Bekyarova, G.

Kozarev, I.

Yankova, T.

English

Varna Medical University Press: Journals

F R E E R A D I C A L O X I D A T I O N A N D E R Y T H R O C Y T E A G G R E G A T I O N A F T E R T H E R M I C I N J U R Y E F F E C T O F A L P H A T O C O P H E R O L G. Bekyarova, I . Kozarev, T. Yankova Key-words: thermic i n j u r y - f r e e radical oxidation — erythrocyte aggregation — alpha-tocopherol —microcirculation Disseminated intravascular coagulation and «sludge» phenomenon deve­lopment are a characteristic manifestation of thermic shock. Ery throcy te aggre­gation presents an important l i nk in the mechanism of this pathological pro­cess (8, 10, 13). Erythrocyte" involvement in this phenomenon is related to a l ­teration of their electrical loading as well .as to loss of their deformabil i ty (3 , 5 ) . The concept that conformational reconstruction of erythrocyte membranes due to essential structural changes is of v i t a l importance for aggregation becomes more and more popular, indeed (2) . I n this sense, the c la r i fy ing of the role of free rad ica l oxidation ( F R O ) as one of the main factors changing membrane structural-functional a c t i v i t y , in the mechanism of erythrocyte aggregation after burning as we l l as in the changing of the erythrocyte sedimentation ra te ( E S R ) and hematocrit (H t ) presents a definite ihterest , indeed. • н • / -I'. л . i , Material and methods Exper imen ta l thermic in jury of I I I r d a — r i l r d b — degree and of 15 — 20 per cent of body surface was moulded in white male rats w i th body mass of 200 — 250 g. A n i m a l s were divided into three groups: a) heal thy b) burned untreated c) burned and treated wi th alphatocopherol. DL-alphatocopherol («Serva») was in t raper i tonea l^ injected i n a dose of 20 mg/kg b. w. immedia­tely after burning, on the 2 4 t h and 4 8 t h hour after thermic injury. Ce r t a in pa­rameters were estimated in the following time intervals: on the 24 t h , 48 t h and 7 2 n d hour. The ac t iv i ty of F R O processes was estimated according to th iobarbi tur ic products ( T B P ) contehts. T B P were spectrophotometrically determined (11) at wfeve lenth of 532 nm w i t h ext inct ion coefficient of 1.56 . 10 5 M 1 . c m ; 1 . Intravascular erythrocyte aggregation was determined after the method of Lo-potnikov and Harash (1982). E S R changes were followed-up after Panchenko and H t level was estimated by using of a microhematocrit centrifuge. Our results were s ta t is t ica l ly processed after thfe method of v a r i a t i o n ana­lys is .and compared according to Student-Fisher 's t-test. Results and discussion Our data demonstrate a significant increase of blood T B P level after ther­mic injury in comparison wi th controls (healthy animals) . L e v e l s increase most 56 G. Bekyarova, I . Кога rev, T. Yankova considerably on the 2 4 l h and 48 t h hour (approximately two times). Then they diminish ( insignif icant ly) without normal iza t ion on the t h i r d day. Alphato-copherol administration results in T B P content reduction in a l l the intervals studied. T h i s decrease is most considerable and re l iable on the 24 t h hour ( p < 0.01) ( f ig . 