[Effect of uneven distribution of elastic recoil pressure change on N2 washout curves (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Horie.
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Two patients who had previously experienced old myocardial infarction and who died suddenly after an attack of chest pain were examined and discussed. In both cases two of the three main coronary arteries showed severe stenosis with canalization. Ruptured atheromatous plaque was found in the unblocked coronary artery. Fibrin was already formed and surrounded the fractured intimal collagen fiber, foam cells, and cholesterin clefts, but a luminal thrombi had not yet been formed. Fresh occluding thrombi were formed at the site of the ruptured atheromatous plaque. Coronary thrombi containing abscess components such as foam cells, cholesterin clefts, and the fractured intimal collagen fiber were found in our preliminary study. These views support the supposition that this fracture between the lumen and the plaque might precede and be responsible for the formation of the thrombus and the onset of acute myocardial infarction. It was confirmed that the attack of preinfarction angina occurred at the time of the rupture of the atheromatous plaque. The rupture of the atheromatous plaque plays an important part as an initiating factor of peinfarction angina and myocardial infarction. Thus, it is necessary to examine coronary arteries by serial histopathological section method.
An extensive histopathological study was carried out on the hearts of 108 patients with electrocardiographically proven acute myocardial infarction dying after admission to a coronary care unit. The occluded or the narrowest segments of the coronary arteries were examined at intervals of 100 mu using serial sections. Serial sectioning is important in such a study because the pathology of the lumen can vary considerably within a 2 to 3 mm segment. A high incidence (80.3%) of thrombus formation corresponding to the site of infarction was observed. These thrombi occluded the vessel lumen, were usually found proximally in the coronary arteries, and were associated with a ruptured atheromatous plaque in 90.8 per cent of cases. It is postulated that an increase of intraplaque pressure resulting from a honeycomb-like accumulation of foam cells, cholesterol clefts, and blood infiltration through the injured endothelial cells is the cause of rupture of the atheromatous plaque. This rupture into the vessel lumen may precede, and be responsible for, formation of thrombus and the onset of acute myocardial infarction.
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The data in our previous paper demonstrated that some alpha-tocopheryl esters administered orally were absorbed in their unchanged form through the lymph, while some other esters were absorbed after being hydrolyzed individually to different degrees. The hydrolysis during absorption seems to be related to the structure of the ester group of alpha-tocopherol at the 6-position. The purpose of this work is to study the metabolism and biological effect of tocopherol esters in vitamin E-deficient rats. Three esters were used on the basis of their behavior during absorption through the lymph, as follows; alpha-tocopheryl acetate (an easily hydrolyzable ester), the nicotinate (a moderately hydrolyzable one) and the pivalate (a scarcely hydrolyzable one). The easily hydrolyzable esters will suffer the same metabolic fate through absorption as alpha-tocopherol. The moderately and scarcely hydrolyzable ones have a tendency to show different physiological effects from alpha-tocopherol due to absorption of the unchanged ester. The effect of these esters on the microsomal enzymes in the liver such as cytochrome P-450, cytochrome b5, aniline and hexobarbital difference spectra and NADPH-dependent cytochrome c reductase was determined. It was shown that the pivalate inhibited the release of NADPH-dependent cytochrome c reductase activity to supernatant in spite of low distribution in the 105,000 X g sediment. The result suggests that the pivalate as a model compound may be interesting to examine for its membrane stabilizing effect of alpha-tocopherol.
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Formation of a free radical from carcinogenic and noncarcinogenic benz[c]acridine derivatives in the presence of proteins was examined. When aqueous mixture of benz[c]acridine and protein was stirred for a long period, shielded from light, benz[c]acridines were converted into free radicals. Albumin had the greatest effect in accelerating the free radical formation, and the effect was smaller in globulin, histone, and deoxyribonuclease. The g-value of the free radicals thus obtained was 2.005. Intensity of the electron spin resonance (ESR) signals of the free radical from carcinogenic derivatives was higher than those of the free radical from noncarcinogenic derivatives. There was a corresponding correlation among the ESR signal intensity of the free radical formed from the mixed system of benz[c]acridine and protein, charge of the K-region or ring nitrogen of the compound, and carcinogenicity of benz[c]acridines.