Abstract
Rats 0, 16, or 48 h after heat shock (42°C core temperature for 15 min) or chemical stress (5 mg/kg sodium arsenfte, i.p.) were exposed to a high ambient temperature (43°C) to induce heatstroke onset. The moment in which the mean arterial pressure and cerebral blood flow began to decrease from their peak values was taken as the onset of heatstroke. Pdor heat shock or chemioal stress conferred significant protection against heatstroke-induced arterial hypotension, cerebral ischemia, cerebral neuronal damage and death, and correlated with expression of HSP72 in brain, heart, liver and kidney at 16 h. However, at 48 h, when HSP72 expression returned to basal values, the above responses that occurred after the onset of heatstroke of two groups (0 h group VS 48 h group) were indistinguishable. The data suggest that HSP72 presence increases survival in rat heatstroke by attenuating arterial hypotension, cerebral ischemia and neuronal damage.
| Original language | English |
|---|---|
| Pages (from-to) | 9-12 |
| Number of pages | 4 |
| Journal | Neuroscience Letters |
| Volume | 252 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1998 Jul 27 |
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Keywords
- Cell death
- Cerebral ischemia
- Heatstroke
- Survival
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Heat shock protein expression protects against death following exposure to heatstroke in rats. / Yang, Yi Ling; Lu, Kwok-Tung; Tsay, Huey Jen; Lin, Chia Hsuan; Lin, Mao Tsun.
In: Neuroscience Letters, Vol. 252, No. 1, 27.07.1998, p. 9-12.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Heat shock protein expression protects against death following exposure to heatstroke in rats
AU - Yang, Yi Ling
AU - Lu, Kwok-Tung
AU - Tsay, Huey Jen
AU - Lin, Chia Hsuan
AU - Lin, Mao Tsun
PY - 1998/7/27
Y1 - 1998/7/27
N2 - Rats 0, 16, or 48 h after heat shock (42°C core temperature for 15 min) or chemical stress (5 mg/kg sodium arsenfte, i.p.) were exposed to a high ambient temperature (43°C) to induce heatstroke onset. The moment in which the mean arterial pressure and cerebral blood flow began to decrease from their peak values was taken as the onset of heatstroke. Pdor heat shock or chemioal stress conferred significant protection against heatstroke-induced arterial hypotension, cerebral ischemia, cerebral neuronal damage and death, and correlated with expression of HSP72 in brain, heart, liver and kidney at 16 h. However, at 48 h, when HSP72 expression returned to basal values, the above responses that occurred after the onset of heatstroke of two groups (0 h group VS 48 h group) were indistinguishable. The data suggest that HSP72 presence increases survival in rat heatstroke by attenuating arterial hypotension, cerebral ischemia and neuronal damage.
AB - Rats 0, 16, or 48 h after heat shock (42°C core temperature for 15 min) or chemical stress (5 mg/kg sodium arsenfte, i.p.) were exposed to a high ambient temperature (43°C) to induce heatstroke onset. The moment in which the mean arterial pressure and cerebral blood flow began to decrease from their peak values was taken as the onset of heatstroke. Pdor heat shock or chemioal stress conferred significant protection against heatstroke-induced arterial hypotension, cerebral ischemia, cerebral neuronal damage and death, and correlated with expression of HSP72 in brain, heart, liver and kidney at 16 h. However, at 48 h, when HSP72 expression returned to basal values, the above responses that occurred after the onset of heatstroke of two groups (0 h group VS 48 h group) were indistinguishable. The data suggest that HSP72 presence increases survival in rat heatstroke by attenuating arterial hypotension, cerebral ischemia and neuronal damage.
KW - Cell death
KW - Cerebral ischemia
KW - Heatstroke
KW - Survival
UR - http://www.scopus.com/inward/record.url?scp=0344157430&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0344157430&partnerID=8YFLogxK
U2 - 10.1016/S0304-3940(98)00508-4
DO - 10.1016/S0304-3940(98)00508-4
M3 - Article
C2 - 9756346
AN - SCOPUS:0344157430
VL - 252
SP - 9
EP - 12
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 1
ER -