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Neutrophil elastase inhibitor improves survival rate after ischemia reperfusion injury caused by supravisceral aortic clamping in rats.
J Surg Res. 2013 Mar; 180(1):e31-6.JS

Abstract

BACKGROUND

Sivelestat sodium hydrate is a specific neutrophil elastase inhibitor effective in acute lung injury (ALI) associated with systemic inflammatory response syndrome. Bowel ischemia reperfusion injury (IRI) induced by supravisceral aortic clamping is associated with an excessive systemic inflammatory response, resulting in remote organ damage, including ALI. In this study, we investigated whether sivelestat can attenuate neutrophil sequestration in the lung, alleviate ALI, and improve survival in a rat bowel IRI model.

METHODS

Adult male Sprague-Dawley rats underwent bowel IRI induced by supravisceral aortic clamping and were randomly assigned to receive sivelestat or saline (control) and monitored for survival. We randomly assigned other rats to undergo laparotomy alone (sham operation), IRI alone, or IRI and sivelestat treatment. We evaluated blood samples for organ function, cytokine levels, and neutrophil elastase activity after reperfusion. Organs were analyzed histologically. We also determined lung injury in another set of rats.

RESULTS

Bowel IRI induced a significant increase in serum variables indicative of organ function, cytokine concentrations, neutrophil elastase activity, and lung permeability and edema, which reflected the presence of both systemic inflammatory response syndrome and compensatory anti-inflammatory response syndrome. Treatment with sivelestat significantly improved survival rate, lung permeability and edema, and significantly decreased levels of creatinine, interleukin 6, interleukin 10, and neutrophil elastase activity. Histological studies showed that sivelestat-treated rats had less bowel IRI-induced damage to lung and liver tissue than controls.

CONCLUSION

In a rat model, administration of sivelestat attenuated the effects of bowel IRI induced by supravisceral aortic clamping, and improved the survival rate.

Authors+Show Affiliations

Department of Surgery, Keio University School of Medicine, Tokyo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22595015

Citation

Fujimura, Naoki, et al. "Neutrophil Elastase Inhibitor Improves Survival Rate After Ischemia Reperfusion Injury Caused By Supravisceral Aortic Clamping in Rats." The Journal of Surgical Research, vol. 180, no. 1, 2013, pp. e31-6.
Fujimura N, Obara H, Suda K, et al. Neutrophil elastase inhibitor improves survival rate after ischemia reperfusion injury caused by supravisceral aortic clamping in rats. J Surg Res. 2013;180(1):e31-6.
Fujimura, N., Obara, H., Suda, K., Takeuchi, H., Miyasho, T., Kawasako, K., Du, W., Yamada, S., Ono, S., Matsumoto, K., Matsuda, S., Yagi, H., Kitago, M., Shinoda, M., Itano, O., Tanabe, M., Sakamoto, M., Maruyama, I., & Kitagawa, Y. (2013). Neutrophil elastase inhibitor improves survival rate after ischemia reperfusion injury caused by supravisceral aortic clamping in rats. The Journal of Surgical Research, 180(1), e31-6. https://doi.org/10.1016/j.jss.2012.04.037
Fujimura N, et al. Neutrophil Elastase Inhibitor Improves Survival Rate After Ischemia Reperfusion Injury Caused By Supravisceral Aortic Clamping in Rats. J Surg Res. 2013;180(1):e31-6. PubMed PMID: 22595015.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neutrophil elastase inhibitor improves survival rate after ischemia reperfusion injury caused by supravisceral aortic clamping in rats. AU - Fujimura,Naoki, AU - Obara,Hideaki, AU - Suda,Koichi, AU - Takeuchi,Hiroya, AU - Miyasho,Taku, AU - Kawasako,Kazufumi, AU - Du,Wenlin, AU - Yamada,Shingo, AU - Ono,Shigeshi, AU - Matsumoto,Kenji, AU - Matsuda,Sachiko, AU - Yagi,Hiroshi, AU - Kitago,Minoru, AU - Shinoda,Masahiro, AU - Itano,Osamu, AU - Tanabe,Minoru, AU - Sakamoto,Michiie, AU - Maruyama,Ikuro, AU - Kitagawa,Yuko, Y1 - 2012/05/08/ PY - 2012/01/13/received PY - 2012/03/27/revised PY - 2012/04/17/accepted PY - 2012/5/19/entrez PY - 2012/5/19/pubmed PY - 2013/4/12/medline SP - e31 EP - 6 JF - The Journal of surgical research JO - J. Surg. Res. VL - 180 IS - 1 N2 - BACKGROUND: Sivelestat sodium hydrate is a specific neutrophil elastase inhibitor effective in acute lung injury (ALI) associated with systemic inflammatory response syndrome. Bowel ischemia reperfusion injury (IRI) induced by supravisceral aortic clamping is associated with an excessive systemic inflammatory response, resulting in remote organ damage, including ALI. In this study, we investigated whether sivelestat can attenuate neutrophil sequestration in the lung, alleviate ALI, and improve survival in a rat bowel IRI model. METHODS: Adult male Sprague-Dawley rats underwent bowel IRI induced by supravisceral aortic clamping and were randomly assigned to receive sivelestat or saline (control) and monitored for survival. We randomly assigned other rats to undergo laparotomy alone (sham operation), IRI alone, or IRI and sivelestat treatment. We evaluated blood samples for organ function, cytokine levels, and neutrophil elastase activity after reperfusion. Organs were analyzed histologically. We also determined lung injury in another set of rats. RESULTS: Bowel IRI induced a significant increase in serum variables indicative of organ function, cytokine concentrations, neutrophil elastase activity, and lung permeability and edema, which reflected the presence of both systemic inflammatory response syndrome and compensatory anti-inflammatory response syndrome. Treatment with sivelestat significantly improved survival rate, lung permeability and edema, and significantly decreased levels of creatinine, interleukin 6, interleukin 10, and neutrophil elastase activity. Histological studies showed that sivelestat-treated rats had less bowel IRI-induced damage to lung and liver tissue than controls. CONCLUSION: In a rat model, administration of sivelestat attenuated the effects of bowel IRI induced by supravisceral aortic clamping, and improved the survival rate. SN - 1095-8673 UR - https://www.unboundmedicine.com/medline/citation/22595015/Neutrophil_elastase_inhibitor_improves_survival_rate_after_ischemia_reperfusion_injury_caused_by_supravisceral_aortic_clamping_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(12)00397-6 DB - PRIME DP - Unbound Medicine ER -