Ho H S, Ueda T, Liu H
Department of Surgery, University of California, Davis School of Medicine 95817-2214, USA.
Surgery. 1998 Aug;124(2):372-9.
Liver dysfunction may be an early event or the end result of multiple organ dysfunction (MOD) in necrotizing pancreatitis. This study measured the early changes in hepatocellular ions and energetics associated with such conditions.
Twenty-five rats, prepared with a 23Na and 31P double-tuned nuclear magnetic resonance surface coil secured over the dome of the liver, were randomized into 5 groups: control, 10 and 20 minutes of total inflow ischemia, pancreatitis induced by deoxycholic acid (DCA), and sham-DCA (saline injection). Dysprosium-TTHA3- solution was used to separate the intracellular and extracellular sodium peaks.
In rat liver, 20 minutes of total inflow occlusion caused irreversible depletion of high-energy phosphates. Changes at 2 hours after the onset of DCA-pancreatitis are compared with changes after 20 minutes of ischemia (mean +/- SEM). Although the DCA-pancreatitis animals did not become hypotensive until 1 hour after the induction of pancreatitis, the changes in hepatic intracellular ions and energetics began soon after such an insult. At 2 hours after the onset of pancreatitis, hepatocellular pHi and [NA+]i were 6.99 +/- 0.16 and 78.4 +/- mmol/L, respectively (P < .01, compared with sham animals). A similar pattern of changes in hepatic bioenergetics also occurred. After the onset of pancreatitis, the hepatic cytostolic phosphorylation potential decreased with time (y = 0.654 - 0.004t, where t is time in minutes and r2 = 0.967 and the rate of hepatic hydrolysis of adenosine triphosphate increased progressively (y = 0.702t + 91.363, where t is time in minutes and r2 = 0.969. These changes correlated well with the accumulated [Na]i.
Unresuscitated necrotizing pancreatitis caused severe hepatocellular acidosis, profound sodium accumulation, and bioenergy depletion early in its course. These effects were as severe as those induced by total liver ischemia. Liver dysfunction may be an early, not terminal, event of MOD in necrotizing pancreatitis.
肝功能障碍可能是坏死性胰腺炎中多器官功能障碍（MOD）的早期事件或最终结果。本研究测量了与此类情况相关的肝细胞离子和能量代谢的早期变化。
25只大鼠，用固定在肝圆顶上的23Na和31P双调谐核磁共振表面线圈制备，随机分为5组：对照组、全血流缺血10分钟和20分钟组、脱氧胆酸（DCA）诱导的胰腺炎组和假DCA组（注射生理盐水）。使用镝 - TTHA3 - 溶液分离细胞内和细胞外钠峰。
在大鼠肝脏中，20分钟的全血流阻断导致高能磷酸盐不可逆消耗。将DCA诱导的胰腺炎发作后2小时的变化与缺血20分钟后的变化进行比较（平均值±标准误）。尽管DCA诱导的胰腺炎动物直到胰腺炎诱导后1小时才出现低血压，但肝细胞内离子和能量代谢的变化在这种损伤后不久就开始了。胰腺炎发作后2小时，肝细胞内pH值和[Na + ]i分别为6.99±0.16和78.4±mmol/L（与假手术动物相比，P < 0.01）。肝脏生物能量代谢也出现了类似的变化模式。胰腺炎发作后，肝细胞胞质磷酸化电位随时间下降（y = 0.654 - 0.004t，其中t为时间，单位为分钟，r2 = 0.967），三磷酸腺苷肝水解速率逐渐增加（y = 0.702t + 91.363，其中t为时间，单位为分钟，r2 = 0.969）。这些变化与积累的[Na]i密切相关。
未复苏的坏死性胰腺炎在病程早期导致严重的肝细胞酸中毒、大量钠蓄积和生物能量消耗。这些影响与全肝缺血诱导的影响一样严重。肝功能障碍可能是坏死性胰腺炎中MOD的早期而非终末期事件。
