Open AccessINVOLVEMENT OF LIVER IN THE DECOMPENSATION OF HEMORRHAGIC SHOCK
Author(s) -
Frank Kobelt,
Ulrike Schreck,
H Henrich
Publication year - 1994
Publication title -
shock
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.095
H-Index - 117
eISSN - 1540-0514
pISSN - 1073-2322
DOI - 10.1097/00024382-199410000-00009
Subject(s) - decompensation , shock (circulatory) , medicine , ketone bodies , anesthesia , endocrinology , metabolism
In a hemorrhagic shock model without adequate volume resuscitation we investigated the question whether a biochemical stabilization of liver function by applying 2-mercaptopropionyl-glycine (2MPG) may influence the shock dynamics especially the transition from compensated to decompensated shock and the development of multiple organ failure (MOF). The application of a bolus of 10 mg/kg 2MPG just after hemorrhage had significantly beneficial effects on shock dynamics. All measured blood parameters demonstrate a less severe liver dysfunction. We found a decisive recovery of systemic pH, prolonged high levels of blood glucose, a better ammonia detoxification, arterial ketone ratios (acetoacetate/beta-OH-butyrat) above about 0.25, and a significantly increased survival time from 200 +/- 10 min to more than 240 min after hemorrhage. Decompensation of the 2MPG group started about 60 min after decompensation of the shock group. The transition to decompensation was combined in the shock group as well as in the 2MPG group with a severe liver dysfunction indicated by an arterial ketone ratio below .25. Decreasing levels of blood thiobarbituric reactive material in compensated shock of both groups demonstrate that production of free radicals did not primarily cause decompensation, but increasing levels of thiobarbituric reactive material during decompensation seems to be one of the factors mediating MOF. Our data support the hypothesis of the liver being a barrier against decompensation of shock and MOF.