Search

The experiments on rats with model traumatic disease showed that melatonin administration produces a dose-dependent positive effect, decreasing the degree and duration of disturbances in platelet hemostasis.

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.

It was shown in experiments on dogs who experienced death from blood loss that regulation of glucocorticoid secretion changes in phases. The changes are characterized by its disturbance in the first 3 days and a tendency to restoration 7 days after return to life. Disorders of function of the hypothalamo-hypophyseal-adrenal system were attended by a change of the intensity of metabolic processes in the leukocytes which depended on the duration of the circulatory arrest. On the 7th day of the postresuscitation period "dexamethasone depression" caused morphological and cytochemical changes of the leukocytes, which resembled those in intact animals.

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.

The reactivity of the autonomous nervous system (ANS) was analysed pharmacologically with phenylephrine hydrochloride and D-L-Dopa in experiments on dogs who experienced 1-, 5-, and 10-minute clinical death. In changes of the pronounced character of the postresuscitation damages to the central nervous system, the changes of the ANS differed not only in intensity but also in the trend. Reactivity from sympatho- and parasympathetic types changed in the direction of vegetative equilibrium and atypical reactions. The occurrence of the last named on the first day after 5- and 10-minute clinical death were an absolute prognostic criterion of unfavourable outcome of resuscitation. Disorders of the synthetic capacity of the sympathoadrenal system in increase of the period of circulatory arrest were very important in ANS dysfunction.

Pharmacological analysis of the functioning of mechanisms responsible for central regulation of temperature homeostasis in the postresuscitation period has been performed in experiments on dogs survived after clinical death of various duration. Thermoregulation disturbances after clinical death are caused by impaired mediator relationships in the CNS and sensor function of thermosensitive hypothalamus neurons. The mechanisms of thermoregulation disturbances are of multifocal nature and are to a great extent dependent on the degree of brain damage in critically ill patients.

Morphological and biochemical indexes of peripheral erythron compartment have been analysed 1, 3, 7 and 14 days after severe mechanical traumas of various locations in human patients, after 5- and 10-min clinical death in dogs and after rotatory polytrauma in rats. It has been shown that rehabilitation period along with usual anemization is characterized by enhanced penetration of newly formed erythrocytes (hyperchromic, fetal, lipoperoxidation-resistant forms) into the circulation. In pathologies with predominant damage of the central nervous system regenerative response of the bone marrow is less marked and normalization of hematologic parameters is less prompt. As erythron changes always take place in terminal and postresuscitation conditions, irrespective of the etiology and species, they are regarded as a typical pathological process.

Administration of dexamethasone (dexasone) to dogs against the background of dysfunction of the hypothalamic-pituitary-adrenal system (HPAS) developing in the first three days of the postresuscitation period causes diverse changes in secretion of hormones of the pancreas. At a relative normalization of HPAS functioning noted 7 days after resuscitation the drug was shown to decrease intensity of glycolysis and processes of lipid peroxidation.