[The role of superoxide anions in regulation of coronary vessel tone and myocardial contractile function in changed redox-state of the myocardium].

The study relates to the character of tirone effect (chemical trap of superoxide--anions) on regulation of coronary vessel tone and myocardial contractile function in normal and changed cell redox-state of coronary and cardiac vessels. The experiments were performed in 64 female Wistar rats (180-320 g). The coronary blood flow and myocardial contractile junction were studied in isolated heart preparations. To determine the role of superoxide-anions in regulation of coronary vessel tone, tirone was added to the perfusion solution (4,5-dihydroxy-1,3-benzene disulfonic acid, 10 mm, Sigma USA). Preliminary injection of N-acetyl-L-cysteine evoked a 16 % increase, whereas injection of L-buthionine-(S,R)-sulfoximine reduced concentration of nonprotein thiol group in the myocardium and erythrocytes of experimental animals by 37%. The influence of superoxide anions on the cardiac vessel tone and myocardial contractile function was due to nitric monoxide participation the concentration of which increased in binding of superoxide anions and was directly dependent on concentration of sulfhydrilis groups in the cardiac cells. The oxygen active forms and cellular redox-state seem to play an important role in the regulation mechanisms of the coronary vessel tone and myocardial contractile function.

[Nitric oxide storage in the cardiovascular system]. / Deponirovanie oksida azota v serdechno-sosudistoi sisteme.

Nitric oxide (NO) is a highly reactive substance with short lifetime. In conditions of a living organism NO can be bound by the complexes used for transport and intracellular storage of NO. The main biological forms of NO store include S-nitrosothiols and dinitrosyl iron complexes capable of interconversion. The NO store formed by these complexes in the vascular wall, on the one hand, provides for protection from excessive free NO after its overproduction and, on the other hand, can be an additional NO source when it is deficient. Apparently, the efficiency of NO storage is genetically determined and corresponds to the inherited level of NO production in the organism. Controlled modulation of formation and dissociation of the NO store is a promising trend for further investigation.

[Autoregulation of coronary vessels following the acute blood loss and its combination with preexisting immobilization stress]. / Autoreguliatsiia koronarnykh sosudov posle ostroi krovopoteri i ee sochetanii s predvaritel'no perenesennym stressom.

A 6-hour immobilization stress and a 2-hour posthaemorrhagic hypotension caused elevation of the coronary flow, deterioration of coronary autoregulation, decreasing of the coronary dilation reserve, and diminishing of the left ventricular pressure. In the "stress + haemorrhage" group, the changes of the coronary vessels autoregulation ability were less obvious. Concentration of NO3-/NO2- in the blood serum was elevated after stress. Inhibition of the NO-synthase decreased the coronary flow. Thereupon, a pre-existing immobilization stress alters the coronary vessels tone.

[The autoregulation of the coronary flow of the isolated heart in rats after saponin damage to the endothelium]. / Autoreguliatsiia koronarnogo potoka izolirovannogo serdtsa krys posle povrezhdeniia éndoteliia saponinom.

The damage of the endothelium with saponin completely abolished the autoregulation of the coronary vessels in the Langendorff isolated heart and reduced the volume velocity of the coronary blood flow by 34% at the perfusion pressure 40 mmHg. Indomethacin and verapamil augmented the coronary flow in intact rats. All these agents decreased the distensibility of the coronary vessels by 43-49% on the average. The damage of the endothelium of coronary vessels reduced the maximum reactive hyperemia and, respectively, the coronary vasodilator reserve.

[NO-synthase inhibition induces a resistant pressor reaction during the 10-minute intravenous infusion of angiotensin-2 to narcotized rats]. / Ingibirovanie NO-sintazy vyzyvaet ustoichivuiu pressornuiu reaktsiiu v usloviiakh 10-minutnoi vnutrivennoi infuzii angiotenzina-2 narkotizirovannym krysam.

With intact NO-synthase, the 10-minute intravenous infusion of angiotensin-2 evoked the escape phenomenon from its pressor action. The intravenous infusion of the same dose of angiotensin-2 with the NO-synthase blocker (NG-monomethyl-arginine) led to a stable pressor response, i.e. no escape phenomenon was observed. L-arginine restored the escape phenomenon from the pressor action of angiotensin-2 almost completely. The findings show that normal functioning of the endothelium relaxing factor (nitric oxide) generation system is significant for reduction of angiotensin-2 pressure action.

[The autoregulation of the coronary flow of the isolated rat heart after NO-synthase blockade]. / Autoreguliatsiia koronarnogo toka izolirovannogo serdtsa krys posle blokady NO-sintazy.

The experiments were performed on 67 rat hearts isolated by the Langendorff method. Perfusion pressure (PP) was stepwise increased from 40 to 120 mm Hg. It was found that NO-synthase blockade by NG-monomethyl-L-arginine (NG-MMLA) decreased volume velocity coronary flow (VVCF) at PP 40 and 60 mm Hg, autoregulation index and shifted the onset of effective autoregulation to the right. In cases of high coronary tone, caused by introduction of pituitrine, the autoregulation and its effectiveness was unchanged. The combination of NG-MMLA and pituitrine decreased the autoregulation index again. In cardiac perfusion under constant pressure, the value of maximal hyperemic coronary flow after introduction of NG-MMLA was decreased by 30-57%, and as a result the coronary reserve was decreased by 28.3%. Thus, NO, which released from endothelium of coronary vessels plays a significant role in mechanism of coronary autoregulation.