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1.
Eur Surg Res ; 46(4): 207-13, 2011.
Article in English | MEDLINE | ID: mdl-21525771

ABSTRACT

Decreasing ischemia-reperfusion injury in intestinal transplantation is of paramount importance for improving graft recovery and function. This study explores the ability of two ischemic preconditioning (IPC) regimens to reduce preservation injury. Sprague-Dawley rats were divided into 3 groups (n = 11 each). In the controls (group C), intestinal grafts were harvested and preserved. IPC was performed either through 4 cycles of mesenteric ischemia of 4 min each followed by 10 min of reperfusion (group BIPC) or 2 ischemic cycles of 12 min each followed by 10 min of reperfusion (group LIPC). Grafts were stored in histidine-tryptophan-ketoglutarate, and samples were taken 0, 3, 6, 9, 12, 18, and 24 h after preservation. Preservation injury was scored using the Park/Chiu scale. Goblet cells (GC), enteroendocrine cells (EEC) and serotonin-producing EEC (SPEEC) were studied for evaluation of the graft conditions. Group C had the most advanced preservation injury followed by group BIPC. GC count was lowest in group C, followed by BIPC. Comparison between groups BIPC and LIPC showed superior parameters (preservation injury, GC, EEC, and SPEEC) in LIPC. In conclusion, an IPC regimen of 2 ischemic cycles of 12 min each followed by 10 min of reperfusion distinctly decreased the preservation injury of intestinal grafts compared with non-manipulated grafts.


Subject(s)
Intestines/blood supply , Intestines/transplantation , Ischemic Preconditioning , Organ Preservation , Reperfusion Injury/prevention & control , Animals , Cell Count , Enteroendocrine Cells/cytology , Goblet Cells/cytology , Intestines/pathology , Male , Rats , Rats, Sprague-Dawley , Reperfusion Injury/pathology , Serotonin/biosynthesis
2.
Ann Transplant ; 14(3): 62-9, 2009.
Article in English | MEDLINE | ID: mdl-19644162

ABSTRACT

BACKGROUND: Intestinal transplantation (ITx) represents difficult life-saving intervention reserved for patients with irreversible intestinal failure. A serious complication of ITx is jejunal graft (JG) damage. The aim of the study was to evaluate the development of JG damage during ITx and determine the share of pathological elements (mechanical manipulation, ischemia, reperfusion) in this damage. MATERIAL/METHODS: Male Wistar rats (n=60; 30 donors and 30 recipients) were used. The harvest of JG as well as heterotopic allotransplantation was performed using a technique adapted from Balaz et al. (2003). In all transplantations, three samples of JG were obtained: immediately after harvest (Sa1), after preservation (Sa2) and 60min after transplantation (Sa3). The samples were stained using the Hematoxylin&Eosin method and histopathological injury index (HII) was assessed using Park/Chiu classification. For detection and quantification of neuroendocrine cells (NECs) Singh's modification of the Masson-Hamperl argentaffin technique was used. RESULTS: The lowest level of HII was detected in Sa1=0.25+/-0.18; higher after preservation Sa2=1.42+/-0.38 and the highest HII was observed after transplantation Sa3=3.08+/-0.38. The percentage share of mechanical manipulation with the graft in jejunal damage during ITx was 8.11% (Sa1), the share of the ischemic element represented 37.98% (Sa2) and reperfusion had 53.91% of the share in jejunal damage (Sa3). The activity of NECs had sinusoidal character (Sa1=0.5+/-0.1; Sa2=1.4+/-0.0; Sa3=0.35+/-0.05). CONCLUSIONS: The development of JG damage during ITx had progressive character. Mechanical manipulation had minimal influence on jejunal damage. One third of damage was caused by the ischemic component and the largest impact on JG damage resulted from reperfusion.


Subject(s)
Intestines/transplantation , Jejunum/injuries , Animals , Humans , Intestinal Mucosa/pathology , Intestines/pathology , Ischemia/pathology , Jejunum/blood supply , Jejunum/pathology , Jejunum/transplantation , Male , Neuroendocrine Cells/pathology , Rats , Rats, Wistar , Reperfusion Injury/etiology , Reperfusion Injury/pathology , Transplantation, Homologous
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