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Biomedical subjects

V N Pirogov

Publications and source records attributed to V N Pirogov.

8 recordsLinked to original sources

[Plasmapheresis and hormone therapy in severe forms of Guillain-Barré syndrome].

Patients with severe Guillain-Barre syndrome were entered into 2 groups: group I was treated with hormones alone, group II with hormones plus plasmapheresis. The results were not significantly different. In view of recognized effectiveness of plasmapheresis for treatment of the syndrome, corticosteroid addition is inappropriate.

Adolescent

[Thrombolytic therapy with streptodekase in ischemic strokes].

Thrombolytic agents previously employed in the treatment of ischemic stroke were associated with adverse side-effects and hemorrhagic complications. The use of streptodekase (S), a Soviet trombolytic drug, which is a long-acting immobilized ensyme proved to be highly effective. The efficacy of S in ischemic stroke was not investigated. The authors report the use of S within the first 6-8 hours after an ischemic stroke in thrombosis of the main stem of the middle meningeal artery in one case and of the vertebral and main arteries with the development of the locked-in syndrome in the other. In both cases the administration of S led to thrombolysis and restoration of the blood flow. The authors discuss the results of the use of S and indicate the necessity of the earliest possible administration of the drug with regard to a high sensitivity of the brain to ischemic lesions.

Brain Ischemia

[Expression of NADPH-diaphorase in the peripheral nerve and its changes at different stages of diphtheritic polyneuropathy].

Distribution and intensity of NADPH-d reactivity, a marker for enzyme of the nitric oxide synthesis, in nervus suralis biopsies in severe DP were studied at light and electron microscopic levels. The study of control specimens has shown that NADPH-d reactivity was permanently present in Schwann cells (SC) and was distributed in all parts of their cytoplasm. Axon and myelin were devoid of NADPH-d reactivity. A decrease of enzyme reactivity in SC cytoplasm of the damaged nerve fibers and rising enzyme reactivity in the cytoplasm of activated SC were observed in DP. High reactivity in SC of small fibers was found at earlier stages and that of thick fibers at later stages. This distinction reflected, apparently, sequence of entering at first thin, then thick fibres in the reparative process. Under the electron microscope, the reaction product was deposited on membranes of endoplasmic reticulum, nuclear membrane and Golgi complex. The enzyme was also located in nucleus of activated SC. Ultrastructural location and the fact that the highest intensity of reaction is present in SC of nervous fibres with morphological signs of remyelination suggest link of this enzyme with the reparative process. This study provides the first evidence of NADPH-d reactivity in SC and shows that NADPH-d histochemistry is a useful tool for peripheral nerve biopsies study.

Diphtheria

[Course of apallic syndrome after clinical death during anesthesia].

Anesthesiological errors after clinical death during narcosis for strumectomy are considered. These errors were continuation of surgery after systole, inadequate management of the systemic arterial pressure and cerebral circulation after global ischemia, early switch-off of artificial ventilation of the lungs. All these steps led to prolonged coma, development of the apallic syndrome, and invalidism of the patient.

Adult

[Diphtheritic polyneuropathy: clinico-morphologic study].

18 patients with grave DP treated with a long-term artificial pulmonary ventilation and feeding through a naso-gastric probe were studied. Biopsies of n. suralis taken at different periods after the appearance of the first signs of DP (from the 19th to the 69th day) were studied at light and electronic microscopy. The basis of DP is toxic myelopathy with paranodal demyelination mainly in the large myelinated neural fibers and a segmentary one in the smaller neural fibers. Axonal degeneration was observed in the gravest cases of DP and was secondary being the result of axon squeezing by a folded myelin and voluminous Schwann cell cytoplasm invaginated into the axon. In no case of DP inflammatory changes and(or) involvement of the immunocompetent cells were found. There was pronounced proliferation and activation of Schwann cells due to intensive utilization of the degradation products of myelin and remyelinization. Morphological signs of remyelinization were observed on the 35th day of DP in the presence of enhancing neurological symptoms. But remyelinization was not complete even on the 69th day of DP.

Adult