies that chronic consumption of the low-Na+ diet had severe effects on hematologic, endocrinological, and thermoregulatory variables as well as thermal sensitivity to prolonged and sedentary exposure to severe heat stress.

scholarly journals Heat Stress Impacts on Cardiac Mortality in Nepali Migrant Workers in Qatar

Cardiology ◽  
2019 ◽  
Vol 143 (1-2) ◽  
pp. 37-48 ◽  
Author(s):  
Bandana Pradhan ◽  
Tord Kjellstrom ◽  
Dan Atar ◽  
Puspa Sharma ◽  
Birendra Kayastha ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Heat Stress ◽  
Migrant Workers ◽  
Heat Stroke ◽  
Heat Exposure ◽  
Health And Safety ◽  
Mortality Data ◽  
Excessive Heat ◽  
Heat Effects ◽  
Cvd Mortality

Background: Qatar is a major destination country for Nepali migrant workers (NMWs; main age range 25–35 years) in the construction trade. These 120,000+ NMWs are exposed to various occupational hazards, including excessive heat, and 3–4 workers die each week. Our study aimed to show whether heat exposure caused deaths. Methods: The worker population and mortality data of NMWs were retrieved from government institutions in Nepal. Heat exposure was assessed by monthly estimates of daily wet bulb globe temperature (WBGT), for in-shade conditions, from data collected at the Doha weather station from 2009 to 2017. Working in the sun during the middle of the day would add 2–3°C to the in-shade WBGT values. Daily deaths and their causes were obtained from the records of the Foreign Employment Promotion Board (FEPB) in Nepal, 2009–2017. Interviews with returning NMWs about their working conditions and the impacts of these conditions added information. The association between the heat variable and mortality was tested with standard statistical methods. Results: The average annual death rate for NMWs in Qatar was 150 deaths/100,000. According to interviews, the majority of NMWs were found working in high WBGT (>31°C) each working day during hot months. The major cause of these deaths was recorded as cardiovascular problems (cardiovascular disease; CVD). Unfortunately, the causes of death were poorly described, and many deaths were listed as “cardiac arrest.” We included these deaths in the broader category of “cardiovascular causes.” There was a strong correlation between average monthly afternoon heat levels (WBGT) and CVD mortality. It is likely that a large proportion of these CVD deaths during hot months were due to serious heat stroke. Global studies show that approximately 15% of deaths in the age group 25–35 years are due to CVD causes. However, in this NMW population, the figures were 22% during the cool season and 58% during the hot season. Conclusions: The increased CVD mortality during hot periods is most likely due to severe heat stress. As many as 200 of the 571 CVD deaths during 2009–2017 could have been prevented if effective heat protection had been implemented as a part of local occupational health and safety programs. There is an urgent need for protection against such heat effects among NMWs, and rising temperatures from ongoing climate change are further increasing the health risks. Cause of death records for workers dying in hot conditions should be more precise than “cardiac arrest.”

scholarly journals Effect of cold and heat stress on rat adrenal, serum and liver ascorbic acid concentration

2006 ◽  
Vol 58 (3) ◽  
pp. 161-164 ◽  
Author(s):  
Jelena Djordjevic ◽  
S. Djurasevic ◽  
Tamara Vuckovic ◽  
N. Jasnic ◽  
Gordana Cvijic
Keyword(s):  
Ascorbic Acid ◽  
Heat Stress ◽  
Cold Stress ◽  
Acid Concentration ◽  
Wistar Rats ◽  
Room Temperature ◽  
Heat Exposure ◽  
Ascorbic Acid Concentration

Changes in ascorbic acid (AA) concentration were examined in the adrenals, serum and liver of Wistar rats exposed to cold (6 ?C) and heat stress (38 ?C) for 60 min. The exposure of animals to cold stress for 60 min did not change concentration of AA in the serum, adrenals and liver as compared to controls maintained at room temperature. After a 60 min heat exposure the concentration of AA in the adrenals decreased (***p<0.001), in the liver remained unchanged whereas it significantly increased in the serum (***p<0.001) in respect to control values. .

