ABSTRACT
A study was made of the possibility of correcting respiratory chain function disorders in hypoxia by means of the naphthoquinone derivative vitamin K3. The antihypoxic activity of that compound is defined by its donor-acceptor properties and its capability to shunt the electron flow from NADH to CoQ. The effect is more pronounced in the tissues that oxidize mostly the NAD-dependent substrates which is related to rapid inactivation of the given enzymatic complex under hypoxia and correlates with low resistance of the cell using the NADH-oxidase pathway of oxidizing energy substrates to oxygen deficiency.
Subject(s)
Energy Metabolism/drug effects , Hypoxia/drug therapy , Vitamin K/therapeutic use , Acute Disease , Animals , Cell Hypoxia/drug effects , Cerebellum/drug effects , Cerebellum/metabolism , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Disease Models, Animal , Drug Evaluation, Preclinical , Heart/drug effects , Hypoxia/metabolism , Male , Myocardium/metabolism , Neurons/drug effects , Neurons/metabolism , Oxidation-Reduction/drug effects , RatsABSTRACT
It was found that infrared laser radiation (IRL) reduces the sparing action of acute hypoxia on ventricular transport function of low-resistant animals and accelerates the recovery of the function during the post-hypoxia period. The effect was caused by the IRL affecting directly the speed of perfusion through the myocardium and thus the latter's breathing rate. The protective effect of the IRL was practically absent in highly resistant animals, which may be indicative of the existence of basic differences in the regulatory systems which is responsible for local vasodilation and supply of oxygen to cells, and which participates in the formation of resistance of cardiomyocytes to oxygen shortage.
Subject(s)
Heart/radiation effects , Hypoxia/physiopathology , Infrared Rays , Lasers , Myocardium/metabolism , Animals , Heart Rate/physiology , Heart Rate/radiation effects , In Vitro Techniques , Male , Myocardial Contraction/physiology , Myocardial Contraction/radiation effects , Perfusion/methods , RatsABSTRACT
The effect of hypoxia of middle severity (H50) has been investigated on the contractile activity, oxidative metabolism and bioenergetic function of the myocardium in the isolated rat heart. It has been shown that differences in the functional-metabolic parameters sensitivity in the resistant and non-resistant to hypoxia animals are defined by the primary utilization of different pathways of substrates oxidation--the succinate-oxidative pathway of oxidation or the NADH-oxidative pathway, correspondingly. It is possible to correct the early hypoxic injuries of the electron-transfer function of the myocardium respiratory chain at the NADH-CoQ region (the first enzyme complex) with the help of quinones (vitamin K3, hydroquinone). The mechanism of this correction depends on the donor-acceptor properties of these compounds and it is the same both in the myocardium of the isolated heart and in the isolated mitochondria. Vitamin K3 is recommended to be utilized on the early stages of hypoxic injuries in myocardium as an antihypoxant of the energized type.
Subject(s)
Heart/drug effects , Myocardium/metabolism , Quinones/pharmacology , Animals , Energy Metabolism , Hydroquinones/pharmacology , Male , Myocardial Contraction/drug effects , Oxidation-Reduction , Rats , Vitamin K/pharmacologyABSTRACT
It was shown that the rate of potassium ferricyanide reduction in erythrocyte suspension recorded potentionmetrically depends on the activity of redox systems of erythrocytes. The rate of this process is increased after an addition of glucose, methylene blue and ascorbate. A sharp decline of the level of reducing equivalents in the hexose monophosphate pathway by tretbutylhydroperoxide stops the ferricyanide reduction. It is concluded that the hexose monophosphate shunt is a source of reducing equivalents for ferricyanide reduction. Ascorbic acid and methylene blue act as "carriers" of the reducing equivalents across the membrane and provide for the reduction of ferricyanide, i.e. compound, which does not penetrate the cell.