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Effect of Hypovolemic Hypotension on Plasma Proteins and Hepatic Energy Status in Jaundiced Rabbits

 

作者: Masayuki Yamamoto,   Kazue Ozawa,   Takayoshi Tobe,   Wolf Isselhard,  

 

期刊: European Surgical Research  (Karger Available online 1982)
卷期: Volume 14, issue 1  

页码: 45-55

 

ISSN:0014-312X

 

年代: 1982

 

DOI:10.1159/000128221

 

出版商: S. Karger AG

 

关键词: Plasma protein;Jaundice;Hypovolemic hypotension;Liver energy charge

 

数据来源: Karger

 

摘要:

Changes in plasma proteins and hematocrit (Ht) were studied in jaundiced rabbits subjected to hemorrhagic hypotension induced by the modified method of Wiggers and compared with changes in the hepatic energy status. At 48 h after common bile duct ligation, jaundiced rabbits showed hypoalbuminemia and a lower hepatic energy charge (EC), (ATP+1/2ADP)/(ATP+ADP+AMP). 30 min after induction of hypovolemic hypotension, in order to maintain a mean arterial pressure of 40 mm Hg, 86% of the blood collected in the reservoir (about 19 % of the normal whole blood volume) had to be successively reinfused over a 2-hour period. Despite increases in Ht and plasma total protein (p-TP) occurring in parallel with the reinfusion, plasma albumin (p-Alb) and the ratio of p-Alb to plasma globulin (A/G) did not increase. On the other hand, in sham-operated rabbits small amounts of blood had to be frequently removed during the first hour (about 34% of the normal whole blood volume), and only 34% of it had to be reinfused over a 2-hour period. Despite removal of more blood and a concomitant decrease in Ht, p-Alb and A/G ratio were higher than in jaundiced rabbits. After marked decreases in EC and total adenine nucleotides (TAN) due to the initial blood loss, EC recovered somewhat and remained higher in sham-operated rabbits than in jaundiced rabbits, whereas TAN did not recover in either group. This seems to indicate that hemodilution functions effectively to maintain microcirculation following hemorrhagic hypotension in sham-operated rabbits, while in jaundiced rabbits a rapid breakdown of protective homeostatic mechanisms results in the earlier deterioration of the hepatic energy status.

 

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