Search

Within the early period after clinical death of various duration, hyperglycemia developed in dogs as a result of increased secretion of catecholamines; the rate of hyperglycemia depended on the severity of postresuscitation impairments of the central nervous system. Content of blood glucose was increased simultaneously with elevation of insulin production. Within 1-2 hrs after administration of dihydroxyphenylalanine the excessive secretion of catecholamines altered adrenoreceptor system sensitivity in Langerhans islands with the subsequent decrease in insulin production. Content of cAMP in brain of resuscitated dogs as compared with controls was increased less drastically.

Hyperglycemia, caused by elevated levels of glucagon simultaneously with inhibition of the hypophysis-hypothalamus-adrenal system, was developed in dogs after clinical death of various duration within the first hour of recirculation. Hyperlactemia produced under these conditions contributed to an increase in catabolism of purines followed by stimulation of lipid peroxidation in erythrocyte membranes. Beginning from the end of the first day of the postresuscitation period the intensity of these processes was decreased and gradually reached the control values.