[Effects of elemental sulphur on the activity of adenylate kinase and performance of isolated rabbit heart]. / Vliianie élementarnoi sery na aktivnost' adenilatkinazy i rabotu izolirovannogo serdtsa krolika.

The experiments performed have shown that elemental sulphur inhibited only cytoplasmic isoenzyme of adenylate kinase without having any effect on mitochondrial isoenzyme. Effect of sulphur is related to its reaction with SH-groups of enzyme. Sulphur also by 50% inhibited cytoplasmic adenylate kinase in intact myocardium during perfusion of isolated rabbit heart. Under this circumstances the amplitude of contractions is diminished but perfusate flow is increased. Thus elemental sulphur must be considered as a new specific SH-reagent and vasodilator drug.

[The state of membrane structures of heart cells during ischemia]. / Izuchenie tselostnosti membrannykh struktur kletok serdtsa pri ishemii.

Under conditions of perfusion of isolated rabbit heart in aerobic medium and, especially, during ischemia, cytochrome c was liberated from heart cells into perfusate, thus indicating that integrity of mitochondrial outer membrane and of cell membrane was impaired. In situ developed deficiency of cytochrome c was distinctly less as compared with isolated mitochondria (50%, 3 hrs perfusion in ischemia), which appears to occur in response to ultrastructural impairments of mitochondria arising during their isolation and to other reasons.

[Effect of ischemia and rotenone on lipid and adenine nucleotide levels and functional activity of heart mitochondria]. / Vliianie ishemii i rotenona na soderzhanie lipidov, adeninnukleotidov i funktsional'nuiu aktivnost' mitokhondrii serdtsa.

Myocardial mitochondria (MCh), isolated with rotenone (MCh + RO) and in absence of rotenone (MCh - RO), were studied in rabbits with ischemia (0.5 hr autolysis) and in controls. Content of acyl-CoA was increased by 50%, linoleic acid - by 49% and lysophosphatidyl choline - by 37% in MCh + RO of control animals as compared with the MCh - RO preparation. In the MCh + RO preparation from rabbits with ischemia content of acyl-CoA was increased by 62%, while concentration of free fatty acids (FFA) and phospholipids was similar to those of the MCh - RO preparation. After isolation of mitochondria with rotenone composition of adenine nucleotides was distinctly altered. Content of ATP was decreased by 27% in mitochondria of both ischemic and control animals, although total amount of adenine nucleotides was decreased only slightly. As shown by estimation of succinate oxidation and membrane potential rotenone did not affect the mitochondrial respiration. In mitochondria of ischemic rabbits concentrations of FFA and lysophosphatidyl choline were increased, whereas content of ATP, total amount of adenine nucleotides, the rate of succinate oxidation and membrane potential were decreased. The method developed, isolation of mitochondria with rotenone, may be used in studies of the role of acyl-CoA in energy metabolism of cells.

[Reasons for disorders of fatty acid oxidation in isolated heart mitochondria during ischemia]. / O prichinakh narusheniia okisleniia zhirnykh kislot v izolirovannykh mitokhondriiakh serdtsa pri ishemii.

The influence of malate and cytochrome c on fatty acid oxidation under control and ischemic conditions was investigated. In the medium without malate, cytochrome did not make fatty acid oxidation decreased during ischemia return to normal. Oxidation in the media containing malate and cytochrome did not differ from control only when it was measured after preliminary oxidation of endogenous substrates. The ratio of palmitoyl-CoA and palmitoyl carnitine to the respiration rates at state 3 was unchanged at 60 min ischemia. Apparently, no changes in carnitine acyltransferase playing a role in oxidation of palmitoyl-CoA took place. Thus, the decrease of fatty acid oxidation at early periods of ischemia is largely caused by a reduction in the content of cytochrome c and intermediates of Krebs cycle in the mitochondria.

[Lipid metabolism of the heart in ischemia and postischemic reperfusion]. / Lipidnyi obmen serdtsa pri ishemii i postishemicheskoi reperfuzii.

Content of unesterified fatty acids (FFA), phospholipids and triglycerides was studied in myocardium of control rabbits, of rabbits with ischemia (1 hr and 4 hrs) of myocardium and in postischemic reperfusion. In the ischemic myocardium content of phospholipids was gradually decreased; FFA increased within the first hour of ischemia. In reperfusion and prolongation of ischemia up to 4 hrs FFA were not altered. The data obtained suggest that a decrease in the ratio between the rates of FFA consumption and of lipid hydrolysis was responsible for an increase in the FFA content and in the phospholipid concentration.

[Fatty acid composition of mitochondrial phospholipids of the ischemic heart]. / Zhirnokislotnyi sostav fosfolipidov mitokhondrii ishemizirovannogo serdtsa.

Gas liquid chromatography was used to study fatty acid (FA) composition of lysophosphatidylcholine (lyso-PC) and phosphatidylcholine in isolated rabbit heart mitochondria. In control, lyso-PC and PC were found to contain 95 and 66% of unsaturated FA, respectively. At 1 hour of ischemia (autolysis at 37 degrees C) the percentage of saturated FA in lyso-PC noticeably increased whereas FA composition remained unchanged. It is concluded that changes in FA composition of lyso-PC are caused by phospholipase A2 action.

[Effect of myocardial ischemia on the phospholipid composition of cardiac tissue and mitochondria]. / Vliianie ishemii miokarda na fosfolipidnyi sostav serdechnoi tkani i mitokhondrii.

Concentration of lysophosphatidyl choline was slightly increased in heart tissue within 30 min after total rabbit myocardial ischemia and it was distinctly decreased within 1 hr as compared with control values. In the mitochondria within the initial periods (0.5 hr, 1 hr) of the ischemia concentration of lysophosphatidyl choline increased most markedly but the phospholipid content became similar to control level within 2 hrs. Alterations in the total phospholipid content whereas separate phospholipid fractions, lysophosphatidyl choline and cardiolipin, altered more distinctly in mitochondria. In ischemically impaired cell phospholipases appear to be initially involved in degradation of mitochondria phospholipids.