[Early reversible changes in the glycolytic system of rat tissues in ischemia]. / Rannie obratimye izmeneniia glikoliticheskoi sistemy tkanei krys pri ishemii.

It is shown that the glycolytic system obtained from the ischemically damaged tissues of rats in the process of the long-term functioning in vitro: partial--after long-term (1.5-2 h) ischemia and completely--after short-term (15-30 min) ischemia. Detection of reversible changes in the glycolytic system under ischemia, besides determination of its activity with the short-term functioning is promoted by isolation of the glycolytic system from tissues as well as prevention of the damage in vitro.

[Glycolysis in the rat kidney shortly after ischemia and administration of calmodulin inhibitors, AMP and NAD]. / Glikoliz v pochkakh krys v rannii period posle ishemii i pri vvedenii ingibitorov kal'modulina, AMP i NAD.

It is shown in experiments on rats that the early postischemic period after 1- and 1.5-hour ischemia of kidneys is characterized by a decrease in the damage of the glycolytic system site which induces glucose-6-phosphate transformation into lactate and by an increase in the inhibition intensity of the initial hexokinase reaction of glycolysis. In the postischemic period after more prolonged (2-, 3-hour) ischemia the damage of the glycolytic system develops also at the site of glucose-6-phosphate transformation into lactate. Administration either of the nucleotide complex (NAD and AMP) or calmodulin inhibitors (aminazine and zinc sulphate) to rats prior to two-hour occlusion of kidneys vessels promotes a decrease in the inhibition of the glycolytic system activity in the postischemic period. At the same time the separate and combined application of zinc sulphate and triftazin (the most intensive calmodulin inhibitor) is not efficient. The positive effect of NAD, AMP and aminazine on the state of the glycolytic kidney system in the postischemic period correlates with the improvement of the blood microcirculation processes in them.

[Effect of NAD and ADP on glycolysis in the kidneys and liver of rats during ischemia]. / Vliianie NAD i ADP na glikoliz v pochkakh i pecheni krys pri ishemii.

Experiments on albino rats have shown that kidney ischemia and its simulation by the anaerobic incubation of postmitochondrial kidney homogenate fraction without a substrate induce a considerable damage of the glycolytic system at the stage of the glucoso-6-phosphate transformation into fructoso-1.6-diphosphate and a less pronounced damage in the fructoso-1.6-diphosphate transformation into lactate. Administration of adenosine diphosphate (ADP) and nicotinamide adenine dinucleotide (NAD) to rats before kidney vessel occlusion or their addition to the postmitochondrial fraction before the anaerobic incubation without a substrate decreased a degree of the glycolytic system damage. The damage of the glycolytic system and protective action of NAD are also detected under simulation of liver ischemia. Possible mechanisms of the ischemic damage in the glycolytic liver and kidney tissue system are discussed.

[Effect of mitochondria and microsomal fractions on glycolytic activity of rat brain and liver tissues under hypoxia]. / Vliianie mitokhondrii i mikrosomnoi fraktsii na glikoliticheskuiu aktivnost' tkanei mozga i pecheni krys pri gipoksii.

It is found that acute hypoxia inhibits the glycolytic activity of postmitochondrial fraction in the liver, activates in the brain, but has no effect on glycolysis under conditions of a preliminary administration of diethylaminoethylamide of parachlorophenoxyacetic acid--antihypoxic preparation. In the processes of two- and four-week interrupted training of adaptation to hypoxia the activity of the liver glycolytic system rises. Suspensions of the mitochondric and microsomal fraction added in definite ratios to the postmitochondrial fraction of the brain and liver intensify its glycolytic activity both in control and hypoxic animals. The activating effect of mitochondria is higher as compared with the control when glycolysis is decreased; when glycolysis is increased the phenomenon is not observed. A mechanism of the found changes in glycolysis and the validity of the tissue glycolysis estimation from the activity of the postmitochondrial fraction are discussed.

[Effect of hypoxia on mitochondrial stability]. / Vliianie gipoksii na ustoichivost' mitokhondrii

The mitochondria isolated from the liver of rats subjected to acute hypoxia (10 km, 2h) are established to 0e less stable to the damage effect of incubation in the substratefree medium than the mitochondria of the control animals. A long interrupted adaptation to hypoxia as well as a single introduciton of p-chlorophenoxyacetic acid diethylaminoethylamide prevents a decrease in stability of the mitochondrial structures which is observed in rats during hypoxia. Addition of p-chlorophenoxyacetic acid diethylaminoethylamide into the incubation medium also inhibits the damage of the liver mitochondria.

[Biochemical mechanisms of the antihypoxic effect of amichlorphen (diethylaminoethylamide parachlorphenoxyacetic acid)]. / K biokhimicheskim mekhanizmam antigipoksicheskogo deistviia amikhlorfena (diétilaminoétilamida parakhlorfenoksiuksusnoi kisloty)

Test set up on albino rats demonstrated a preliminary introduction of amichlophene to prevent a hypoxic fall in the level of highly ergastic compounds in the tissues owing to stimulation of the mitochondrial respiration processes and increased energy-producting effectiveness of the latter. The beneficial effect of amichlophen on the bioenergetics of the tissues in acute hypoxia is largely caused by the continued structural and functional integrity of the mitochondria, lysosomes and other cellular organellae which is due to the inhibitory action of the compound on the prosses of lipids reoxidation and to the activity of phospholipase A.