HYDROGEN SULPHIDE-INDUCED HYPOTHERMIA ATTENUATES STRESS-RELATED ULCERATION IN RATS

  1. Li-Xia Lou1,
  2. Bin Geng1,
  3. Jun-Bao Du3,4,
  4. Chao-Shu Tang1,2

Article first published online: 17 OCT 2007

DOI: 10.1111/j.1440-1681.2007.04812.x

Issue

Clinical and Experimental Pharmacology and Physiology

Clinical and Experimental Pharmacology and Physiology

Volume 35, Issue 2, pages 223–228, February 2008

Additional Information

How to Cite

Lou, L.-X., Geng, B., Du, J.-B. and Tang, C.-S. (2008), HYDROGEN SULPHIDE-INDUCED HYPOTHERMIA ATTENUATES STRESS-RELATED ULCERATION IN RATS. Clinical and Experimental Pharmacology and Physiology, 35: 223–228. doi: 10.1111/j.1440-1681.2007.04812.x

Author Information

  1. 1

    Institute of Cardiovascular Diseases, Peking University First Hospital,

  2. 2

    Department of Physiology and Pathophysiology, Peking University Health Science Center,

  3. 3

    Department of Pediatrics, Peking University First Hospital and

  4. 4

    Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, China

* Bin Geng, Institute of Cardiovascular Research, Peking University First Hospital, Beijing 100034, China. Email: bingeng@bjmu.edu.cn

Publication History

  1. Issue published online: 17 OCT 2007
  2. Article first published online: 17 OCT 2007
  3. Received 26 May 2007; revision 19 August 2007; accepted 20 August 2007.

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Keywords:

  • endoplasmic reticulum stress;
  • hydrogen sulphide;
  • induced hypothermia;
  • rats;
  • stress gastric ulcer

SUMMARY

  • 1
    Hydrogen sulphide (H2S) acts as a gaseous cellular messenger and has recently been reported to induce a suspended animation-like state in mice. The aim of the present study was to investigate the protective role of H2S exposure in stress gastric ulcer.
  • 2
    In the present study, we used a rat model of water immersion and restraint stress (WRS) to induce the typical stress disease, namely stress gastric ulcer. Rats were treated with WRS for 4 h, with or without pre-exposure to H2S (160 p.p.m. H2S for 2.5 h).
  • 3
    In H2S-exposed rats, body temperature was significantly reduced by 2.5C (P < 0.01) and oxygen consumption was reduced by 37.1% (P < 0.01) compared with control rats. Plasma levels of H2S were increased by 20.8% (P < 0.01) following pre-exposure. Pre-exposure to H2S significantly reduced the gastric ulcer index, from 24 ± 9 to 9 ± 2 (P < 0.01), in WRS rats. In addition, WRS increased plasma levels of adrenocorticotropin (ACTH) and corticosterone 4.7- and 4.8-fold, respectively (both P < 0.01). Pre-exposure to H2S markedly suppressed plasma ACTH and corticosterone level by 34.4 and 53.2%, respectively (both P < 0.01), and reduced WRS-elevated myeloperoxidase (MPO) activity by 19%. In the present study, WRS increased gastric malondialdehyde and conjugated diene content by 42 and 68%, respectively (both P < 0.01), and H2S exposure reduced lipid peroxide production. Finally, H2S exposure inhibited the WRS-elevated expression of glucose-regulated protein 78 and caspase 12, markers of endoplasmic reticulum stress.
  • 4
    In conclusion, a low concentration of H2S may be a new pharmacological tool for induced hypothermia to prevent severe stress-induced diseases and multifarious trauma in the clinical setting.
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