Changes in body temperature of rats acclimated to heat with different acclimation schedules

1989 ◽  
Vol 67 (5) ◽  
pp. 2154-2157 ◽  
Author(s):  
O. Shido ◽  
Y. Yoneda ◽  
T. Nagasaka
Keyword(s):  
Wistar Rats ◽  
Heat Exposure ◽  
Heat Acclimation ◽  
Dark Phase ◽  
Light Phase ◽  
Dark Cycle ◽  
Hypothalamic Temperature ◽  
Male Wistar Rats ◽  
The Mean ◽  
Low Levels

Male Wistar rats, initially maintained at an ambient temperature (Ta) of 23.8 degrees C, were subjected to one of seven different heat acclimation schedules under a 12:12-h light-dark cycle (lights on at 0600 h). Two groups of rats were exposed to Ta of 32.4 degrees C all day for 5 (HC5) or 10 (HC10) days. The other four groups were exposed to Ta of 32.8 degrees C for 5 h/day during the last half of the dark phase for 5 (NI5) or 10 (NI10) consecutive days or during the last half of the light phase for 5 (DI5) or 10 (DI10) consecutive days. Control rats (C) were kept at 23.8 degrees C throughout the experiment. Hypothalamic temperature (Thy) was measured every 5 min with a chronically implanted thermocouple from 1 day before the beginning to 2 days after the end of the heat acclimation periods. During the heat acclimation periods, daily mean Thy rose significantly in HC5 and HC10 rats but decreased significantly in NI5 and NI10 rats. Daily mean Thy did not change in C, DI5, and DI10 rats. Thy in HC10 rats sharply decreased at the end of the heat acclimation periods and remained at low levels for approximately 3 h. On the 2nd postacclimation day, however, mean Thy returned and remained at a significantly higher level. In NI10 rats, the mean Thy in the postacclimation period was significantly lower than the preacclimation values. No such changes in mean Thy were observed in DI10 rats. Five-days of heat exposure had little effect on the postacclimation Thy.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals NLRP3 ablation enhances tolerance in heat stroke pathology by inhibiting IL-1β-mediated neuroinflammation

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Zi-Teng Zhang ◽  
Xiao-Lei Gu ◽  
Xin Zhao ◽  
Xian He ◽  
Hao-Wei Shi ◽  
...  
Keyword(s):  
Heat Tolerance ◽  
Knockout Mice ◽  
Nlrp3 Inflammasome ◽  
Heat Stroke ◽  
Heat Exposure ◽  
Neutralizing Antibody ◽  
Underlying Mechanism ◽  
Stroke Severity ◽  
Inflammasome Activation ◽  
Prior Infection

Abstract Background Patients with prior illness are more vulnerable to heat stroke-induced injury, but the underlying mechanism is unknown. Recent studies suggested that NLRP3 inflammasome played an important role in the pathophysiology of heat stroke. Methods In this study, we used a classic animal heat stroke model. Prior infection was mimicked by using lipopolysaccharide (LPS) or lipoteichoic acid (LTA) injection before heat stroke (LPS/LTA 1 mg/kg). Mice survival analysis curve and core temperature (TC) elevation curve were produced. NLRP3 inflammasome activation was measured by using real-time PCR and Western blot. Mice hypothalamus was dissected and neuroinflammation level was measured. To further demonstrate the role of NLRP3 inflammasome, Nlrp3 knockout mice were used. In addition, IL-1β neutralizing antibody was injected to test potential therapeutic effect on heat stroke. Results Prior infection simulated by LPS/LTA injection resulted in latent inflammation status presented by high levels of cytokines in peripheral serum. However, LPS/LTA failed to cause any change in animal survival rate or body temperature. In the absence of LPS/LTA, heat treatment induced heat stroke and animal death without significant systemic or neuroinflammation. Despite a decreased level of IL-1β in hypothalamus, Nlrp3 knockout mice demonstrated no survival advantage under mere heat exposure. In animals with prior infection, their heat tolerance was severely impaired and NLRP3 inflammasome induced neuroinflammation was detected. The use of Nlrp3 knockout mice enhanced heat tolerance and alleviated heat stroke-induced death by reducing mice hypothalamus IL-1β production with prior infection condition. Furthermore, IL-1β neutralizing antibody injection significantly extended endotoxemic mice survival under heat stroke. Conclusions Based on the above results, NLRP3/IL-1β induced neuroinflammation might be an important mechanistic factor in heat stroke pathology, especially with prior infection. IL-1β may serve as a biomarker for heat stroke severity and potential therapeutic method.

scholarly journals Gene and Metabolite Integration Analysis through Transcriptome and Metabolome Brings New Insight into Heat Stress Tolerance in Potato (Solanum tuberosum L.)

