Clinical Physiology of Circulation

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery


Pharmacological correctionof endothelial dysfunction and disturbance ofstructured organization of thrombocyte membranesin ischemic heart disease

Abstract

According to the treatment results in 46 patients with ischemic heart disease, exertional angina and rest angina of II-IV functional classes, arterial hypertension of II-III severity degree, rhythm and conduction disturbance of different genesis, it was shown that introduction of anti-ischemic drug with pronounced antioxidant activity of nadzin into conventional mode of treatment leads to decreased angina functional class by 23%, rarity of angina attack cases by 78%. Cyanosis disappears in 95% of cases. The myocardial demand for oxygen decreases by 30%. This is accompanied (unlike the group which was not given nadzin) by elevation of oxidation-reduction potential of pyridine nucleotide system and their absolute number, normalization of NADFN-oxidase and decrease of endothelin-1 up to its normal level. Nazin helps to restore thrombocyte membrane resistance to oxidation, reduce the level of malone dyaldehyde, increase the activity of catalase and superoxide dismutase. Antiischemic effect of nadzin expands not only on myocardium, but also on other tissues, what helps to cut down on the doses of anti-hypertension and diuretic drugs when treating with nadzin, what helps to obtain required diuretic effect without disturbing electrolyte balance. Treatment with nadzin helps to decrease ST-segment and/or T-wave depths. Good tolerance to nadzin was noted.

References

1. Бокерия Л. А., Голухова Е. З. Кардиология в кардиохирургии: эффективный симбиоз // Бюллетень НЦССХ им. А. Н. Бакулева РАМН. - 2004. - № 3. - С. 8-18.
2. Бокерия Л. А., Маликов В. Е., Сукоян Г. В. и др. Способы кардиопротекции при кардиохирургии. - М., 2004.
3. Каган В. Е., Орлов О. Н., Прилипко Л. Л. Проблема анализа эндогенных продуктов перекисного окисления липидов. - М., 1986.
4. Pагино Ю. И., Душкин М. И. Простой метод исследования резистентности к окислению гепаринсодержащих липопротеинов сыворотки крови // Клин. лаб. диагностика. - 1998. - № 3. - С. 6-9.
5. Сукоян Г. В., Галенко-Ярошевский В. П., Петров Ю. М. Ишемическая болезнь сердца: стратегия фармакологического вторжения и коррекция метаболизма миокарда // Ишемическая болезнь сердца / Под ред. П. А. Галенко- Ярошевского. - М.: Медицина, 2007. - С. 310-363.
6. Adler A., Messina E., Sherman B. et al. NADP(H) oxidasegenerated superoxide anion axxounts for reduced control of myocardium O2 consumption by NO in old fischer 344 rats // Am. J. Ph. Heart. - 2003. - Vol. 285, № 10. - P. 1015-1022.
7. Giordano F. Oxygen, oxidative stress, hypoxia, and heart failure // J. Clin. Invest. - 2005. - Vol. 115, № 3. - P. 55-58.
8. Griendling K. K., Sorescu D., Ushio-Fukai M. NAD(P)H oxidase. Role in cardiovascular biology and disease // Circul. Res. - 2000. - Vol. 86. - P. 494-507.
9. Hornstein P. S., Zaugg C. E., Zhu P. et al. Combined blockade of endothelin-1 and thromboxane A2 receptors against postischaemic contractile dysfunction in rat hearts // British J. Pharmacol. - 2001. - Vol. 132. - P. 234-240.
10. Ide T., Tsutsui H., Kinugawa Sh. et al. Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium // Circ. Res.-1999.-Vol. 85. - P. 357-363.
11. Keidar S., Kaplan M., Pavlotzky E. et al. Aldosterone administration to mice stimulates macrophage NADPH oxidase and increases atherosclerosis development. Possible role for angiotensin-converting enzyme and the receptors for angiotensin II and aldosterone // Circulation. - 2004. - Vol. 109. - P. 2213-2220.
12. Landmesser U., Hornig B., Drexler H. Endothelial function. A critical determinant in atherosclerosis? // Circulation. - 2004. - Vol. 109 (Suppl. 2). - P. II27-II33.
13. Li J.-M., Wheatcroft S., Fan L. M. et al. Opposing roles of p47phox in basal versus angiotensin II-stimulated alterations in vascular O2 - production, vascular tone, and mitogenactivated protein kinase activation // Circulation. - 2004. - Vol. 109, № 10. - P. 1307-1313.
14. Liu Y., Zhao H., Li H. et al. Mitochondrial sources of H2O2 generation play a key role in flow-mediated dilatation in human coronary resistance arteries // Circ. Res. - 2003. - Vol. 93. - P. 573-580.
15. Miura H., Bosnjak J. J., Ning G. et al. Role for hydrogen peroxide in flow-induced dilation of human coronary arterioles // Circ. Res. - 2003. - Vol. 92. - P. 31-40.
16. Paravicini T. M., Chrissobolis S., Drummons G. R., Sobey C. G. Increased NADPH-oxidase and nox-4 expression during chronic hypertension is associated with enhances cerebral vasodilatation to NADPH in vivo // Stroke. - 2004. - Vol. 35, № 2. - P. 584-589.
17. Rajagapola S., Kurz S. Angiotensin II mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation: contribution to alteration of vascular tone // J. Clin. Invest. - 1996.-Vol. 97.- P. 1916-1923.
18. Takimoto E., Kass D. A. Role of oxidative stress in cardiac hypertrophy and remodeling // Hypertension. - 2007. - Vol. 49. - P. 241-248.
19. Umeki S. Human Neutrophil cytosolic activation factor of the NADPH oxidase // J. Biol. Chem. - 1990. - Vol. 9, № 3. - P. 5049-5054.

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