Minei J P, Fong Y, Marano M A, Moldawer L L, Jones W G, Wei H, Richardson R P, Yurt R W, Shires G T, Lowry S F
Department of Surgery, New York Hospital- Cornell Medical Center, New York 10021.
J Surg Res. 1989 Apr;46(4):311-6. doi: 10.1016/0022-4804(89)90193-5.
Hepatocellular membrane dysfunction, as indicated by depolarization of the membrane potential, occurs after acute injury and early bacteremia. To determine whether hepatocellular membrane dysfunction occurs in the setting of ongoing thermal injury and infection, Wistar rats were divided into four groups: (1) sham-burned, freely fed controls (FF); (2) rats sustaining approximately 30% total body surface area dorsal full-thickness scald burn (Burn); (3) rats sustaining burns as in group 2 followed by immediate inoculation of 1 x 10(8) CFU Pseudomonas aeruginosa (Burn/Inf); and (4) sham-burned rats pair-fed to the food intake of the Burn/Inf group (PF). On the third and seventh days postburn, body and liver weights were determined. In vivo hepatocellular transmembrane potentials were measured and hepatic ATP, RNA, DNA, and protein contents were assayed. By Day 7, despite greater weight loss in the Burn/Inf group than due to starvation alone (P less than 0.01 Burn/Inf vs FF and PF), hepatic mass was conserved. This was associated with hyperpolarization of the hepatic transmembrane potential (-46.6 +/- 1.5 vs -32.1 +/- 0.6 mV, Burn/Inf vs FF, P less than 0.01) and increases in RNA (141 +/- 9 vs 91 +/- 4 mg/liver, Burn/Inf vs FF, P less than 0.01) and DNA (37 +/- 5 vs 22 +/- 2 mg/liver, Burn/Inf vs FF, P less than 0.05) contents, with no change in ATP or hepatic protein contents. There was a significant hypercorticosteronemia observed in the Burn/Inf group (43 +/- 9 vs 2.8 +/- 0.7 micrograms/dl, Burn/Inf vs FF, P less than 0.01). This hepatic membrane hyperpolarization and augmented RNA content were not secondary to burn or starvation alone as the response in these groups was significantly less than that of the Burn/Inf group. It is suggested that this hepatic membrane hyperpolarization is one mechanism by which hepatic function is maintained during ongoing burn infection in the rat.
肝细胞细胞膜功能障碍，表现为膜电位去极化，发生在急性损伤和早期菌血症之后。为了确定在持续热损伤和感染的情况下是否会发生肝细胞细胞膜功能障碍，将Wistar大鼠分为四组：（1）假烧伤、自由进食对照组（FF）；（2）全身表面积约30%背部全层烫伤的大鼠（烧伤组）；（3）如第2组那样烧伤的大鼠，随后立即接种1×10⁸CFU铜绿假单胞菌（烧伤/感染组）；（4）假烧伤大鼠，按烧伤/感染组的食物摄入量进行配对喂养（PF组）。在烧伤后第3天和第7天，测定体重和肝脏重量。测量体内肝细胞跨膜电位，并测定肝脏ATP、RNA、DNA和蛋白质含量。到第7天时，尽管烧伤/感染组的体重减轻比单纯饥饿更严重（烧伤/感染组与FF组和PF组相比，P＜0.01），但肝脏质量得以保留。这与肝跨膜电位的超极化有关（-46.6±1.5对-32.1±0.6mV，烧伤/感染组与FF组相比，P＜0.01），以及RNA（141±9对91±4mg/肝脏，烧伤/感染组与FF组相比，P＜0.01）和DNA（37±5对22±2mg/肝脏，烧伤/感染组与FF组相比，P＜0.05）含量增加，而ATP或肝脏蛋白质含量没有变化。在烧伤/感染组观察到明显的高皮质醇血症（43±9对2.8±0.7μg/dl，烧伤/感染组与FF组相比，P＜0.01）。这种肝细胞膜超极化和RNA含量增加并非仅继发于烧伤或饥饿，因为这些组的反应明显小于烧伤/感染组。提示这种肝细胞膜超极化是大鼠在持续烧伤感染期间维持肝功能的一种机制。
