Effects of estrogen on thermoregulatory evaporation in rats exposed to heat

1994 ◽  
Vol 267 (3) ◽  
pp. R673-R677 ◽  
Author(s):  
M. A. Baker ◽  
D. D. Dawson ◽  
C. E. Peters ◽  
A. M. Walker
Keyword(s):  
Heat Exposure ◽  
Plasma Osmolality ◽  
Ovariectomized Rats ◽  
Body Core Temperature ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Evaporative Water ◽  
Sprague Dawley Rats ◽  
Body Core ◽  
Opposite Order

The purpose of this study was to determine the effects of estrogen (E2) replacement on thermoregulation in ovariectomized rats exposed to heat. Female Sprague-Dawley rats were ovariectomized and splenectomized and implanted with a temperature-sensitive transmitter. Each rat was studied when E2 treated (after an E2 pellet implant) and untreated. Animals were divided into two groups with opposite order of treatment and were studied over a 9-wk period. Measurements of body core temperature (Tc) and evaporative water loss (EWL) were made on unrestrained animals resting at 38 degrees C air temperature. E2-treated animals increased EWL at all levels of Tc, reduced the threshold Tc for onset of saliva spreading, and regulated Tc at a lower level during heat exposure. E2 treatment elevated plasma E2 and reduced hematocrit but did not affect plasma osmolality. These effects of E2 on evaporative cooling and Tc in heat-stressed rats are similar to those that have been reported in human females. The mechanisms of the thermoregulatory effects of E2 remain to be studied.

scholarly journals Pregnancy alters body-core temperature response to a simulated open field in rats

1997 ◽  
Vol 82 (5) ◽  
pp. 1406-1410 ◽  
Author(s):  
James E. Fewell ◽  
Patricia A. Tang
Keyword(s):  
Open Field ◽  
Core Temperature ◽  
Temperature Response ◽  
The Body ◽  
Body Core Temperature ◽  
Sprague Dawley ◽  
Induced Hyperthermia ◽  
Sprague Dawley Rats ◽  
Functional Consequences ◽  
Body Core

Fewell, James E., and Patricia A. Tang. Pregnancy alters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4): 1406–1410, 1997.—Exposure of a rat to a novel environment (e.g., a simulated open field) induces a transient increase in body-core temperature, which is often called stress-induced hyperthermia. Although pregnancy is known to influence thermoregulatory control, its effect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied to test the hypothesis that pregnancy would alter the development of stress-induced hyperthermia after exposure to a simulated open field. Body-core temperature index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but not in gestation day-15 and day-20 rats. Thus our data provide evidence that pregnancy influences the body-core temperature response of rats exposed to a simulated open field in a gestation-dependent fashion. The functional consequences as well as the mechanisms involved remain to be determined.

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson
Keyword(s):  
Body Weight ◽  
Arginine Vasopressin ◽  
Plasma Catecholamines ◽  
Plasma Osmolality ◽  
Sprague Dawley ◽  
Prolonged Administration ◽  
Chronic Stimulation ◽  
Sustained Hypertension ◽  
Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

The recommended Threshold Limit Values for heat exposure fail to maintain body core temperature within safe limits in older working adults

2017 ◽  
Vol 14 (9) ◽  
pp. 703-711 ◽  
Author(s):  
Dallon T. Lamarche ◽  
Robert D. Meade ◽  
Andrew W. D'Souza ◽  
Andreas D. Flouris ◽  
Stephen G. Hardcastle ◽  
...  
Keyword(s):  
Core Temperature ◽  
Heat Exposure ◽  
Body Core Temperature ◽  
Limit Values ◽  
Threshold Limit Values ◽  
Working Adults ◽  
Threshold Limit ◽  
Body Core ◽  
Safe Limits

