[A revised classification of hypoxic conditions]. / Utochnenie klassifikatsii gipoksicheskikh sostoianii.

The precised classification of circulatory hypoxia described in the paper is principally different from those published earlier by that it discriminates between hypoxia preconditioned by impaired cardiac-muscle constriction, on the one hand, and hypoxia due to malfunctions of smooth muscles (SM), on the other hand. The genesis of SM malfunctions is predetermined by impaired interactions of serotonin with SM serotonin receptors. The clinical use of serotonin adipinat reduces the local organic and total-tissue hypoxia in different pathologies and provides for better treatment results. The mentioned precised classification can be used to gain more data on the tissue-hypoxia pathogenesis and to schedule the clinical-and-experimental research on the purpose-oriented basis.

Role of serotoninergic structures in coordination of electric activity in the gastroduodenal complex.

Myoelectric activity in various portions of the stomach and duodenum in normal and after vagotomy and intravenous injection of serotonin adipinate was studied in acute experiments on cats. Vagotomy disturbed coordination of myoelectric activity in the stomach and duodenum. Intravenous injection of serotonin adipinate restored coordination and increased myoelectric activity in the stomach, particularly, in the pylorus. Under these conditions the pacemaker of myoelectric activity in the gastric corpus and autonomic regulation of the duodenum were preserved. Intravenous injection of serotonin adipinate most significantly changed myoelectric activity in the pylorus. Myoelectric activity in the cardia increased after vagotomy against the background of serotonin adipinate. Our findings suggest that serotoninergic structures maintain functional heterogeneity of digestive organs and coordinate their interrelationships.

[Endogenic vasomotor function and smooth muscle insufficiency in the vascular microcirculation]. / Makhanizm éndogennoi vazomotoriki i gladkomyshechnoi nedostatochnosti mikrotsirkuliatornogo rusla.

The paper outlines the previously unknown smooth muscle insufficiency in terms of its etiology, pathogenesis, diagnosis and treatment. It has been shown that drug administration leads to smooth muscle insufficiency which is eliminated by serotonin both in vitro and in vivo. The clinical manifestations of smooth muscle (SM) insufficiency are eliminated by serotonin, irrespective of whether it has been caused by the use of drugs or impaired smooth muscle innervation. The mechanism of vascular rhythmic oscillations in the microcirculatory bed, the so-called endogenous vasomotility (EV) has been decoded. The mechanism of EV regulation is due to the fact that platelets constantly (continuously) adsorb serotonin from the enterochromaffin cells of the gastrointestinal tract and constantly (continuously) release it into the microcirculatory bed, thereby providing the continuum of entry of the stimulant to the SM fibers which are able to contract at this time. The summation of these contractions of smooth muscle contractions in the microcirculatory bed maintains their vascular tone and yields the pattern of EV. The paper also describes the earlier unknown properties of hemoglobin and myoglobin to cause smooth muscle spasm and to accelerate platelet destruction. A correlation between the EV and vascular platelet hemostasis is described in terms of these properties. The continuous mechanism of EV is impaired and it transforms to intermittent (final) vascular platelet hemostasis.