J.Jpn. Surg. Soc.. 79(6): 453-472, 1978

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Original article

HEPATIC HEMODYNAMIC AND METABOLIC CHANGES FOLLOWING CANINE ENDOTOXIN SHOCK: COMPARISON WITH HEMORRHAGIC SHOCK

We examined the hepatic dysfunction within two weeks after surgical shock in 207 patients and noticed that its incidence was much higher in septic shock (17%) than in hemorrhagic shock (7.4%). In 17 cases of gram-negative bacteremic shock, we also found six cases of severe hypoglycemia less than 60 mg/dl.
To elucidate the pathophysiology of the liver in septic shock, we studied at first the serum hepatic enzyme levels, hepatic blodo flow changes and hepatic glucose output in canine endotoxin shock, compared with canine hemorrhagic shock. In dogs administered 3 mg/kg E. coli endotoxin, levels of serum GOT, Al-Pase and LDH increaseds harply within a few hours, whereas these values did not change significantly in hemorrhagic shock maintained at 50-60 mmHg mean arterial blood pressure for 4 hours. While blood glucose levels in hemorrhagic shock showed consistent hyperglycemia more than 200mg/dl for 6 hours, progressive hypoglycemia was characteristic in endotoxin shock soon after the transient initial hyperglycemia.
Although cardiac output (CO) and total hepatic blood flow (HBF) decreasedl argely in the course of both shock, hepatic fracti on of CO in hemorrhagic shock was mostly constant at 36% all through the experiment, whereas the hepatic fraction in endotoxin shock was gradually decreased from 36% before shock down to 28% two hours after endotoxin administration. These results suggested hepatic ischemia following endotoxin shock might be more severe than hemorrhagic shock, especially in terms of greater reduction of portal venous flow.
We also obtained the differences of blood glucose concentrations between hepatic and portal venous blood during shock. These differences were rapidly enlarged and maintained at high levels at least for 4 hours in hemorrhagic shock, but these values in endotoxin shock were diminished progressively soon after the initial transient increase, suggesting the depression of hepatic gluconeogenesis. The role of these hepatic hemodynamic and metabolic changes in pathophysiology of shock was discussed in detail.
Pretreatment of large doses of dexamet has one in endotoxin shock increased the hepatic fraction of cardiac output as well as the differences between hepatic and portal venous blood glucose levels, and showed protective effect against generalc irculatory and metabolic deteriolations.

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