350 rub
Journal Technologies of Living Systems №4 for 2013 г.
Article in number:
Evaluation of hyperhomocysteinemia and induced hyperlipidemia affecting endothelium functions in patients with coronary artery disease
Authors:
E.I. Sokolov, S.P. Shtin, N.B. Bayurova, V.V. Vikent-ev, A.G. Goncharova, L.H. Bragin
Abstract:
Initiating stage of development of atherosclerotic defeat of coronary vessels is dysfunction an endoteliy which arises under the influence of these or those factors of environment which are called as risk factors of IBS, being shown as an imbalance between vazodilatation and vazokonstriktor effects of these or those biologically active substances. We have studied the nature of the effect of risk factors such as induced hyperlipidemia, and hyperhomocysteinemia induced by the functional state of vascular endothelial cells in ischemic heart disease. The study included 44 patients with chronic forms of coronary artery disease and 40 healthy individuals. In a study in patients with coronary heart disease found Manifestation available atherogenic changes in the lipid-transport system of the blood under the influence of induced hyperlipidemia, positive correlation between the severity and extent of violations of atherogenic increase of endothelin-1, reflecting the vasoconstrictive potential. Peripheral blood levels of homocysteine reliably reflect the severity of coronary artery disease, the presence of its complications. Lipid loading at sick IBS reveals a manifistation of atherogenous shifts already available on an empty stomach in a lipid - transport system of blood. Positive correlation communication between expressiveness of atherogenous violations in plasma of blood and extent of increase of level of endothelin - 1, reflecting vazokonstriktor function an endoteliy is revealed. Level of of homocysteine blood reflects character of a current of IBS. The simultaneous assessment of level of homocysteine blood plasma, endothelin-1 - atherogenous changes of a lipidny range of plasma of blood and induced by food loading allows in earlier terms and more precisely to predict character of a current of IBS against influence of the specified risk factors.
Pages: 31-39
References

 

  1. Ageev F.T. Rol ehndotelialnojj disfunkcii v razvitii i progressirovanii serdechno-sosudistykh zabolevanijj // Serdechnaja nedostatochnost. 2003. № 1. S. 22 - 25.
  2. Almazov V.A., Berkovich O.A., Sytnikova M.JU. i dr. EHndotelialnaja disfunkcija u bolnykh s debjutom ishemicheskojj bolezni serdca v raznom vozraste // Kardiologija. 2001. T. 41. № 5. S. 26 - 29.
  3. Aronov D.M. Lechenie i profilaktika ateroskleroza. M.: Triada KH. 2000. 412 s.
  4. Barkagan Z.S., Kostjuchenko G.I., Kotovshhikova E.F.Gipergomocisteinemija kak samostojatelnyjj faktor riska porazhenija i trombirovanija krovenosnykh sosudov i vozmozhnost ee korrekcii lekarstvennym preparatom «Angiovit» // Terra medica nova. 2005. № 4.
  5. Belova L.A. Biokhimija processov vospalenija i porazhenija sosudov. Rol nejjtrofilov // Biokhimija. 1997. T. 62. Vyp. 6. S. 659 - 668.
  6. Gomazkov O.A. EHndotelin v kardiologii: molekuljarnye, fiziologicheskie i patologicheskie aspekty // Kardiologija. 2001. № 2. S. 50 - 56.
  7. Efimov V.S., Cakalof A.K. «Gomocistein v patogeneze trombovaskuljarnojj bolezni i ateroskleroza» // Laboratorija mediciny. 1994. № 2. S. 44 - 48.
  8. ZHdanov V.S. Morfologicheskie osobennosti razvitija i techenija koronarnogo ateroskleroza // Kardiologija. 1989. T.29. № 11. S. 43 - 46.
  9. Zatejjshhikov D.A., Manushkina L.O., Kudrjashova O.JU. i dr.Polimorfizm genov NO-sintetazy i receptora angiotenzina ІІ 1-go tipa i ehndotelialnyjj gemostaz u bolnykh ishemicheskojj boleznju serdca // Kardiologija. 2000. T. 40. № 11. S. 28 - 32.
  10. Zotova I.V., Zatejjshhikov D.A., Sidorenko B.A. Sintez oksida azota i razvitie ateroskleroza // Kardiologija. 2002. T. 42. № 4. S. 58 - 67.
  11. Ivanishina N.S., Deev A.D., Oganov R.G. Svjaz razlichnykh faktorov riska s sostojaniem ehndotelialnojj funkcii // Kardiovaskuljarnaja terapija i profilaktika. 2003. T. 2. № 2. S. 23 - 27.
