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肝硬化大鼠部分肝切除术后残余肝脏中线粒体增强现象的缺失。

Absence of mitochondrial enhancement in the remnant liver after partial hepatectomy in cirrhotic rats.

作者信息

Morimoto T, Isselhard W

机构信息

Second Department of Surgery, Faculty of Medicine, Kyoto University, Japan.

出版信息

Res Exp Med (Berl). 1992;192(2):89-97. doi: 10.1007/BF02576262.

Abstract

Changes in energy metabolism after 70% partial hepatectomy were investigated in normal and carbon-tetrachloride-(CCl4)-induced-cirrhotic rats by evaluating hepatic mitochondrial ATP synthesizing activity as well as liver tissue levels of adenine nucleotides and lipid peroxide. Preoperative concentrations of ATP and total adenine nucleotides (TAN: ATP + ADP + AMP) in mumol/g dry weight (dw) and the energy charge potential (ECP) in the cirrhotic livers were 8.53 SEM 0.25, 14.73 SEM 0.54, and 0.74 SEM 0.01, respectively, and were significantly lower than those of normal livers (12.04 SEM 0.34, 15.75 SEM 0.12, and 0.86 SEM 0.01, P less than 0.01 in TAN). There was no difference in the preoperative mitochondrial phosphorylation rate (PR = x 10(-10) mol ATP/sec per mg mitochondrial protein) between normal and cirrhotic livers (21.01 SEM 0.95 and 21.55 SEM 1.03, respectively). After hepatectomy, in the normal livers these values decreased slightly after 12 h, remained low until 48 h, and returned to the preoperative value at 72 h. PR was remarkably enhanced and reached the maximum level of 32.54 SEM 2.07 at 24 h (P less than 0.001, compared to the sham-operated rats) and gradually returned to the preoperative value at 72 h. In the cirrhotic livers, ATP and ECP levels were drastically decreased at 12 h and recovered to the preoperative levels within 24 h, while TAN level remained unchanged. Enhancement of PR was not observed in any of the cirrhotic livers during the experiment. Lipid peroxidation was transiently increased postoperatively with no difference between normal and cirrhotic livers both in the sham-operated and the hepatectomized rats. These findings suggest that the energy status was more depressed in the cirrhotic livers than in normal livers both before and after hepatectomy. This depressed energy status might be attributed to the low preoperative tissue levels of adenine nucleotides and ECP level in the cirrhotic livers as well as to the absence of the enhancement of PR in the remnant livers.

摘要

通过评估肝线粒体ATP合成活性以及肝组织中腺嘌呤核苷酸和脂质过氧化物的水平,研究了正常大鼠和四氯化碳(CCl4)诱导的肝硬化大鼠在70%部分肝切除术后能量代谢的变化。肝硬化肝脏中ATP和总腺嘌呤核苷酸(TAN:ATP + ADP + AMP)的术前浓度以每克干重(dw)的微摩尔数计分别为8.53±0.25、14.73±0.54,能量电荷电位(ECP)为0.74±0.01,均显著低于正常肝脏(分别为12.04±0.34、15.75±0.12和0.86±0.01,TAN的P值小于0.01)。正常肝脏和肝硬化肝脏术前的线粒体磷酸化率(PR = x 10(-10) 摩尔ATP/秒/毫克线粒体蛋白)无差异(分别为21.01±0.95和21.55±1.03)。肝切除术后,正常肝脏中的这些值在12小时后略有下降,直到48小时一直保持较低水平,并在72小时恢复到术前值。PR显著增强,在24小时达到最高水平32.54±2.07(与假手术大鼠相比,P小于0.001),并在72小时逐渐恢复到术前值。在肝硬化肝脏中,ATP和ECP水平在12小时急剧下降,并在24小时内恢复到术前水平,而TAN水平保持不变。在实验过程中,任何肝硬化肝脏均未观察到PR增强。假手术和肝切除的大鼠术后脂质过氧化均短暂增加,正常肝脏和肝硬化肝脏之间无差异。这些发现表明,肝切除术前和术后,肝硬化肝脏的能量状态均比正常肝脏更受抑制。这种能量状态受抑制可能归因于肝硬化肝脏术前腺嘌呤核苷酸组织水平和ECP水平较低,以及残余肝脏中PR未增强。

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