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Acute intestinal ischemia represents a broad spectrum of diseases with variousclinical and pathological manifestations. The primary causes of insufficient bloodflow to the intestine arc diverse and include thromboembolism, neoplasms, vasculitis,abdominal inflammatory conditions, trauma, chemotherapy, radiation and corrosiveinjury (Rha et aI., 2000). Despite of the advances in the pathophysiological, laboratorydiagnosis and imaging techniques acute intestinal ischemiais still one ofthe major etiological causes of multiple organ failure (Schlichting et aI., 1995). Ischemiainduces continuous distrubance of hepatic microcirculation leading to liverdysfunction (Nakamura et al., 2001). Furthermore, it triggers the development oflung dysfunction (Ito et aI., 2003). Ischemia is often associated with mortality ratesmore than 60% and thus it represents a major challenging clinical problem (Lock,2001).Reviewing the literature re ,e1led that the intestinal mucosa in particular is oneof the most sensitive tissues to ischemia and ischemia reperfusion injury in the humanbody (Ikeda et aI., 1998; Kalia et aI., 2001). Although the histopathological alterationsin the intestinal mucosa after ischemic injury have been extensively described(Puglisi et al., 1995; Takeyoshi et al., 1996; Ikeda et al., 1998) yet most ofthe previous models of ischemia were achieved by complete occlusion of the superiormesenteric artery which often resulted in shock and early death of the experimentalanimalshence rendering it rather difficult to examine the delayed morphologicalchanges in the ischemic intestinal mucosa. Moreover. the intestinal segments distalto ischemia though clinically showed decreased contraction frequency. decreased relaxationresponses and altered responses to norepinephrine (Malone and Kanaan  2001) yet the morphological changes in locations distal to ischemia were not properlyinvestigated.Recently, the role ofmodulators particularly nitric oxide has received specialattention. It is hypothesized that nitric oxide might be involved in tissue protectionand provide partial preservation of intestinal mucosa as the first line of defense followingischemia reperfusion (Kalia et al., 20ot). Detection of nitric oxide could beachieved via the estimation of endothelial nitric oxide synthase (NOS) which is amember of a family of enzymes responsible for synthesis of nitric oxide from L arginineand molecular oxygen (Chan et al., 2002).Accordingly, it was the aim of the current work to illustrate the delayed morphologicaland morphometric changes following segmental ischemia and ischemiareperfusion produced by selective occlusion of terminal branches of superior mesentericartery. Moreover an attempt of detection of nitric oxide production wasachieved via the estimation of nitric oxide synthase. The changes in both the ischemicsegment as well as the segment distal to it were investigated. Such a study mightbe beneficial in post-ischemic resection anastomosis procedures, or in surgical revascularization.

THE DELAYED HISTOLOGICAL CHANGES OF SEGMENTAL ISCHEMIA AND ISCHEMIA - REPERFUSION ON THE JEJUNAL VILLI 01