Wang Bin, Luo Bing-de, Zou Fei, Wang Wei-ren, Guo Jin-qiang
Institute of High-temperature Medicine, Department of Tropical Hygiene, First Military Medical University, Guangzhou 510515, China.
Di Yi Jun Yi Da Xue Xue Bao. 2004 Mar;24(3):300-2.
To investigate the preventive effects of heat-shock response (HSR) against circulatory collapse induced by hyperthermia and understand its mechanism.
Twenty-four SD rats were randomized equally into heat-shock group (HS group), high temperature control group (HC group) and normal temperature control group (NC group). The rats in HS group, but not HC group, were subjected to heat shock pretreatment. After a recovery period for 20 h at room temperature, the rats in HS and HC groups were exposed to high temperature environment, and their blood pressures and electrocardiograms were measured continuously. Heat exposure was terminated at 73 min and the contents of myocardial malondialdehyde (MDA) and NO were measured. Using Chart software, the data of the mean arterial pressure (MAP), systolic pressure (SP), diastolic pressure (DP), heart rate (HR) were acquired. The rats in NC group did not receive any treatment to obtain the measurements in normal condition.
Compared with NC group, the MAP, SP and DP were significantly lowered (P P<0.01) in HS and HC group and HR accelerated (P P<0.01) after a 73-min heat exposure, and HS group had significantly higher measurements of the above indices than HC group did. In comparison with NC group, the contents of MDA and NO in the myocardium in HC group were significantly elevated after the exposure (P P<0.01). The MDA content in HS group, which was comparable with that of NC group, was significantly lower than that of HC group (P P<0.05), and compared with HC group, HS also had lower NO content (P<0.01).
HSR may relieve circulatory collapse induced by hyperthermia, which involves the inhibitory effect of HSR on the production of MDA and NO in the myocardium.
