Acute intestinal ischemia represents a broad spectrum of diseases with various
clinical and pathological manifestations. The primary causes of insufficient blood
flow to the intestine arc diverse and include thromboembolism, neoplasms, vasculitis,
abdominal inflammatory conditions, trauma, chemotherapy, radiation and corrosive
injury (Rha et aI., 2000). Despite of the advances in the pathophysiological, laboratory
diagnosis and imaging techniques acute intestinal ischemiais still one of
the major etiological causes of multiple organ failure (Schlichting et aI., 1995). Ischemia
induces continuous distrubance of hepatic microcirculation leading to liver
dysfunction (Nakamura et al., 2001). Furthermore, it triggers the development of
lung dysfunction (Ito et aI., 2003). Ischemia is often associated with mortality rates
more 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 one
of the most sensitive tissues to ischemia and ischemia reperfusion injury in the human
body (Ikeda et aI., 1998; Kalia et aI., 2001). Although the histopathological alterations
in the intestinal mucosa after ischemic injury have been extensively described
(Puglisi et al., 1995; Takeyoshi et al., 1996; Ikeda et al., 1998) yet most of
the previous models of ischemia were achieved by complete occlusion of the superior
mesenteric artery which often resulted in shock and early death of the experimental
animalshence rendering it rather difficult to examine the delayed morphological
changes in the ischemic intestinal mucosa. Moreover. the intestinal segments distal
to ischemia though clinically showed decreased contraction frequency. decreased relaxation
responses and altered responses to norepinephrine (Malone and Kanaan  2001) yet the morphological changes in locations distal to ischemia were not properly
investigated.
Recently, the role ofmodulators particularly nitric oxide has received special
attention. It is hypothesized that nitric oxide might be involved in tissue protection
and provide partial preservation of intestinal mucosa as the first line of defense following
ischemia reperfusion (Kalia et al., 20ot). Detection of nitric oxide could be
achieved via the estimation of endothelial nitric oxide synthase (NOS) which is a
member of a family of enzymes responsible for synthesis of nitric oxide from L arginine
and molecular oxygen (Chan et al., 2002).
Accordingly, it was the aim of the current work to illustrate the delayed morphological
and morphometric changes following segmental ischemia and ischemia
reperfusion produced by selective occlusion of terminal branches of superior mesenteric
artery. Moreover an attempt of detection of nitric oxide production was
achieved via the estimation of nitric oxide synthase. The changes in both the ischemic
segment as well as the segment distal to it were investigated. Such a study might
be beneficial in post-ischemic resection anastomosis procedures, or in surgical revascularization.