MK801 impairs thermoregulation in the heat

2002 ◽  
Vol 80 (3) ◽  
pp. 226-232 ◽  
Author(s):  
Frédéric Canini ◽  
Nadine Simler ◽  
Lionel Bourdon
Keyword(s):  
Locomotor Activity ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Core Temperature ◽  
Exposure Duration ◽  
Heat Exposure ◽  
Nmda Receptor Antagonist ◽  
Dopamine Metabolism ◽  
Body Core Temperature ◽  
Body Core

The effects of MK801 (dizocilpine), a glutamate NMDA receptor antagonist, on thermoregulation in the heat were studied in awake rats exposed to 40°C ambient temperature until their body core temperature reached 43°C. Under these conditions, MK801-treated rats exhibited enhanced locomotor activity and a steady rise in body core temperature, which reduced the heat exposure duration required to reach 43°C. Since MK801-treated rats also showed increased striatal dopaminergic metabolism at thermoneutrality, the role of dopamine in the MK801-induced impairment of thermoregulation in the heat was determined using co-treatment with SCH23390, a dopamine D1 receptor antagonist. SCH23390 normalized the locomotor activity in the heat without any effect on the heat exposure duration. These results suggest that the MK801-induced impairment of thermoregulation in the heat is related to neither a dopamine metabolism alteration nor a locomotor activity enhancement.Key words: heatstroke, NMDA receptor, thermoregulation, dopamine, locomotion.

scholarly journals Elevated Core Temperature in Florida Fernery Workers: Results of a Pilot Study

2019 ◽  
Vol 67 (9) ◽  
pp. 470-480
Author(s):  
Valerie Vi Thien Mac ◽  
Jose Antonio Tovar-Aguilar ◽  
Lisa Elon ◽  
Vicki Hertzberg ◽  
Eugenia Economos ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Core Temperature ◽  
Heat Exposure ◽  
Body Core Temperature ◽  
Adaptation Measures ◽  
Heat Stress Response ◽  
Increased Risk ◽  
Body Core ◽  
Outdoor Worker ◽  
Occupational Heat Exposure

With expected increases in extreme weather, there may be a greater risk of injury from extreme heat in outdoor worker populations. To plan for future adaptation measures, studies are needed that can characterize workers’ physiologic responses to heat in outdoor settings such as agriculture. The objective of this study was to characterize occupational heat exposure, key vulnerability factors (e.g., gender, energy expenditure), and physiologic heat stress response in a sample of fernery workers. Forty-three fernery workers over 86 workdays were examined regarding heat-related illness (HRI) during the summer months of 2012 and 2013. The key outcome measure was whether a participant’s body core temperature (Tc) reached or exceeded 38.0°C (100.4ºF; Tc38). Participants’ Tc exceeded 38.0°C on 49 (57%) of the workdays, with 30 of 40 participants reaching or exceeding Tc38 on at least one workday. Adjusting for sex, there was a 12% increase in the odds of Tc38 for every 100 kilocalories of energy expended (OR: 1.12; 95% Confidence Interval [CI]: [1.03, 1.21]). Adjusting for energy expenditure, females had 5 times greater odds of Tc38 compared with males (OR: 5.38; 95% CI: [1.03, 18.30]). These findings provide evidence of elevated Tc in Florida fernery workers, indicating an increased risk of occupational HRI, and the need for policy and interventions to address this health risk.

scholarly journals Thermal dehydration-induced thirst in spontaneously hypertensive rats

1999 ◽  
Vol 276 (5) ◽  
pp. R1302-R1310 ◽  
Author(s):  
Christopher C. Barney ◽  
Gina L. Smith ◽  
Michael M. Folkerts
Keyword(s):  
Water Status ◽  
Heat Exposure ◽  
Plasma Osmolality ◽  
Thermal Response ◽  
Hemoglobin Concentration ◽  
Water Losses ◽  
Evaporative Water ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto

Spontaneously hypertensive (SH) rats and normotensive Wistar-Kyoto (WKY) rats were exposed to either 25 or 37.5°C for 3.5 h, and their thermal and water balance responses were compared. After exposure, either a blood sample was obtained or the rats were allowed to rehydrate for 4 h. SH rats had both higher core temperatures and evaporative water losses during heat exposure. Measurements of hematocrit, hemoglobin concentration, plasma protein and sodium concentrations, and plasma osmolality indirectly showed that the SH rats were dehydrated relative to the WKY rats after exposure to either 25 or 37.5°C. SH rats drank significantly more water but also had significantly higher urine volumes than the WKY rats and thus rehydrated only slightly better than the WKY rats. SH and WKY rats had similar levels of water intake and urine output after 24 h of water deprivation. The elevated thermal response of SH rats to heat exposure does not appear to lead to uncompensatable changes in body water status.

scholarly journals Posttraumatic therapeutic hypothermia alters microglial and macrophage polarization toward a beneficial phenotype

2016 ◽  
Vol 37 (8) ◽  
pp. 2952-2962 ◽  
Author(s):  
Jessie S Truettner ◽  
Helen M Bramlett ◽  
W Dalton Dietrich
Keyword(s):  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Macrophage Polarization ◽  
Temperature Sensitive ◽  
Sprague Dawley ◽  
Rt Pcr ◽  
M2 Microglia ◽  
Sprague Dawley Rats ◽  
Inflammatory Processes ◽  
Clinical Models

Posttraumatic inflammatory processes contribute to pathological and reparative processes observed after traumatic brain injury (TBI). Recent findings have emphasized that these divergent effects result from subsets of proinflammatory (M1) or anti-inflammatory (M2) microglia and macrophages. Therapeutic hypothermia has been tested in preclinical and clinical models of TBI to limit secondary injury mechanisms including proinflammatory processes. This study evaluated the effects of posttraumatic hypothermia (PTH) on phenotype patterns of microglia/macrophages. Sprague-Dawley rats underwent moderate fluid percussion brain injury with normothermia (37℃) or hypothermia (33℃). Cortical and hippocampal regions were analyzed using flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR) at several periods after injury. Compared to normothermia, PTH attenuated infiltrating cortical macrophages positive for CD11b+ and CD45high. At 24 h, the ratio of iNOS+ (M1) to arginase+ (M2) cells after hypothermia showed a decrease compared to normothermia. RT-PCR of M1-associated genes including iNOS and IL-1β was significantly reduced with hypothermia while M2-associated genes including arginase and CD163 were significantly increased compared to normothermic conditions. The injury-induced increased expression of the chemokine Ccl2 was also reduced with PTH. These studies provide a link between temperature-sensitive alterations in macrophage/microglia activation and polarization toward a M2 phenotype that could be permissive for cell survival and repair.

Restoration of thermoregulation after exercise

2017 ◽  
Vol 122 (4) ◽  
pp. 933-944 ◽  
Author(s):  
Glen P. Kenny ◽  
Ryan McGinn
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Current Knowledge ◽  
Thermal Control ◽  
The Body ◽  
Body Core Temperature ◽  
Whole Body ◽  
Temperature Sensitive ◽  
Internal Core ◽  
Body Core

Performing exercise, especially in hot conditions, can heat the body, causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole body heat loss; a response mediated by temperature-sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body’s ability to dissipate heat during exercise. These include the activation of the body’s sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases (e.g., diabetes). The influence of these factors extends into recovery such that marked impairments in thermoregulatory function occur, leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body’s physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifest most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.

