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L Cicalese

Publications and source records attributed to L Cicalese.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Bacterial translocation and its surgical implications].

The passage of viable bacteria through epithelial mucosa into lamina propria and then to mesentheric lymphnodes, and possibly other tissues was defined bacterial translocation (BT) by Berg and Garlington. The transepithelial passage of bacteria out of the intestinal lumen seems to occur in a variety of surgical conditions, and it is suspected to be involved in systemic inflammatory response syndrome, sepsis and multiorgan failure. There is increasing evidence that many nosocomial infections are caused by enteric translocating microorganisms, although the exact incidence of BT in humans is difficult to establish. Consensus is emerging that the barrier function of the gut is relevant in established critical illness and in patients at risk of developing sepsis and clinical studies have provided strong evidence that systemic infections often originate from intestinal flora in high risk patients. So the suspect of BT is made when there is infection after trauma, burns, major surgery, chemotherapy and immuno suppression. Bacterial translocation is also associated with organ transplantation, especially with small bowel transplantation. The Authors have summarized published experimental and clinical studies that have tried to understand the occurrence, mechanisms and effects of this complex process. At the present time there is a near full understanding of the relevance of BT like an interplay of diverse factors in a physiologically, immunologically and microbiologically complex intestinal tract. However additional experimental and clinical studies are needed to clarify the relationship between these phenomena and the development of sepsis or multiple organ dysfunction syndrome.

Bacterial Infections↗
PubMed1998

Phenotypic and functional characteristics of intestinal intraepithelial lymphocytes during acute rejection of small intestinal allografts.

Infiltration of a transplanted organ by host lymphoid cells is the hallmark of acute rejection. However, after intestinal transplantation, physiological lymphocyte migration may lead to host cell infiltration of the graft even in the absence of rejection. It is unclear whether this lymphocyte migration also involves the intraepithelial compartment of the graft or whether infiltration there is indicative of acute rejection. We demonstrate here that host cell infiltration of the intestinal mucosa occurs both during acute rejection of a small bowel allograft and, to a lesser extent, when rejection is prevented by immunosuppression with FK506. The infiltrating host cells consisted of CD3+ T cells with a predominant CD4-CD8+ phenotype resembling intraepithelial lymphocytes (IELs). Functional studies showed that the nonspecific cytolytic activity of IELs was not affected by acute rejection or by immunosuppression with FK506. These findings indicate that host cell infiltration of the intestinal mucosa does not connote an ongoing acute rejection. Furthermore, the decreased mucosal barrier function during acute rejection of intestinal allgrafts is probably not due to impaired cytolytic activity of IELs.

Animals↗
PubMed1996

Oxygen free radical content and neutrophil infiltration are important determinants in mucosal injury after rat small bowel transplantation.

Mucosal injury is an immediate event following revascularization of small intestinal grafts in the context of transplantation (SBTx). The generation of oxygen free radicals (OFR) and tissue infiltration by activated neutrophils are consequences of ischemia and reperfusion and known causative factors of tissue injury; to delineate their role in the reperfusion injury occurring after cold preservation of the intestine and subsequent transplantation was the aim of this study. Prior to orthotopic SBTx in Sprague-Dawley rats, grafts were stored in cold (4 degrees C) Ringer's lactate solution for 1 (n=6), 2 (n=7), and 4 hr (n=7). Small bowel biopsy specimens were obtained before harvesting, at the end of the (cold) ischemic period and immediately before unclamping (i.e., before revascularization) and 30, 60, 120 min, and 24 hr after transplantation to evaluate tissue injury by histology, OFR production, (measured by luminol-enhanced chemiluminescence [LCL]), and the degree of neutrophil infiltration by myeloperoxidase staining. Reperfusion of the graft significantly worsened the histologically graded mucosal injury compared with that seen before unclamping. However, 24 hr after engraftment, mucosal morphology was restored almost completely. OFR production increased significantly during the early phases of reperfusion (30, 60, and 120 min) and returned to control values after 24 hr. Reperfusion of the graft was associated with a marked increase in the number of mucosal neutrophils. The present study indicates that OFR production and neutrophilic infiltration commence and progressively increase with graft reperfusion. These changes parallel the mucosal injury. Ischemic intervals of 4 hr were not associated with a statistically significant greater ischemic-injury patterns compared with 1- and 2-hr intervals. The profound changes associated with reperfusion probably overshadow the minor, yet likely, progressive injury patterns associated with longer ischemia times.

Animals↗
PubMed1996

Pyruvate prevents ischemia-reperfusion mucosal injury of rat small intestine.

BACKGROUND: Since reactive oxygen intermediates (ROI, or free radicals) have been implicated in the pathogenesis of ischemia-reperfusion injury of the small bowel, we evaluated the pretreatment effect of pyruvate, a 3-carbon compound recently shown to inhibit superoxide production, on reperfusion mucosal injury in the rat. METHODS: The small bowel of the ACI rat (n = 6) was divided into 2 5-cm segments, and 10 mL of a liquid diet containing pyruvate (0.32 g) or placebo (0.26 g) was instilled into the lumen of one of the segments for 10 minutes. The bowel was then made completely ischemic for 45 minutes by clamping the superior mesenteric artery, which was followed by 60 minutes of reperfusion. RESULTS: The production of ROI in bowel biopsy samples, estimated by luminol-enhanced chemiluminescence, was at least 80% decreased in the segment containing pyruvate compared with placebo immediately after ischemia (time 0), and compared with 30 and 60 minutes of reperfusion (P < 0.05 for each time point). After 60 minutes of reperfusion, the bowel segment containing the placebo diet showed villus sloughing with destruction of lamina propria and crypts, and mucosal neutrophil infiltration had increased by 80%. Electron microscope evaluation revealed a reduction in number and size of microvilli, dilatation of intercellular spaces, and intracellular vacuoles. The bowel segment containing pyruvate showed the villi and crypts to be intact, without enhanced neutrophil infiltration. CONCLUSION: Pyruvate pretreatment of the rat small bowel inhibits postischemic reperfusion mucosal histologic injury, neutrophil infiltration, and ROI production.

Animals↗
PubMed1995

Mucosal perfusion and reactivity of the rat small intestinal allograft.

During acute rejection (AR), the endothelial targeting seen in the mucosal vessels of the intestinal allograft (IA) could impair the blood supply and response to luminal stimuli. To study the effect of AR in the perfusion and reactivity of the IA mucosa, we measured the mucosal blood flow in the ileum (IL) of 2 groups of control rats (Lewis and ACI) and in the native and grafted IL of syngeneic (ACI to ACI) and allogeneic (donor ACI to recipient Lewis) rats. Using reflectance spectrophotometry and laser-Doppler flowmetry, parameters of mucosal oxygen saturation (ISO2), hemoglobin content (IHB), and blood flow (FLOW) were obtained at baseline and after saline and 50% dextrose (D50) stimulation. When compared to controls, the isograft IL had similar perfusion (ISO2, IHB, and FLOW). The allograft IL showed ischemia (similar ISO2, and lower ISO2 and FLOW). In the allografts, the ISO2 and FLOW were lower than in the isografts. In response to D50, the native IL of all groups showed an increased IHB and FLOW (hyperemia); the isografts showed an increase only in IHB (partial response); the allografts did not show any response at all. In summary, the mucosal perfusion in the rejecting allografts, but not in the isografts, showed ischemia. The response to D50 seen in the native ilea was only partial in the isografts and absent in the allografts. Because these changes occurred before the onset of mucosal ulcerations, we postulate that they could be used as early indicators of AR.

Animals↗