THE DELAYED HISTOLOGICAL CHANGES OF SEGMENTAL ISCHEMIA AND ISCHEMIA - REPERFUSION ON THE JEJUNAL VILLI 01<' RABBITS | ||||
| The Egyptian Journal of Anatomy | ||||
| Article 3, Volume 26, Issue 2, July 2003, Page 45-86 PDF (2.32 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/ejana.2003.5880 | ||||
 View on SCiNiTO | ||||
| Author | ||||
| Shahira Youssef | ||||
| Anatomy Department. Faculty of Medicine, Ain Shams University | ||||
| Abstract | ||||
| 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. | ||||
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