[The effect of the antioxidant, butylhydroxyanisole on experimental myocardial necrosis in rats. Morphologic study]. / Vplyv antioxidacnej látky butylhydroxyanizolu na experimentálnu nekrózu myokardu potkanov. Morfologické sledovanie.

The present paper aimed to investigate a possible effect of the antioxidant butylhydroxyanisole (BHA) on the extent of experimental necroses of the myocardial cells. Administration of BHA in a daily dose of 10 mg.kg-1 i. m. lasted 20 days. The isoprenaline model in a single-dose subcutaneous administration of IP 25 mg.kg-1 was used to induce experimental necrosis. Tables 1-7 show quantification and morphometry of histological and electron-microscopic images. The protective effect of BHA was manifested by influencing the extent of myocardial necroses (p < 0.01) (Table 1). In the morphometric electron-microscopic examinations, the protective influence of BHA was recorded in the parameter of cristolysis, i.e. equipment of mitochondria with cristae (Table 5), in comparison of the control group with IP and the BHA group with IP (p < 0.01). No statistically significant differences in the two above-mentioned experimental groups were found in the other compartments.

[The effect of butylhydroxyanisole, an antioxidant, on oxidative phosphorylation of myocardial mitochondria in experimental ischemia]. / Vliv antioxidacní látky butylhydroxyanizolu na oxidacní fosforylaci mitochondrií myokardu pri experimentálne vyvolané ischemii.

The present paper evaluated the effect of the antioxidatively acting agent butylhydroxyanisole (BHA) on the oxidative and energetic processes in the mitochondria of the myocardium, both normal and damaged with isoprenaline. BHA was administered for 20 days in a daily dose of 10 mg.kg-1. Experimental necrosis of the myocardium was induced by a single-dose administration of a dose of 25 mg.kg-1 s.c. The results shown in Graphs 1-7 indicate that BHA in the above-mentioned concentration did not act protectively on the metabolic processes taking place in the mitochondria during experimentally induced necroses of the myocardium.

[The effect of butylhydroxyanisole, an antioxidant, on experimental atherosclerosis in Japanese quail]. / Vplyv antioxidantu butylhydroxyanizolu na experimentálnu aterosklerózu u japonských prepelíc.

The present paper aimed to examine a possible influence of the antioxidant butylhydroxyanisole (BHA) on the extent of atherosclerotic changes in coronary arterioles, in arcus aortae, and on the influencing of the extent of myocardial necroses. The model of atherosclerosis was worked out by administering 1% cholesterol diet to Japanese quails for the period of 40 days. The above-mentioned changes were examined on histological preparations and they were evaluated morphometrically. Quantification and morphometry of atherosclerotic changes in the individual experimental groups are shown in Table 1 and statistical evaluation of findings using the t-test in Tables 2, 3 and 4. The protective effect of butylhydroxyanisole was demonstrated to be statistically significant in the examination of the extent of atheromatous changes in arterioles. In arcus aortae, the findings were neither extensive, nor statistically significant. The findings concerning the extent of necroses in the myocardium provide documentary evidence for subendothelial micronecroses in the group with BHA in contrast to blended necroses in the group with Epavit + cholesterol. The model of cholesterol diet used in Japanese quails proved to be suitable to examine the pathogenesis of atherosclerosis and its possible influencing by pharmaceuticals. The dose of butylhydroxyanisole (BHA), 20 mg.kg-1, was selected in the optimal manner with regard to possible inhibition of atherosclerotic changes.

[Ultrastructure of the myocardium in the calcium channel blocker withdrawal syndrome]. / Syndróm vynechania podávania blokátorov kalciového vstupu v obraze ultrastruktúry myokardu.

Changes in the ultrastructure of rat myocardial cells were investigated after withdrawal of therapy with the calcium entry blockers diltiazem, nifedipine, and verapamil. Two hours after the last administration the ultrastructure was without significant changes in comparison to the control group. However the incidence of contracture bands, dehiscence of intercalated discs and lesions of mitochondria observed 30 hours after therapy withdrawal demonstrated serious damage of myocardial tissue. The recorded changes, practically identical with changes associated with the calcium paradox, were the consequence of withdrawal of calcium entry blocker therapy. The reported morphological changes reflected biochemical and functional changes characteristic of the calcium entry blocker withdrawal syndrome.