Protective effects of heat shock response on circulatory collapse induced by hyperthermia.
- Author:
Bin WANG
1
;
Bing-de LUO
;
Fei ZOU
;
Wei-ren WAN
;
Jin-qiang GUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Heat-Shock Proteins; analysis; Heat-Shock Response; physiology; Hot Temperature; Male; Nitric Oxide; analysis; Rats; Rats, Sprague-Dawley; Shock; metabolism; physiopathology; Time Factors
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2004;22(2):115-118
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects and mechanism of heat shock response (HSR) on circulatory collapse induced by hyperthermia.
METHODSTwo experiments were carried out: (1) Protective effects of HSR. Rats were divided into 2 groups: heat shock (HS) group, sham control (SC) group. After HS group was pretreated with heat shock and recovered for 20 h at room temperature, both groups were exposed to heat till death, and blood pressure, electrocardiogram were measured continuously during exposure. Mean arterial pressure (MAP), survival time etc were acquired through Chart software. (2) Mechanism of effects. Rats were divided into 3 groups: HS group, SC group and normal control (NC) group. The treatment in HS and SC groups was identical with that in the first experiment, but it would be terminated at 73 min after heat exposure. Systolic pressure (Ps), diastolic pressure (Pd) etc were recorded and content of NO and HSP70 in myocardium were measured.
RESULTS(1) The survival time in HS group [(102.3 +/- 11.4) min] was longer than that in SC group [(87.9 +/- 7.7) min] and shock revealed later (P < 0.01); (2) During early heat exposure MAP in HS group was not different from that in SC group, but after 60 min MAP in HS group were higher than that in SC group; (3) MAP, Ps, Pd, HR and HSP70 in HS group were significantly higher but content of NO was lower than those in SC group (P < 0.01, P < 0.05).
CONCLUSIONHSR may induce upregulation of HSP70 and inhibit excessive production of NO in myocardium, thus result in relief of circulatory collapse induced by hyperthermia.