| Ischemia - Reperfusion (I/R) injury is a limiting factor in pancreas transplatation. There are many reasons to cause pancreas injury in the I/R ,In these circumstance ,cell death can occur by either necrosis or apoptosis . Direct cell necrosis is consequent to anoxia or to the direct toxic effect of ROI . The necrosis cells, with the lysis of the membrance and the release of intracellular substance , can pontentate the inflammatory response in the surrounding tissue. In contrast, apoptosis is medicated by intra - and extracellular signal that induce a genetic response of these cells, leading to cell death with minimal alteration of tissue architecture, but the Oxygen - Derive Free radical producing and Calcium overloading are important metabolism in I/R . I/R injury is the consequence of Oxygen deprivation with decrease of cellular energy level followed by the production of toxic reactive oxygen intermediates (ROI) and recruiment and activation of leukocytes. Resultly, lead them to apoptosis and necrosis.Since ROI have been implicated in the pathogenesis of I/R injury ,many agents have been propose as ROI scavengers to reduce or prevent I/R - induced injury, we have recently shown that the PY( pyru-vate) inhibits intestinal, renal liver I/R injury in rats, PY is a 3 -carbon compound physiologically present in tissue and used by the cells as energy substrate during anaerobic glycolysis. PY has been shown to directly or indirectly act as an ROI scavenger by reactingwith hydrogen peroxide to form water carbon dioxide, thereby preventing the formation of the toxic hydroxyl ion. It has also been shown that PY can directly inhibit superoxide formation. This study aims to evaluate the protective effect of PY on pancreas I/R injury in rats.MATERIALS AND METHODSSixty male ACI rats (CMU Lab. center provide) weighing 200 -250g were used for the study. Rats were divided into two groups. Study animals were fed for 7 days with a liquid diet containing 15 mmol/day of PY, wheres control animals received the same liquid diet containing an isoenergetic amount of placeco ( glucose). Rats were anesthetized using inhalation of methoxyflurance for induction and in-traperitoneal injection of 25mg/kgsodium pentobarbital for maintain. Through a midlineancision, the pancreas was dissected free of its ligaments and artery, With a small vascular clamp as schematically indicated , after SOminule of ischemia of the median and 2,6 12hour of reperfusion. Samples from the parenchyma of pancreas was divided and part was immediately fixed , stain with H - E for light microscopy, while the rest was used to evaluate apoptosis cells with TUNEL. Additionally , at these time, examinate TNF - a by injucting vein blood and evaluate necrosis state. The results obtained were statistically e-valuated using the Students't test.RESULTS2hour AI after I/R was the most peak (PY:35. 34 ±4. 35: Control 48.45 ± ) , wheres 6hour AI after I/R in PY group was 25. 74 ±3.28;ControL 42. 59 ±9. 59 , The PY - treated group compare between 2 and 4hour , the count was significant ( P < 0. 05 ). TNF -cdevels in PY - treated group varied litter ( 13 ± 2. 02; 10. 51 ± 1. 57; 9. 82±2. 64) , wheres in control increased significantly ( 27. 16 . 91;19.44±3.43;56.73 ±6.44).Histolosic alteration of the pancreas after I/R was characterized as sinusoidal congestion and edema, vacuolization of pancreas, focal necrosis, and leukocyte infiltration in the control group. 2hour after reperfusion, the pancreas showed histologic alteration characterized by extensive coagulation necrosis, mostly localized around the centrolobu-lar zones. The pancreas were generally intact, but large sinusoidal dilatation and congestion were present. Necrotic pancreas showed marked eosinophilic and condensed cytoplasm, at 6and 12hour after reprefusion, the necrotic pancreas underwent lysis, being replaced with zones of coalescent necrosis.CONCLUSSIONThis study confirms previous observation that showed a protective effect of PY in numerous models of I/R. Since...
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