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The role of tumour necrosis factor-alpha in renal dysfunction following mild haemorrhage in rats.
Int J Exp Pathol. 2004 Dec; 85(6):345-53.IJ

Abstract

Mild haemorrhage occasionally causes delayed death following failure of kidney or multiple organs, but the precise mechanisms have not yet been identified. We investigated the role of tumour necrosis factor-alpha (TNF-alpha), known as a major pro-inflammatory cytokine that leads to multiple organ failure, on the renal damage induced by mild haemorrhage. A mild haemorrhagic state was induced in male anaesthetized rats by bleeding via a common carotid catheter for 20 min at 16.7% of total body blood, 1.09 ml/100 g body weight, without fluid resuscitation. Mean arterial pressure and heart rate decreased soon after haemorrhaging but returned to baseline level up to 5 h after bleeding. TNF-alpha mRNA expression in the kidney and serum TNF-alpha levels were highest at 1 h after bleeding. Intraperitoneal pretreatment with FR167653, an inhibitory compound of TNF-alpha production, as well as of interleukin (IL)-1beta, significantly inhibited the increase in TNF-alpha. The inflammatory cell infiltration and tubular cell injury induced by haemorrhage were suppressed, and the renal dysfunction was dramatically improved by the FR167653 treatment. The morphological changes were also less in the treated group than in those that had not been treated. TNF-alpha has been reported to have striking effects on IL-1beta release and activation of neutrophils, and to play a pivotal role in the expression of the other pro-inflammatory cytokines. Our data show that endogenously-derived TNF-alpha does play a key role in the renal dysfunction during mild haemorrhage. These results should be useful to forensic pathologists to explain the pathogenesis of renal dysfunction induced by a mild haemorrhage and to identify the cause of death where there are no significant morphological changes after mild haemorrhage.

Authors+Show Affiliations

Department of Forensic Medicine, School of Medicine, University of Occupational and Environmental Health Japan, Yahata Nishi-ku, Kitakyushu 807-8555, Japan. h-sato@med.uoeh-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15566431

Citation

Sato, Hiroaki, et al. "The Role of Tumour Necrosis Factor-alpha in Renal Dysfunction Following Mild Haemorrhage in Rats." International Journal of Experimental Pathology, vol. 85, no. 6, 2004, pp. 345-53.
Sato H, Tanaka T, Kita T, et al. The role of tumour necrosis factor-alpha in renal dysfunction following mild haemorrhage in rats. Int J Exp Pathol. 2004;85(6):345-53.
Sato, H., Tanaka, T., Kita, T., Yamaguchi, H., & Tanaka, N. (2004). The role of tumour necrosis factor-alpha in renal dysfunction following mild haemorrhage in rats. International Journal of Experimental Pathology, 85(6), 345-53.
Sato H, et al. The Role of Tumour Necrosis Factor-alpha in Renal Dysfunction Following Mild Haemorrhage in Rats. Int J Exp Pathol. 2004;85(6):345-53. PubMed PMID: 15566431.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of tumour necrosis factor-alpha in renal dysfunction following mild haemorrhage in rats. AU - Sato,Hiroaki, AU - Tanaka,Toshiko, AU - Kita,Toshiro, AU - Yamaguchi,Hiroki, AU - Tanaka,Noriyuki, PY - 2004/11/30/pubmed PY - 2005/1/19/medline PY - 2004/11/30/entrez SP - 345 EP - 53 JF - International journal of experimental pathology JO - Int J Exp Pathol VL - 85 IS - 6 N2 - Mild haemorrhage occasionally causes delayed death following failure of kidney or multiple organs, but the precise mechanisms have not yet been identified. We investigated the role of tumour necrosis factor-alpha (TNF-alpha), known as a major pro-inflammatory cytokine that leads to multiple organ failure, on the renal damage induced by mild haemorrhage. A mild haemorrhagic state was induced in male anaesthetized rats by bleeding via a common carotid catheter for 20 min at 16.7% of total body blood, 1.09 ml/100 g body weight, without fluid resuscitation. Mean arterial pressure and heart rate decreased soon after haemorrhaging but returned to baseline level up to 5 h after bleeding. TNF-alpha mRNA expression in the kidney and serum TNF-alpha levels were highest at 1 h after bleeding. Intraperitoneal pretreatment with FR167653, an inhibitory compound of TNF-alpha production, as well as of interleukin (IL)-1beta, significantly inhibited the increase in TNF-alpha. The inflammatory cell infiltration and tubular cell injury induced by haemorrhage were suppressed, and the renal dysfunction was dramatically improved by the FR167653 treatment. The morphological changes were also less in the treated group than in those that had not been treated. TNF-alpha has been reported to have striking effects on IL-1beta release and activation of neutrophils, and to play a pivotal role in the expression of the other pro-inflammatory cytokines. Our data show that endogenously-derived TNF-alpha does play a key role in the renal dysfunction during mild haemorrhage. These results should be useful to forensic pathologists to explain the pathogenesis of renal dysfunction induced by a mild haemorrhage and to identify the cause of death where there are no significant morphological changes after mild haemorrhage. SN - 0959-9673 UR - https://www.unboundmedicine.com/medline/citation/15566431/The_role_of_tumour_necrosis_factor_alpha_in_renal_dysfunction_following_mild_haemorrhage_in_rats_ L2 - https://doi.org/10.1111/j.0959-9673.2004.00403.x DB - PRIME DP - Unbound Medicine ER -