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Published on: March 22, 2024
BIOCHEMICAL STUDIES ON SHOCK : I. THE METABOLISM OF AMINO ACIDS AND CARBOHYDRATE DURING HEMORRHAGIC SHOCK IN THE RAT
F L Engel1, M G Winton, C N Long
1Department of Physiological Chemistry, Yale University School of Medicine, New Haven.
Abstract:
During and following the production of shock by hemorrhage in the normal, suprareno-demedullated, and suprarenalectomized rat, the following significant changes in amino acid and carbohydrate metabolism have been observed. 1. In the intact, suprareno-demedullated, and suprarenalectomized rat there is a progressive rise in the whole blood and plasma amino acid nitrogen levels during and after a fatal, shock-inducing hemorrhage. The rate of rise varies inversely with the survival time. In animals surviving the hemorrhage there is little or no elevation in whole blood amino acid levels during the 8 hours following hemorrhage, and a decrease in 24 hours due to hemodilution. The plasma amino acids, however, rise slightly. 2. The blood amino acid nitrogen elevation occurs only after the blood pressure has fallen to between 85 and 90 mm. of Hg. 3. The blood keto acids, as pyruvate, and the blood lactate become elevated during shock in the normal, suprareno-demedullated and suprarenalectomized rat. 4. In the normal fasted rat with low liver glycogen stores the blood sugar may rise moderately or may not rise at all during hemorrhagic shock. In animals with high liver glycogen levels (fed rats or fasted rats previously fed high protein diets) shock generally induces a marked hyperglycemia. In both groups hypoglycemia may occur terminally. 5. In the suprareno-demedullated and suprarenalectomized rats shock is always accompanied by a fall in the blood sugar. 6. There is no significant difference between the liver glycogen levels of suprareno-demedullated rats fasted 48 hours and those similarly fasted but surviving 24 hours after a hemorrhage. The blood chemical changes have been interpreted as due to a decrease in hepatic function resulting from early anoxia of the liver and to the later effects of anoxia on the peripheral tissues causing an increased rate of protein breakdown and of glucose utilization and an accumulation of lactate and pyruvate in the blood and tissues.
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