Pancreatitis-induced ascitic fluid and hepatocellular dysfunction in severe acute pancreatitis.
Pancreatitis-induced ascitic fluid and hepatocellular dysfunction in severe acute pancreatitis.
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重症急性胰腺炎中胰腺炎引起的腹水和肝细胞功能障碍。
DOI：
10.1006/jsre.1998.5539
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Takeyama,Y
中科院分区：
文献类型：
--
作者：
Ueda,T;Ho,HS;Anderson,SE;Takeyama,Y
多器官功能衰竭(MOF)是重症急性胰腺炎最严重的并发症，病死率高。高能磷酸盐、细胞内pH和细胞内阳离子稳态的变化与MOF所致肝细胞损伤密切相关。方法用31P和23Na核磁共振波谱测定DCA诱导的胰腺炎大鼠肝脏磷代谢产物、细胞内pH(Phi)和细胞内Na+浓度([Na+]i)。肝脏出现明显的细胞内酸中毒(pH=6.99±0.16)和钠负荷(75±9 mm)，能量状态降低(β-ATP/PI=0.2±0.0 3和PI=16 4±12)。健康大鼠IP注射PAF后，虽未出现全身性低血压，但肝细胞离子动态平衡严重失调，生物能量耗竭。腹部暴露于PAF的时间越长，变化越严重。注射PAF后3h，肝组织[Na+]i显著升高(42±3 mm)，pHi显著降低(7.30±0.03)。IP注射PAF后6h，肝β-ATP/Piratio降至0.34±0.0 5，PI值上升至97±2 7。结论PAF可引起肝细胞酸中毒，肝细胞内钠离子迅速积聚，肝细胞浆磷酸化能力受损，肝细胞对三磷酸腺苷的利用率增加。这些影响可能是坏死性胰腺炎所致肝功能障碍最终发展的原因。
BackgroundMultiple organ failure (MOF) is the most serious complication in severe acute pancreatitis, contributing to its high mortality. It has been suggested that changes of high-energy phosphates, intracellular pH, and intracellular cation homeostasis are closely related to hepatocellular injury associated with MOF.MethodsPhosphorus metabolites, intracellular pH (pHi), and intracellular Na+concentration ([Na+]i) were measured in rat liversin vivousing31P and23Na NMR spectroscopy after deoxycholic acid (DCA)-induced pancreatitis or intraperitoneal injection (ip) of pancreatitis-induced ascitic fluid (PAF).ResultsTwo hours after induction of DCA-pancreatitis, the liver experienced significant intracellular acidosis (pHi= 6.99 ± 0.16) and sodium loading (75 ± 9 mM) and a reduction in its energy state (β-ATP/Pi= 0.2 ± 0.03 and Pi= 164 ± 12). Although ip injection of PAF into healthy rats did not induce systemic hypotension, the livers under these conditions also developed severe disturbances in hepatocellular ion homeostasis and depletion of its bioenergetics. The longer the abdomen was exposed to the PAF, the worse the changes were. At 3 h after ip injection of PAF, hepatic [Na+]isignificantly increased (42 ± 3 mM) along with a significant decrease in pHi(7.30 ± 0.03). At 6 h after ip injection of PAF, the hepatic β-ATP/Piratio decreased to 0.34 ± 0.05 and Piincreased to 97 ± 27.ConclusionsPAF induced severe hepatocellular acidosis, rapid accumulation of hepatic intracellular sodium, impaired hepatic cytosolic phosphorylation potential, and increased hepatic utilization of ATP. These effects may account for the eventual development of liver dysfunction associated with necrotizing pancreatitis.
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影响因子：
15.9
作者：
GORES, GJ;NIEMINEN, AL;LEMASTERS, JJ
通讯作者：
LEMASTERS, JJ
健康大鼠和急性肝损伤大鼠对果糖负荷肝反应的体内外31P磁共振波谱研究
影响因子：
3.3
作者：
Wuhua Lu;S. Locke;M. Brauer
通讯作者：
M. Brauer
DOI：
10.1006/bbrc.1996.5777
发表时间：
1997-02-13
影响因子：
3.1
作者：
Gressner, AM;Lahme, B;Roth, S
通讯作者：
Roth, S
与出血性胰腺炎相关的出血性腹水的毒性。
影响因子：
--
作者：
C. Frey;H. N. Wong;D. Hickman;T. Pullos
通讯作者：
T. Pullos
影响因子：
11.2
作者：
M. Barry;J. Reynolds;A. Eastman
通讯作者：
M. Barry;J. Reynolds;A. Eastman