%0 Journal Article
%T TNF-a and plasma D(-)-lactate levels in rats after intestinal ischemia and reperfusion<br>TNF-α and plasma D(-)-lactate levels in rats after intestinal ischemia and reperfusion
%A Yongming YAO
%A Ning DONG
%A Yan YU
%A Zhiyong SHENG
%A Ailan REN
%A Shengli DONG
%A <br>Yongming YAO
%A Ning DONG
%A Yan YU
%A Zhiyong SHENG
%A Ailan REN
%A Shengli DONG
%J 老年心脏病学杂志(英文版)
%D 2004
%I Science Press
%X Objective To study the potential role of tumor necrosis factor-a (TNF-a) induction in the development of mucosal barrier dysfunction in rats caused by acute intestinal ischemia-reperfusion injury, and to examine whether pretreatment with monoclonal antibody against TNF-a (TNF-a MoAb) would affect the release of D(-)-lactate after local gut ischemia followed by reperfusion. Methods Anesthetized Sprague-Dawley rats underwent superior mesenteric artery occlusion for 75 min followed by reperfusion for 6 hr. The rats were treated intravenously with either TNF-a MoAb (20 mg/kg) or albumin (20 mg/kg) 30 min prior to the onset of ischemia. Plasma D(-)-lactate levels were measured in both the portal and systemic blood by an enzymatic spectrophotometric assay. Intestinal TNF-a mRNA expression as well as protein levels were also measured at various intervals. In addition, a postmortem examination was performed together with a macropathological evaluation based on a four-grade scoring system. Results Intestinal ischemia resulted in a significant elevation in D(-)-lactate levels in the portal vein blood in both the control and treatment groups ( P < 0.05). However, animals pretreated with TNF-a MoAb at 6 hr after reperfusion showed significant attenuation of an increase in both portal and systemic D(-)-lactate levels when compared with those only receiving albumin (P < 0.05). In the control animals, a remarkable rise in intestinal TNF-a level was measured at 0.5 hr after clamp release ( P < 0.01), however, prophylactic treatment with TNF-a MoAb completely annulled the increase of local TNF-a levels seen in the control animals. Similarly, after anti-TNF-a MoAb administration, intestinal TNF-a mRNA expression was markedly inhibited, which showed significant differences when compared with the control group at 0. 5 hr, 2 hr and 6 hr after the release of occlusion ( P < 0. 05-0. 01). In addition, the pathological examination showed marked intestinal lesions that formed during ischemia, which were much worse upon reperfusion, particularly at the 6 hr time point. These acute injuries were obviously attenuated in animals receiving TNF-a MoAb. Conclusions It appeared that acute intestinal ischemia was associated with failure of the mucosal barrier, resulting in increased plasma D(-)-lactate levels in both portal and systemic blood. These results suggest that TNF-a appears to be involved in the development of local damage associated with intestinal ischemic injury. Moreover, prophylactic treatment with TNF-a MoAb exerts preventive effects on ischemia/ reperfusion-induced circulating D (-)-lactate elevation and gut injury.
%K D (-)-lactate
%K ischemia/reperfusion
%K injury
%K intestinal
%K tumor necrosis
%K factor-a
%K monoclonal antibody
%K intestinal mucosal barrier<br>D(-)-lactate
%K ischemia/reperfusion
%K injury
%K intestinal
%K tumor
%K necrosis
%K factor-α
%K monoclonal
%K antibody
%K intestinal
%K mucosal
%K barrier
%U http://www.alljournals.cn/get_abstract_url.aspx?pcid=A9DB1C13C87CE289EA38239A9433C9DC&cid=AD36F34DDC3BA7B0&jid=4DC702B3A2386A4814E2FF9CFB799B27&aid=88DB9EF5A5FDF19328DA409EFF760A64&yid=D0E58B75BFD8E51C&vid=CA4FD0336C81A37A&iid=0B39A22176CE99FB&sid=EFD65B51496FB200&eid=2F56B21F91C9B05B&journal_id=1671-5411&journal_name=Journalofgeriatriccardiology:JGC&referenced_num=0&reference_num=0