Abstract

The purpose of the paper was experimental study of activity of energy production of the heart, liver and kidney after harmful action of general vibration with 8 and 44 Hz frequency. The functional state of native mitochondria in tissue homogenates was studied by polarographic method by means of closed oxygen device of halvanic type in thermostated cuvette of 1 ml volume in the salt medium of incubation. Metabolic states of mitochondria of the rabbit heart, liver and kidney were modeled in vitro in oxidation of endogenous substrates (before and after administration of inhibitors of different stages of breath chain) varying exogenous substrates (before and after administration of 2.4-DNP into the cell). In order to synchronize the changes in short time, the incomplete cycle of metabolic states “endogenous breath → rest → activity” was used. The velocity of mitochondrial oxidation of endogenous substrates was determined by tissue type, and was 16.3 ± 4.3, 5.2 ± 0.6 and 8.13 ± 1.4 ng-atom О min-1mg-1 protein for the heart, liver and kidney of intact animals respectively. In the heart, after high frequent vibration, the reduction of oxidation velocity of NAD-dependent substrates in rest and in active metabolic state of mitochondria was 43 % (р ≤ 0.05) and 30 % (р ≤ 0.01) respectively, while the velocity of oxidation for endogenous succinic acid increased by 77 % (р ≤ 0.05) to 21st session of vibration, then constantly decreasing to the end of vibration sessions. The same changes but in less degree were registerted in the liver and kidney. The systems of energy production of the heart and the studied parenchimatic organs were involved in reaction on vibration exposure and reacted typically by low energetic shift with hyperactivation of endogenous succinic acid system of oxidation and inhibition of NAD-depended part of the breath chain of mitochondria. Therefore, the study of bioenergetics mechanisms of hypoxia in different tissues allows to clear the molecular targets for pharmacological action by means of substrate antihypoxants.

Highlights

  • The velocity of mitochondrial oxidation of endogenous substrates was determined by tissue type, and was 16.3 ± 4.3, 5.2 ± 0.6 and 8.13 ± 1.4 ng-atom О min–1mg–1 protein for the heart, liver and kidney of intact animals respectively

  • After high frequent vibration, the reduction of oxidation velocity of NAD-dependent substrates in rest and in active metabolic state of mitochondria was 43 % (р ≤ 0.05) and 30 % (р ≤ 0.01) respectively, while the velocity of oxidation for endogenous succinic acid increased by 77 % (р ≤ 0.05) to 21st session of vibration, constantly decreasing to the end of vibration sessions

  • The same changes but in less degree were registerted in the liver and kidney

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Summary

НAУчНЫЕ ОБЗОРЫ

Тканеспецифические особенности вибрационноопосредованной гипоксии сердца, печени и почки кролика. Резюме Целью работы явилось экспериментальное изучение активности системы энергопродукции сердца, печени и почки кролика при неблагоприятном действии общей вибрации с частотой 8 и 44 Гц. Системы энергопродукции сердца и паренхиматозных органов, вовлекаясь в ответную реакцию на воздействие вибрации, претерпевали качественно однотипные изменения функциональной активности по типу низкоэнергетического сдвига с гиперактивацией системы окисления янтарной кислоты и торможением НАД-зависимого звена дыхательной цепи митохондрий. Несмотря на то что в ряде экспериментальных работ доказана вибрационно-опосредованная трансформация энергетического обмена [94,95,96,97,98], роль нарушения тканевой биоэнергетики в развитии вибрационно-обусловленных миокардиодистрофии и висцеропатий остается изученной недостаточно, поэтому для повышения эффективности профилактических и лечебных мероприятий [58, 67, 95] целью исследования явилось изучение тканеспецифических особенностей биоэнергетической гипоксии сердца, печени и почки кролика под влиянием вибрации в эксперименте

Материалы и методы
Чувствительность Vэ к ингибиторам вычисляли по формуле
Результаты исследования
Vэнд почки
Findings
SS df MS
Full Text
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