Biomedical subjects
Publications and source records attributed to Y Taira.
This report describes two patients with dilated cardiomyopathy associated with angiographically proven left ventricular aneurysm. There was no apparent history of myocardial infarction and coronary arteries were angiographically normal in both cases.
A 37-year-old woman was admitted with an acute anterior myocardial infarction. Coronary arteriography revealed a dissecting aneurysm of the left main coronary artery. The patient died from perioperative myocardial infarction following aortocoronary bypass surgery on the 102nd hospital day. Histologic sections of the aneurysm revealed that granulation tissue had replaced the aneurysm, suggesting spontaneous healing of the dissecting aneurysm.
We have previously reported that cimetidine, a histamine H2-receptor blocker, augments the histamine-induced coronary vasoconstriction at the site of spastic segments in the atherosclerotic coronary arteries of swine. To elucidate whether cimetidine has a coronary vasoconstrictive effect in humans, 14 patients with vasospastic angina (group 1) and 14 controls with atypical chest pain (group 2) were examined angiographically. Nitroglycerin-effective spontaneous angina with electrocardiographic ST-T changes and ergonovine-induced coronary artery spasm were confirmed in group 1, but not in group 2. Cimetidine was administered intravenously in a dose of 200 mg. Cimetidine induced coronary artery spasm in 4 patients in group 1 but none in group 2(29% vs. 0%, p less than 0.01). The extent of coronary vasoconstriction induced by cimetidine was greater at the site of spastic coronary segments than that at the site of non-spastic segments in group 1 or all segments in group 2 [14% vs. 4%, (p less than 0.01) or 14% vs. 2%, (p less than 0.01)] as well as the extent of ergonovine-induced coronary vasoconstriction [46% vs. 14%, (p less than 0.01) or 46% vs. 14%, (p less than 0.01)] and nitroglycerin-induced coronary vasodilatation [58% vs. 25%, (p less than 0.01) or 58% vs. 17%, (p less than 0.01)]. As it was suggested that cimetidine has potential vasoconstrictive effects in patients with coronary artery spasm, it should be administered with caution in patients with the vasospastic angina pectoris.
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Effects of retrograde coronary venous perfusion on oxygen supply and energy metabolism of ischemic myocardium of the isolated perfused rat heart were examined by means of NADH fluorescence photography. Occlusion of the left coronary artery produced regional ischemia of the left ventricular free wall, as evidenced by the sharply demarcated increase in NADH fluorescence. During ischemia, a narrow area of minimal fluorescence (140 +/- 10 microns), indicating sufficient oxygenation for oxidative phosphorylation, was observed around the epicardial coronary veins in the ischemic lesion. Retrograde perfusion was introduced through the coronary vein (left cardiac vein) that drained off the ischemic area, which resulted in a marked reduction of the area of increased NADH fluorescence in the epicardial surface. In the cross-sectional view, although the myocardium of the entire ischemic area induced by left coronary artery occlusion could be perfused by venous retroperfusion, the effect on reduction of the area of increased NADH fluorescence was seen only in the epicardial half of the myocardium. Retrograde coronary venous perfusion also resulted in a small increase in tension development (P less than 0.05), a decrease in resting tension (P less than 0.01), and partial preservation of myocardial high energy phosphate content (P less than 0.01). We propose that coronary venous retroperfusion improves oxygenation, partially preserves oxidative phosphorylation in the epicardium, and improves contractile function in the ischemic region.
Right ventricular systolic and diastolic function was studied in patients with ischemic heart disease using equilibrium radionuclide ventriculography. In patients with inferior myocardial infarction and proximal right coronary lesions, the right ventricular ejection fraction (0.43 +/- 0.06, n = 10, mean +/- SD) and peak filling rate (1.7 +/- 0.4 EDV/sec) were lower than normals (0.57 +/- 0.07 and 2.7 +/- 0.4 EDV/sec, n = 10, p less than 0.001, respectively). In these patients, the right ventricular time to peak filling rate was longer than in normals (225 +/- 36 msec vs 136 +/- 45 msec, p less than 0.001), while the left ventricular ejection fraction remained normal. In patients with inferior myocardial infarction and distal right coronary lesions, the right ventricular ejection fraction, peak filling rate and time to peak filling rate were not different from those in normals. Even in patients with proximal right coronary lesions, the right ventricular ejection fraction was normal unless they had an inferior myocardial infarction. A decreased left ventricular ejection fraction and abnormal motion of the ventricular septum did not affect the right ventricular ejection fraction. The present results suggest that patients with an inferior myocardial infarction and proximal right coronary lesion often develop right ventricular systolic and diastolic dysfunction.
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Ischaemia induced in Wistar rat hearts by ligation of the main coronary arteries, was studied by NADH-fluorescence photography. The coronary anatomy was examined by barium angiography and intravascular resin infusion and it was confirmed that the main arteries were the left and right coronaries and the septal artery. The septal artery branched from the right coronary orifice in 90% of hearts examined. The long-axial cross-sectional view of the heart showed the ischaemic area to be limited to the left ventricular free wall following ligation of the left coronary, to the right ventricular free wall following ligation of the right coronary artery and to the ventricular septum after ligation of the septal artery. When the left coronary artery was ligated at its origin, the ratio of ischaemic area to cross-sectional area increased from the base to the apex of the heart. The borders of the epicardial ischaemic area induced by left and right coronary ligation made contact without any overlapping or broad separation. This indicates that the area perfused by the left and right coronary arteries was contiguous but physically separated.
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NADPH-cytochrome c reductase (NADPH : ferricytochrome oxido-reductase, EC 1.6.2.4), the flavoprotein which mediates the NADPH-dependent reduction of cytochromes P-450 in adrenocortical microsomes, has been localized immunohistochemically at the light microscopic level in rat adrenal glands. Localization was achieved through the use of sheep antiserum produced against purified, trypsin-solubilized rat hepatic microsomal NADPH-cytochrome c reductase in both an unlabeled antibody peroxidase-antiperoxidase technique and an indirect fluorescent antibody method. The sheep antibody to rat hepatic microsomal NADPH-cytochrome c reductase concomitantly inhibited the NADPH-cytochrome c reductase and progesterone 21-hydroxylase activities catalyzed by isolated rat adrenal microsomes. When sections of rat adrenal glands were exposed to the reductase antiserum in both immunohistochemical procedures, positive staining for NADPH-cytochrome c reductase was observed in parenchymal cells of the three cortical zones but not in medullary chromaffin cells. The intensity of staining, however, was found to differ among the three cortical zones, with the most intense staining being found in the zona fasciculata and the least in the zona glomerulosa. The intensity of staining was also found to differ among cells within the zona fasciculata. These immunohistochemical observations demonstrate that microsomal NADPH-cytochrome c reductase is not distributed uniformly throughout the rat adrenal cortex.