EFFECTS OF SIMVASTATIN ON FEMORAL BIOMECHANICS IN OVARIECTOMIZED RATS

2013 ◽  
Vol 13 (02) ◽  
pp. 1350048
Author(s):  
XIAOCHONG JIAN ◽  
JIANG CHEN ◽  
LINLIN ZHANG ◽  
FUHUA YAN ◽  
YANJUN ZENG
Keyword(s):  
Bending Test ◽  
Ovariectomized Rats ◽  
Sprague Dawley ◽  
Simvastatin Treatment ◽  
Three Point Bending ◽  
Sprague Dawley Rats ◽  
Biomechanical Parameters ◽  
Inorganic Constituents ◽  
Time Of Administration ◽  
Maximal Strain

Objective: To investigate the effect of simvastatin on the biomechanical characteristics of the femur in ovariectomized rats. Material and methods: Fifty-four female Sprague-Dawley rats, aged three months old, were randomly divided into three groups: sham-operated group ( SHAM; n = 18), ovariectomized group (OVX; n = 18), and ovariectomized with simvastatin treatment group (OVX+SIM; n = 18). Eight weeks after being ovariectomized, simvastatin was administered orally at 5 mg/kg each day in the OVX + SIM group. The animals were sacrificed at either four or 12 weeks after administration and femurs were obtained. Biomechanical parameters were measured by the three-point bending test. Results: There were no significant differences in the maximal strain and flexibility strain between the OVX and OVX + SIM groups at either four or 12 weeks after administration (p > 0.05). In contrast, significant differences in flexibility loading at four weeks and in maximal loading, flexibility loading, and the coefficient of bending ductility between the OVX and OVX + SIM groups at either four or 12 weeks (p < 0.05 and p < 0.01, respectively). Intergroup comparisons showed that maximal loading and flexibility loading have significant differences in the OVX + SIM group (p < 0.01). Conclusion: Simvastatin shows potential in promoting bone remodeling, changing bone micro-architecture, and influencing the integration and distribution ratio of organic and inorganic constituents in bone tissue of ovariectomized rats. In addition, a longer time of administration with simvastatin could enhance the femoral strength.

Role of plasma osmolality in the delayed onset of thermal cutaneous vasodilation during exercise in humans

1998 ◽  
Vol 275 (1) ◽  
pp. R286-R290 ◽  
Author(s):  
Akira Takamata ◽  
Kei Nagashima ◽  
Hiroshi Nose ◽  
Taketoshi Morimoto
Keyword(s):  
Regression Line ◽  
Plasma Osmolality ◽  
Peak Oxygen Consumption ◽  
Body Core Temperature ◽  
Temperature Threshold ◽  
Moderate Exercise ◽  
Cutaneous Vasodilation ◽  
Body Core ◽  
The Relationship

To elucidate the role of increased plasma osmolality (Posmol), which occurs during exercise in the regulation of cutaneous vasodilation (CVD) during exercise, we determined the relationship between the change in esophageal temperature (ΔTes) required to elicit CVD (ΔTes threshold for CVD) and Posmol during light and moderate exercise (30 and 55% of peak oxygen consumption, respectively) and passive body heating. Then we compared the relationship with the data obtained in our previous study [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 ( Regulatory Integrative Comp. Physiol.42): R197–R204, 1997], in which we determined the relationships during passive body heating following isotonic (0.9% NaCl) or hypertonic (2 or 3% NaCl) saline infusions in the same subjects. Posmol values at 5 min after the onset of exercise were 287.5 ± 0.9 mosmol/kgH2O during light exercise and 293.0 ± 1.2 mosmol/kgH2O during moderate exercise. Posmol just before passive body heating was 289.9 ± 1.4 mosmol/kgH2O. The ΔTes threshold for CVD was 0.09 ± 0.05°C during light exercise, 0.31 ± 0.09°C during moderate exercise, and 0.10 ± 0.05°C during passive body heating. The relationship between the ΔTes threshold for CVD and Posmol was shown to be on the same regression line both during exercise and during passive body heating with or without infusions [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 ( Regulatory Integrative Comp. Physiol.42): R197–R204, 1997]. Our data suggest that the elevated body core temperature threshold for CVD during exercise could be the result of increased Posmol induced by exercise and is not due to reduced plasma volume or the intensity of the exercise itself.

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