[Reactive-inflammatory process in the spinal canal after implantation of autologous intervertebral disk cartilage].

The results of 6-month follow-up morphologic and immunomorphologic studies on 34 rabbits after the implantation of an autologous intervertebraldisk cartilage into the epidural space are presented. The data indicate of the reactive inflammatory process with a specific two-phase course of development. The cellular structure and the change of immunocompetent cell populations in the inflammation foci suggest the formation of hypersensitivity reaction 3 weeks after implantation.

[Effect of preliminary adaptation on 99mTc pyrophosphate accumulation and the development of structural changes in the heart muscle under stress].

It is established that preliminary adaptation of animals to physical exertion and short-term stress prevents the contracture and necrotic changes, as well as 99mTc-pyrophosphate accumulation in the heart muscle caused by durable emotional stress.

[Accumulation of 99mTc-pyrophosphate and structural changes in cardiac muscle during pharmacologic correction of stress injuries of the heart].

It has been established that natrium oxybutirate, prolactin, inderal and ionol affecting different links of pathogenetic chain of stress injury, efficiently prevent structural damage to cardiomyocytes and the accumulation of 99mTc-pyrophosphate in the myocardium.

[Evaluation of the protective effect of gamma-hydroxybutyric acid in stress].

Administration of GHBA during emotional stress reduces the stress syndrome that manifests in the lesser increase of the corticosterone content in blood plasma, while the noradrenaline level in the heart remains unchanged. GHBA prevents necrosis and contracture injuries of heart muscle cells during the stress. Quantitative evaluation of GHBA protective effect on the organism exposed to stress helped determine that the preliminary administration of GHBA reduces twofold the time necessary for the appearance of eosinophilia after eosinopenia.

[Lipid peroxidation activation and the focal contracture injuries in the myocardium under emotional-pain stress].

Emotional-pain stress reproduced in the form of so called anxiety-neurosis provokes long-term activation of lipid peroxidation associated with an increased content of its products in the myocardium and the development of focal lesions of the contracture type in myocytes. These heart lesions are likely to be related to the impairment of active calcium release from myofibrils due to lipid hydroperoxides-induced injury to cell membranes responsible for the cation transport. While progressing the morphologic changes in the heart reach maximum, i.