  12. Klimov A.N., Nikulcheva N.G. Obmen lipidov i lipoproteidov i ego narushenija. SPb.: Piter Kom. 1999. 512 s.
  13. Perova N.V. Narushenija lipidnogo obmena, ikh diagnostika i korrekcija. V kn.: Bolezni serdca / pod red. R.G. Oganova, I.G. Fominojj. M.: Litera. 2006. S. 125 - 172.
  14. Perova N.V., Metelskaja V.A. Metabolicheskie narushenija v patogeneze ateroskleroza i metody ikh korrekcii. M. 2008. 64 s.
  15. Sokolov E.I., Metelskaja V.A., Perova N.V. Vzaimosvjaz agregacii trombocitov s disliproteidemijami i polinenasyshhennymi zhirnymi kislotami // Kardiovaskuljarnaja terapija i profilaktika. 2006. № 5. S. 87 - 93.
  16. SHmeleva V.M. Gipergomocisteinemija i tromboz // Tromboz, gemostaz, reologija. 2000. № 4. S. 28-32.
  17. SHHukina G.N.Tolerantnost k zhirovojj nagruzke u bolnykh ishemicheskojj boleznju serdca: Diss. - kand. med. nauk. / MGMSU. 1991. 145 s.
  18. AndersonT.J., MeredithI.T., CharbonneauF., YeungA.C., Frei V., SelwynA.P., GanzP.Endothelium-dependentcoronaryvasomotion relates to the susceptibility of LDL to oxidation in humans // Circulation. 1996. V. 93. № 9. P. 1647 - 1650.
  19. Berliner J.A., Navab M., Fogelman A.M. et al. Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics // Circulation. 1995. V. 91. P. 2488 - 2496.
  20. Brown M.S., Goldstein J.L. A receptormediated pathway for cholesterol heamostatsis // Science. 1986. V. 232. P. 34 - 37.
  21. Chowienczyk P.J., Watts G.F., Cockroft J.R., Ritter J.M. Impaired endothelium ? dependent vasodilation of forearm resistance vessels in hypercholesterolaemia // Lancet. 1992. V. 340. P. 1430 - 1432.
  22. Comwell T.L., Arnold E., Boerth N.J., Lincoln T.M.Inhibition of smooth muscle cell growth by nitric oxide and activation of cAMP-dependent protein kinase by cGMP // Amer. J. Physiol. 1994. V. 267. P. 1405 - 1413.
  23. Davies M.J. Coronary disease: The pathophysiology of acute coronary syndromes // Heart. 2000. V. 83. P. 361 ? 366.
  24. Dyslipidemia and coronary heart disease // The ILIB LipidHandbook for Clinical Practice. 3rd ed.  N.Y.: ILIB. 2003. P. 242.
  25. Gordon S. Macrophage heterogeneity and tissue lipids. // J. Clin. Invest. 2007. V.117. P. 89 - 93.
  26. Graham I., Atar D., Borch-Johnsen K. et al.  European guidelines on cardiovascular disease prevention in clinical practice (Fourth Joint Task Force of the European Society of Cardiology and other societies on cardiovascular disease prevention in clinical practice) // Eur. J. Cardiovasc. Prev. Rehabil. 2007. V. 14. (Suppl 2). P. S1 - 113.
  27. Griendling K.K., Minieri C.A., Ollerenshaw J.D., Alexander R.W.Angiotensin II stimulates NADH and NADH oxidase activity in cultured vascular smooth muscle cells // Circ. Res. 1994. V. 74. P. 1141 - 1148.
  28. Lipid Research Clinics Prorgamm. The Lipid Research Clinics Coronary Primary Prevention trial results. 1. Reduction in incidence of coronary heart disease // JAMA. 1984. V.251. P.351 - 364.
  29. Thompson G.R. The proving of the lipid hypothesis // Current Opinion in Lipidology. 10th Anniversary issue. 1999. V. 10(3). P.201 - 205.
  30. Thompson G.R., Maher V.G.M., Matthews S. et al. Familial Hypercholesterolaemial Regression Study: a randomized trial of lowdensity lipoprotein apheresis // Lancet. 1995. V. 345. P. 81 - 116.
  31. Zechner R. The tissue specific expression of lipoprotein lipase: implication for energy and lipoprotein metabolism // Current Opinion in Lipidology. 1997. V.8. P. 77 - 88.