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AIM:To investigate the effect of epidural anaesthesia(EA)on pancreatic microcirculation during acute pancre-atitis(AP).METHODS:AP was induced by injection of sodium tau-rocholate into the pancreatic duct of Sprague-Dawleyrats.To realize EA,a catheter was introduced into theepidural space between T7 and T9 and bupivacaine wasinjected.Microcirculatory flow was measured by laserDoppler flowmetry.Arterial blood gas analyses were per-formed.At the end of the experiment(≤5 h),pancreaswas removed for histology.The animals were dividedinto three groups:Group 1(n=9),AP without EA;Group2(n=4),EA without AP;and Group 3(n=6),AP treatedby EA.RESULTS:In Group 1,pancreatic microcirculatory flowprior to AP was 141±39 perfusion units(PU).After AP,microcirculatory flow obviously decreased to 9±6 PU(P<0.05).Metabolic acidosis developed with base ex-cess(BE)of-14±3 mmol/L.Histology revealed exten-sive edema and tissue necrosis.In Group 2,EA did notsignificantly modify microcirculatory flow.BE remainedunchanged and histological analysis showed normal pan-creatic tissue.In Group 3,AP initially caused a significantdecrease in microcirculatory flow from 155±25 to 11±7PU(P<0.05).After initiation of EA,microcirculatory flow obviously increased again to 81±31 PU(P<0.05).BE was-6±4 mmol/L,which was significantly differentcompared to Group 1(P<0.05).Furthermore,histologyrevealed less extensive edema and necrosis in pancreatictissue in Group 3 than that in Group 1.CONCLUSION:AP caused dramatic microcirculatorychanges within the pancreas,with development of meta-bolic acidosis and tissue necrosis.EA allowed partialrestoration of microcirculatory flow and prevented devel-opment of tissue necrosis and systemic complications.Therefore,EA should be considered as therapeutic op-tion to prevent evolution from edematous to necrotic AP.
AIM: To investigate the effect of epidural anaesthesia (EA) on pancreatic microcirculation during acute pancreat-atitis (AP). METHODS: AP was induced by injection of sodium tau-rocholate into the pancreatic duct of Sprague-Dawleyrats. To realize EA, a catheter was introduced into the epidural space between T7 and T9 and bupivacaine was injected. Microcirculatory flow was measured by laser Doppler flowmetry. Arterial blood gas analyzes were per- formed. At the end of the experiment (≤ 5 h), pancreaswas removed for histology. animals Groups 2 (n = 4), EA without AP; and Group 3 (n = 6), AP treated by EA.RESULTS: In Group 1, pancreatic microcirculatory flowprior to AP was 141 ± 39 perfusion units (PU). After AP, microcirculatory flow decreased decreased to 9 ± 6 PU (P <0.05). Metabolic acidosis developed with base ex-cess (BE) of -14 ± 3 mmol / L. Histology revealed exten-sive edema and tissue necrosis.In Group 2, EA did not significantly modify microcirculatory flow.BE remaine dunchanged and histological analysis showed normal pan-creatic tissue.In Group 3, AP initially caused significant depletion in microcirculatory flow from 155 ± 25 to 11 ± 7 PU (P <0.05) .After initiation of EA, microcirculatory flow increased again to 81 ± 31 PU (P <0.05) .BE was-6 ± 4 mmol / L, which was significantly differentcompared to Group 1 (P <0.05) .Furthermore, histologyrevealed less extensive edema and necrosis in pancreatic lesion in Group 3 than that in Group 1. CONCLUSION: AP caused dramatic microcirculatory changes within the pancreas, with development of meta-bolic acidosis and tissue necrosis. EA allowed partialrestoration of microcirculatory flow and prevented devel-opment of tissue necrosis and systemic complications. Before, EA should be considered as therapeutic op- tion to prevent evolution from edematous to necrotic AP.