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The fate of aflatoxin B1 (AFB1) in the blood of various species of animals was studied in vitro. Examination of the distribution of radioactivity in blood incubated with [14C]AFB1 at 37°C showed that high levels of radioactivity were associated with blood cells. The radioactivity was readily removed from the blood cells by washing with fresh plasma, indicating loose binding of AFB1 to blood cells. Most of the radioactivity in plasma was bound to protein. These results suggest that a large part of the AFB1 in blood in vivo may be carried not only by the plasma proteins but also by the blood cells. When chloroform extracts of plasma of [14C]AFB1-treated mouse, rat, duckling, and hamster blood were developed by thin-layer chromatography, high levels of radioactivity were found in both the AFB1 region and the aflatoxicol (AFL) region. Incubation of blood with nonradioactive AFB1 and AFL showed marked interconversion of AFB1 and AFL in the blood of rats, hamsters, mice, and Mongolian gerbils, but not in the blood of guinea pigs, rhesus monkeys, squirrel monkeys, or humans. Interconversion occurred in red blood cell suspensions but not in plasma, indicating that the red blood cells are responsible for AFB1-AFL interconversion in the blood. 相似文献
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The absorption and secretion of ochratoxin A (OA) by the gastrointestinal tract were studied in the rat. When OA was introduced into the lumen at various sites of the gastrointestinal tract, the largest concentration of OA in portal blood was found after the toxin was injected into the lumen at the proximal jejunum. After the injection of OA into a closed loop at the proximal jejunum, the rate of appearance of OA in the mesenteric venous plasma was higher than that in lymph. The rate of appearance in the venous plasma increased with an increase in the luminal concentration of OA while in the lymph the rate remained almost constant with respect to the luminal OA concentration. These results suggest that the site of maximal absorption is the proximal jejunum and that the primary route of absorption is the portal vein although the contribution of the lymphatic route cannot be excluded when low-dose levels of OA are given. When various parts of the gastrointestinal tract were perfused after iv injection of OA, noticeable amounts of the toxin appeared in the intestinal perfusate, suggesting that intestinal secretion may be another route of excretion of OA. Comparison of intestinal secretion and absorption showed asymmetric transfer of OA across the intestinal mucosa, the lumen-to-blood transfer being greater than that in the opposite direction. 相似文献
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S Inamura Y Sakurai S Kawada A Shohtsu S Kuribayashi 《Kyobu geka. The Japanese journal of thoracic surgery》1990,43(3):219-221
A two-year-and-ten-month-old female with tetralogy of Fallot with major aortopulmonary collateral arteries (MAPCAs) developed a persistent heart failure after an intracardiac repair. Angiograms revealed four MAPCAs originating from the upper portion of the descending thoracic aorta and draining into the left pulmonary artery, one MAPCA from the inferior phrenic artery into bilateral pulmonary arteries, and remaining one from the left subclavian artery into left pulmonary artery. Three of these MAPCAs were occluded by transcatheter embolization by the use of the steal coil. The heart failure was improved dramatically by this treatment. 相似文献
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S Kuribayashi 《Nihon Igaku Hōshasen Gakkai zasshi. Nippon acta radiologica》1989,49(7):899-914
Normal values of left ventricular (LV) function were determined angiographically in 50 normal infants and children. With these normal control data, LV function was assessed in 44 patients with a variety of cardiac diseases. LV volumes were calculated from 30 degrees right anterior oblique cineangiograms using area-length method. Normal values for LV end-diastolic volume (LVEDV) was expressed as a function of body surface area (BSA): LVEDV = 72.4 (BSA). The ratio of measured value to predicted normal value was calculated in the evaluation of diseased hearts. Mean LV ejection fraction (LVEF) in the normal group was 58.9 +/- 5.7%. There was no apparent correlation between LVEF and BSA or age of the patients. For the objective analysis of regional wall motion, the most adequate method was Area method which divides left ventriculogram into 5 regions. Mean ejection change in each region in the normal group was as follows; segment 1 (anterobasal) 52.4 +/- 6.9 (SD)%, segment 2 (anterolateral) 42.6 +/- 7.8%, segment 3 (apical) 46.3 +/- 6.7%, segment 4 (diaphragmatic) 37.0 +/- 7.0% and segment 5 (posterobasal) 29.0 +/- 5.6%. In the group of congenital heart disease with L-R shunt, 16 of 20 patients showed apparent increase of LVEDV. It remained within the normal range in 3 patients who had small shunt. There was no case which showed decreased LVEF or impaired regional wall motion. Both of the 2 patients with congestive cardiomyopathy showed increased LVEDV and decreased LVEF. Generalized hypokinesis of LV was recognized in one of them. In the group of Kawasaki disease with abnormal coronary arteries, which consisted of 27 ventriculograms in 22 patients, increased LVEDV and decreased LVEF were recognized in patients with coronary artery occlusion or large aneurysm. Decreased wall motion was observed in the territories of abnormal coronary arteries presenting occlusion or large-to-medium-sized aneurysm. 相似文献
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