1). Hematocri t values are max ima l on the 5 t h hour (p < 0.01). Then they decrease and tend to fa l l below the normal l imits on the 7 2 n d hour. However, when alphatocopherol is injected H t values do not change essentially in comparison wi th burned untreated animals ' ones (fig. 2) . Dur ing the acute period after thermic injury intravascular eryth­rocyte aggregation increases r e l i a ­bly in the aforementioned intervals by 5 1 , 76, 60 and 34 per cent, respectively, as compared wi th that in control animals. Alphatocopherol induces erythrocyte aggregation reduction which is most statisti­cal ly significant on the 24 hour (p<0.01) when compared with that in burned untreated rats (f ig. 3) . E S R increases considerably s t i l l on the 5 t h hour after thermic injury and then this rate decreases but remains re l iab ly higher than nrnol/gHb 80 70 60 50 40 30 24 48 72 hours Fig. 1. Change of ТВ-product concentration in the blood after thermic injury in rats ( I I P — I I I е degree, 15—20 per cent of body surface). Legend: 0 — controls — intact # — burned untreated 1 — burned treated with alphatocopherol. * P 2 . i < 0 . 0 5 ; ** P 2 1 < 0.01; ** + P 2 i > < 0.001 + p < 0.05 < p + 0.01. % 16№ 50 40 30-20 10 I r ? m ni i0\r 5 -24 4Ь 72 hours Fig. 2. Hematocrit changes' after thermic injury in rats ( I I I 3 — I I I b degree, 15— ^ 20 per cent of body surface). Legend — see fig. 1. 48 72 hours Fig. 3. Change of erythrocyte aggregation after thermic injury in rats ( M l a — H I * degree, 15 — 20 per cent of body surface). Y-axis—changes in per centage in com­parison with control values. X-axis —-interval of observation. Legend see fig. 1. Free radical oxidation and. 57 IT 0.60 050 24 48 7? hours | e normal level . After alphatocopherol application, except for the 4 8 t h hour, S P decreases but does not normalize t i l l the 72 n d hout (fig. 4 ) . Data presented show that F R O ac t iv i ty increases s t i l l on the 5 t h hour and mains high (luring the first days after thermic trauma. Pa ra l e l ly , erythrocyte aggregation, E S R and Ht elevates, too. W e suppose that the increased aggregation capaci ty is due to serious structural alterations of erythrocyte membrane influenced by the accumu-lated endogenous F R O derivat ives. Probably, peroxide modification re-sults in redistribution of ionized groups on erythrocyte membrane sur-face and in electrokinetic potential reduction (2,9) . The close relationship between activation of F R O processes and erythrocyte aggregation is in concordance wi th literature data available ( 1 , 9, 14). I t can be assumed that aggrega-tion capacity increase is due to a change of elastic properties and to transformation of discocytes into spherocytes because of conformational al terations in l i p id and polypeptide components during the direct action of F R O derivatives on erythrocytes (15) . F R O activation induce the formation of high-molecular compounds of the type of lysolecithine and of the free fat ty acids which st imulate disc-spherocytic transformation probably by means of PL-ase ac t iv i ty increase (7, 14). I t can be presumed that F R O is an important l i n k i n the mechanism of erythrocyte aggregation and, of course, not the only one l i n k . Probably , to that process changes o£ plasma blood composition ( i . e . decreased albumin level , increased concentration of high-molecular components, f ibrinogen, gammaglo-bul in 121) wh ich disturb erythrocyte suspension s t ab i l i ty i n hemoconcentration as w e l l as the more insufficient effect of alphatocopherol on these parameters contribute to a cer ta in extent , too. Alphatocopherol due to its ant ioxidat ive properties diminishes F R O ac-t ivat ion and this results i n electrokinetic potential s tab i l iza t ion (12) . B y this way , it contributes to the creation of an electromagnetic balance between eryth-rocytes and vascular w a l l (4) . Alphatocopherol prevents erythrocyte aggrega-t ion and thus contributes to blood viscosi ty reduction and microcirculat ion improvement after burn ing . Our results obtained argue for the statement that F R O is one of the deter-minant factors st imulating erythrocyte aggregation. T h i s conclusion is confirm-ed by our data demonstrat ing a close relationship between F R O , erythrocyte aggregation as' well as alphatocopherol protective act ion. Fig. 4. F.SR changes after thermic in/nrv in rast ( I I P - I I I a degree, 15 —2.0 per cent of boyd surface/ Legend — see fig. 1. 58 Ё. Bekyarova, I . Rozarev, Т. Yankova R E F E R E N C E S I. A p v T ю и я и, P. А., С. Л. Б а д ж и н я н, А. К. А б р а м я н, Н. Р. О в и е я н . Делон, рукопись в В1ШНПМИ МЗ СССР. Москва, № 6130—83. — 2. Г а-б р и е л я и, 3. С , С. 3. Л г о п о в. Клетки крови и кровообращение. Ереван, 198:?, 399 с. — 3. t у с е н о в а, Ф. М., В. А. С о к о л о в а, В. П. М а т в е е н к о, и др. Патол. физиол..эксперим. тер., 1986, № 2, И —14. — 4. К а з а н о в , Ю. М. Карбио-логия, 1981, 1981, № 8 > ПО—116. — 5. Л е в и и, Г. Р. И. M y р а з я н, Ю. /А. Ill е р е м е т и е в , / I . Р. П а н ч е и к о . Гематол. и трансфузиол., 1983, № 2, 52—58. — 6, Л о и о т и и к о в, В. А., Л. М. X а р а ш. Лабор. дело, 1982, № 7, 5—7. — 7. М е е р с о н, Ф. 3. Адаптации, стресс, профилактика. Москва, Медицина, 1981, 288 с. -8. М ч е е д л и ш в и л и, Г. И. Патол. физиол. эксперим. тер., 1986, № 2, 3— И. — 9. П а и а с е и к о , О. М., Р. И. Ш а л и н а, О. А. А в и з о в а. Бюлл. эксперим. биол. и мед., 1985, № 4, 434—439. — 10. Ш т ы х н о, Ю. М., 3. Р. А т а д ж а и о в а. Патол. физиол. эксперим. тер., 1985, № 2, 30—35. — 11. G г е е n w a 1 d, R. A.' Boca Raton, Florida, C R C Press Inc., 1936, 197-204. — 12. Е s с i n, C . W., К. Е s с i n. Biochemistry, 11, 1972, 606—610. — 13. G u е s t, M. M., D. J . W a i n , M. E . F г a-w i е г. / . Burn Care RehabiL, 4, 1983, No 3, 158—162. — 14. L a C e l l , И. P. В и н ц, Л. А. С а н т я и о. Мембраны и болезнь. Москва, 1980. — 15. Н о с h s t е i n, D. , S. K. J a i n . Fed. Proc, 40, 1981, 183-188. СВОБОДНОЕ РАДИКАЛЬНОЕ ОКИСЛЕНИЕ И АГРЕГАЦИЯ ЭРИТРОЦИТОВ ПОСЛЕ ТЕРМИЧЕСКОЙ ТРАВМЫ. ЭФФЕКТ АЛЬФА ТОКОФЕРОЛ А Г. Бек проза, И. Козырев, Т. Янкова Р Е З Ю М Е Повышеинаяа грегация клеток крови является одним из наиболее важных патогенных факторов нарушений микроциркуляции. Авторы поставили перед собой цель изучить влия­ние активирования продуктов свободного радикального окисления на агрегационную спо­собность эритроцитов, реакции оседания эритроцитов и гематокрита в первые часы и дни после получения термической травмы Ш а и 1П6 степени (15—20% поверхности тела) у белых крыс самцов. Устанавливается, что параллельно с нарастанием содержания ТБК.-продуктов крови, агрегация эритроцитов, скорост оседания эритроцитов и гематокрит повышаются. Применение альфатокоферола приводит к уменьшению количества ТБК-продуктов, по­нижению агрегации и скорости оседания эритроцитов и не оказывает влияния на гема­токрит. Полученные результаты дают основание предполагать, что повышенное количество продуктов свободного радикального окисления стимулирует агрегацию эритроцитов при термической травме, а альфатокоферол имеет защитную функцию. 

FREE RADICAL OXIDATION AND ERYTHROCYTE AGGREGATION AFTER THERMIC INJURY EFFECT OF ALPHATOCOPHEROL

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FREE RADICAL OXIDATION AND ERYTHROCYTE AGGREGATION AFTER THERMIC INJURY EFFECT OF ALPHATOCOPHEROL

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