Plants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 103
Author(s):  
Bailin Liu ◽  
Lingshuang Kong ◽  
Yu Zhang ◽  
Yuncheng Liao
Keyword(s):  
Heat Stress ◽  
Heat Tolerance ◽  
Elevated Temperatures ◽  
Solanum Tuberosum L ◽  
Heat Exposure ◽  
Differentially Expressed ◽  
Heat Response ◽  
Negative Ionization ◽  
Stress Related Genes ◽  
Prolonged Heat

Potatoes are particularly vulnerable to elevated temperatures, with short heat stress (6 h) inducing stomatal opening and reducing membrane stability and prolonged heat stress (3-day) decreasing the photosynthetic capacity of potato leaves. The integration of transcriptomics and metabolomics methods demonstrated that 448 heat upregulated and 918 heat downregulated genes and 325 and 219 compounds in the positive and negative ionization modes, respectively, were up- or downregulated in leaves in response to short and prolonged heat stress. Differentially expressed genes enriched in photosynthesis, cell wall degradation, heat response, RNA processing, and protein degradation were highly induced during heat exposure, and differentially expressed metabolites involved in amino acid biosynthesis and secondary metabolism were mostly induced during heat exposure, suggesting a possible role of these genes and metabolites in the heat tolerance of the potato. Metabolite and transcript abundances for the upregulation of flavone and flavonol biosynthesis under prolonged heat stress were closely correlated. Heat-induced gene expression in Arabidopsisthaliana shoots and potato leaves overlapped, and heat stress-responsive genes overlapped with drought stress-related genes in potato. The transient expression of four heat-induced genes in Nicotiana benthamiana exhibited increased heat tolerance. This study provides a new transcriptome and metabolic profile of the potato’s response to heat.

scholarly journals Impact of different temperature stimuli on the expression of myosin heavy chain isoforms during recovery from bupivacaine-induced muscle injury in rats

2019 ◽  
Vol 127 (1) ◽  
pp. 178-189
Author(s):  
Tsubasa Shibaguchi ◽  
Mizuki Hoshi ◽  
Toshinori Yoshihara ◽  
Hisashi Naito ◽  
Katsumasa Goto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Stress ◽  
Myosin Heavy Chain ◽  
Muscle Mass ◽  
Heavy Chain ◽  
Muscle Injury ◽  
Heat Exposure ◽  
Control Level ◽  
Male Wistar Rats ◽  
The Impact

Limited information exists regarding the impact of different temperature stimuli on myosin heavy chain (MyHC) expression in skeletal muscle during recovery from injury. Therefore, this experiment investigated the impact of both cold and heat exposure on the MyHC isoform profile in the rat soleus during recovery from injury. Male Wistar rats were randomly divided into control, bupivacaine-injected (BPVC), BPVC with icing, and BPVC with heat stress groups. Muscle injury was induced by intramuscular injection of bupivacaine into soleus muscles of male Wistar rats. Icing treatment (0°C for 20 min) was performed immediately after the injury. Intermittent heat stress (42°C for 30 min on alternating days) was carried out during 2–14 days after bupivacaine injection. In response to injury, a transient increase in developmental, IId/x, and IIb MyHC isoforms, as well as various types of hybrid fibers, followed by the recovery of the MyHC profile toward the control level, was noted in the regeneration of the soleus. The restoration of the MyHC profile in the regenerating muscle at whole-muscle and individual myofiber levels was partially delayed by icing but facilitated by heat stress. In addition, the application of repeated heat stress promoted the recovery of soleus muscle mass toward the control level following injury. We conclude that compared with acute and immediate cold (icing) treatment, chronic and repeated heat stress may be a more appropriate treatment for the enhancement of both normalization of the MyHC profile and restoration of muscle mass following injury. NEW & NOTEWORTHY Cold exposure (icing), but not heat exposure, has been well accepted as a first-aid treatment for accidental and/or sports-related injuries. However, recent evidence suggests the negative impact of icing treatment on skeletal muscle regeneration following injury. Here, we demonstrated that acute/immediate icing treatment delayed the restoration of the myosin heavy chain (MyHC) profile, but intermittent hyperthermia, repeated for several days, facilitated the recovery of both muscle mass and the MyHC profile in the regeneration of skeletal muscle following injury.

Sign in / Sign up

Export Citation Format

Share Document