hyperthermic condition
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2010 ◽  
Vol 643 (2-3) ◽  
pp. 162-169 ◽  
Author(s):  
Jalal Pourahmad ◽  
Mohammad Reza Eskandari ◽  
Masoumeh Nosrati ◽  
Farzad Kobarfard ◽  
Ali Reza Khajeamiri

2008 ◽  
Vol 109 (3) ◽  
pp. 522-529 ◽  
Author(s):  
Alireza P. Shabanzadeh ◽  
Ashfaq Shuaib ◽  
Chen Xu Wang

Object Statins have been used for induction of ischemic tolerance after cerebral ischemia. The authors have previously shown that simvastatin is protective after ischemic cerebral injury in normothermic conditions. In this study they further examined whether treatment with simvastatin can reduce ischemic brain injury in a hyperthermic condition. Methods Focal ischemic brain injury was induced by embolizing a preformed clot into the middle cerebral artery in rats. The authors initially examined whether treatment with simvastatin could reduce ischemic brain injury without or with hyperthermia. The infarct volume, edema, and neurological deficits were examined. They then studied whether simvastatin could reduce the perfusion deficits, damage to the blood–brain barrier (BBB), and degeneration of neurons in the ischemic injured brain. Results Simvastatin significantly reduced the infarct volume in both normothermic and hyperthermic conditions, compared with appropriate controls. Concomitantly, this treatment also significantly reduced neurological deficits and brain edema. Administration of simvastatin significantly decreased perfusion deficits, BBB permeability, and degenerated neurons. Conclusions These studies suggest that simvastatin is an effective agent for ischemic brain injury not only in normothermic but also in hyperthermic conditions, which may be through the decrease of BBB permeability, degenerated neurons, and perfusion deficits.


2005 ◽  
Vol 98 (6) ◽  
pp. 2011-2018 ◽  
Author(s):  
Gregg R. McCord ◽  
Christopher T. Minson

The dramatic increase in skin blood flow and sweating observed during heat stress is mediated by poorly understood sympathetic cholinergic mechanisms. One theory suggests that a single sympathetic cholinergic nerve mediates cutaneous active vasodilation (AVD) and sweating via cotransmission of separate neurotransmitters, because AVD and sweating track temporally and directionally when activated during passive whole body heat stress. It has also been suggested that these responses are regulated independently, because cutaneous vascular conductance (CVC) has been shown to decrease, whereas sweat rate increases, during combined hyperthermia and isometric handgrip exercise. We tested the hypothesis that CVC decreases during isometric handgrip exercise if skin blood flow is elevated using local heating to levels similar to that induced by pronounced hyperthermia but that this does not occur at lower levels of skin blood flow. Subjects performed isometric handgrip exercise as CVC was elevated at selected sites to varying levels by local heating (which is independent of AVD) in thermoneutral and hyperthermic conditions. During thermoneutral isometric handgrip exercise, CVC decreased at sites in which blood flow was significantly elevated before exercise (−6.5 ± 1.8% of maximal CVC at 41°C and −10.5 ± 2.0% of maximal CVC at 43°C; P < 0.05 vs. preexercise). During isometric handgrip exercise in the hyperthermic condition, an observed decrease in CVC was associated with the level of CVC before exercise. Taken together, these findings argue against withdrawal of AVD to explain the decrease in CVC observed during isometric handgrip exercise in hyperthermic conditions.


1992 ◽  
Vol 107 (6_part_1) ◽  
pp. 769-774 ◽  
Author(s):  
Ann M. Thompson ◽  
J. Gail Neely

The effect of hyperthermia on Induction of the 72 kllodalton (kDa) heat shock protein (HSP72) was examined In interdental cells of the guinea pig cochlea. After being Immersed in a water bath of either normal body temperature (37° C, control condition) or 43° C (hyperthermic condition), animals were killed either 0, 1, 2, 6, or 18 hours later. Cochlear sections were incubated with a monoclonal antibody raised against HSP72 and relative staining densities were quantified with a light microscopic image analysis system. Optical densities of the interdental cell region of animals receiving hyperthermia treatment were significantly greater than those of animals in the control group. Further analysis revealed that levels of HSP72 Immunoreactlvlty began increasing by 1 hour after hyperthermia and continued to increase thereafter, to reach maximal levels at 6 hours. The maximal levels were maintained for the rest of the experiment—18 hours. The results indicate that hyperthermia leads to an increase in the synthesis of HSP72 in guinea pig Interdental cells.


1975 ◽  
Vol 38 (6) ◽  
pp. 969-973 ◽  
Author(s):  
P. Thaxton ◽  
W. P. Yonushonis ◽  
G. R. Baughman

Juvenile chickens that had previously received mercuric chloride intramuscularly were subjected to an acute exposure of high ambient temperature in the presence or absence of a 140 mpm air velocity. This level of mercury did not retard growth of affect the resting body temperature. However, following heating the birds experienced a greater hyperthermia than similarly heated controls and consequently thermal death occurred earlier. When a high air velocity was maintained during heating the hyperthermic condition was further amplified, as was the event of thermal death. It is concluded that a synergistic relationship exists between mercury, when administered at a nontoxic level, and the climatic factors of temperature and air velocity.


1963 ◽  
Vol 18 (3) ◽  
pp. 600-602
Author(s):  
Abbott T. Kissen

Supersonic or hypersonic aircraft flight can produce hyperthermia in crew members. Dark adaptation is a physiologic response possibily influenced by such stress. Biochemical regeneration rate of rhodopsin might be altered if retinal blood or tissue temperatures are raised by this hyperthermia. Peripheral dark adaptation curves were obtained on five subjects at comfort (21.0 C) and 65.6 C temperatures alternately, using a modified Hecht-Schlaer adaptometer. In 24 heat experiments, subjects were exposed to 65.6 C ambient air temperature for 55 min after which the heat was shut off. Chamber temperature declined but the subjects remained in a relatively constant hyperthermic condition during the subsequent 35-min dark adaptation test. The criterion used here for hyperthermia is the elevation and maintenance of the rectal temperature at least 0.56 C above corresponding control temperature. Curves obtained under hyperthermic conditions (with the exception of the initial and terminal values) differ, with statistical significance, from controls, indicating a facilitation of dark adaptation under the imposed thermal stress conditions. Submitted on July 9, 1962


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