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Myocardial high-energy phosphates and hepatic redox state in jaundiced rats
K Katsuyama1, K M Ozawa, S Morikawa
1Second Department of Surgery, Molecular Neurobiology Research Center, Shiga University of Medical Science, Kitano Hospital, Seta Tsukinowa-cho, Shiga, Otsu, 520-21, Japan. katuyama@belle.shiga-med.ac.jp
Background:
The mechanism underlying the fatal complications in jaundiced states after shock has not been fully clarified. The present study was designed to examine the effect of hemorrhagic shock on myocardial high-energy phosphate stores and the arterial ketone body ratio (AKBR:acetoacetate/beta-hydroxybutyrate), which reflects the redox state of the liver mitochondria, in normal and jaundiced rats.
Materials And Methods:
At 1 week after ligation of the common bile duct, hemorrhagic shock was induced by exsanguination (mean arterial blood pressure = 40 mmHg) and maintained for 2 h. Serial changes in AKBR were measured. The myocardial adenine nucleotides phosphocreatine (PCr) and inorganic phosphate (Pi) were determined before and after hemorrhagic shock.
Results:
Before shock, myocardial ATP in the jaundiced group was lower than that in the sham group. However, the myocardial PCr levels in the two groups did not differ. After reinfusion of the shed blood, ATP and PCr recovered to the preshock levels in the sham group. However, ATP and PCr were further increased in the jaundiced group. At 60 min after reinfusion, AKBR recovered to the normal level in the sham group, but decreased below 0.7 in the jaundiced group. Metabolic acidosis was more severe in the jaundiced group than in the sham group.
Conclusions:
The decrease in AKBR indicated irreversible metabolic acidosis. As a result, fatal circulatory failure occurred, although the phosphoenergetic level in the myocardium was sufficiently maintained.