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MISC - 中村　一文

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Effects of Low-Dose Aspirin on Endothelial Function in Hypertensive Patients.

Monobe H, Yamanari H, Nakamura K, Ohe T

Clin. Cardiol 2000年

Involvement of Ca2+ in antiarrhythmic effect of ischemic preconditioning in isolated rat heart

Kui Hong, Kengo Fukushima Kusano, Hiroshi Morita, Yoshihisa Fujimoto, Kazufumi Nakamura, Hiroshi Yamanari, Tohru Ohe

Japanese Journal of Physiology 50 ( 2 ) 207 - 213 2000年

記述言語：英語出版者・発行元：The Physiological Society of Japan

We investigated the relationship between the effects of ischemic preconditioning (IPC) and Ca2+ preconditioning (CPC) on reperfusion-induced arrhythmias. In the control group (noPC), Langendorff-perfused rat hearts were subjected to 5-min zero-flow global ischemia (I) followed by 15-min reperfusion (I/R). In ischemic preconditioning groups (IPC), the hearts were subjected to three cycles of 3-min global ischemia and 5-min reperfusion. In the CPC group, the hearts were exposed to three cycles of 3-min perfusion of higher Ca2+ (2.3 mmol/l Ca2+) followed by 5-min perfusion of normal 1.3 mmol/l Ca2+, and the hearts were then subjected to I/R. Verapamil was administered in several hearts of the IPC group (VR+IPC). Ventricular arrhythmias upon reperfusion were less frequently seen in the IPC and CPC groups than in the noPC and VR+IPC groups. IPC and CPC could attenuate conduction delay and enhance shortening of the monophasic action potential duration during ischemia. The ventricular fibrillation threshold measured at 1-min reperfusion was significantly higher in the IPC and CPC groups than in the noPC and VR+IPC groups. Verapamil completely abolished the salutary effects of IPC. These results demonstrate that Ca2+ plays an important role in the antiarrhythmic effect of IPC during reperfusion.

DOI： 10.2170/jjphysiol.50.207

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Hepatitis C Virus Infection in a Patient With Dermatomyositis and Left Ventricular Dysfunction(共著)

Japanese Circulation Journal 64 ( 8 ) 617 - 618 2000年

Relatively Benign Clinical Course in Asymptomatic Patients with Brugada-Type Electrocardiogram Without Family History of Sudden Death.

Takenaka S, Fukushima K K, Hisamatsu K, Nagase S, Nakamura K, Morita H, Matsubara H, Emori T, Ohe T

Journal of Cardiovascular Electrophysiology 2000年

Lone AFにおける心房心筋炎の関与．

草野研吾, 中村陽一, 中村一文, 垣下幹夫, 永瀬聡, 斉藤博則, 松原広己, 山成洋, 大江透, 磯村寛樹, 山田雅夫

Therapeutic Research 22,3,29-32 2000年

Involvement of Ca2+ in Antiarrhythmic Effect of Ischemic Preconditioning in Isolated Rat Heart(共著)

Japanese Journal of Physiology 50 ( 2 ) 207 - 213 2000年

Manumycin A, inhibitor of ras farnesyltransferase, inhibits proliferation and migration of rat vascular smooth muscle cells

Hirosuke Kouchi, Kazufumi Nakamura, Kazuo Fushimi, Masakiyo Sakaguchi, Masahiro Miyazaki, Tohru Ohe, Masayoshi Namba

Biochemical and Biophysical Research Communications 264 ( 3 ) 915 - 920 1999年11月

記述言語：英語出版者・発行元：Academic Press Inc.

Restenosis after angioplasty is thought to be caused by proliferation and migration of vascular smooth muscle cells (VSMCs), and it is a most serious problem in medical treatment. A low dose (50 ng/ml) of manumycin A, an inhibitor of p21(ras) (ras) farnesylation, significantly inhibited proliferation of rat VSMCs stimulated by the platelet-derived growth factor (PDGF). The mitoinhibitory effect of manumycin A was dose- and time-dependent but was independent of cell density. Western blot analysis showed that manumycin A reduced the amount of functional ras localized at the cytoplasmic membrane and inhibited the phosphorylation of p42/44 mitogen-activated protein kinase (MAPK). Manumycin A also inhibited VSMC migration and disorganized α actin fibers, as shown by immnofluorecence staining. These results indicate that the interruption of the ras/MAPK signal transduction pathway and the disorganization of α actin fibers are the main cause of manumycin A inhibition of VSMC proliferation and migration induced by PDGF.

DOI： 10.1006/bbrc.1999.1546

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Manumycin A, Inhibitor of ras Farnesyltransferase, Inhibits Proliferation and Migration of Rat Vascular Smooth Muscle Cells(共著)

Biochemical and Biophysical Research Communications 264 ( 3 ) 915 - 920 1999年11月

24) 右室流出路起源特発性心室頻拍におけるQRS波形からみた起源の推定

森田宏, 福島研吾, 中村一文, 藤本義久, 垣下幹夫, 山成洋, 大江透

Japanese circulation journal 63 ( 3 ) 914 - 914 1999年10月

83) Atriofascicular connectionのMahaim束の一例

中村一文, 福島研吾, 伴場主一, 垣下幹夫, 森田宏, 山成洋, 大江透

Japanese circulation journal 63 ( 3 ) 921 - 921 1999年10月

APICAL HYPERTROPHY ASSOCIATED WITH RAPID T-WAVE INVERSION ON THE ELECTROCARDIOGRAM

H YAMANARI, D SAITO, K MIKIO, K NAKAMURA, T NANBA

HEART AND VESSELS 10 ( 4 ) 221 - 224 1995年

記述言語：英語掲載種別：記事・総説・解説・論説等（学術雑誌）出版者・発行元：SPRINGER VERLAG

A 53-year-old man who had no chest pain and no family history of heart disease demonstrated a rapid T wave change on an electrocardiogram, from a positive T wave to a giant negative T wave, within 1 year. Echocardiography showed no left ventricular hypertrophy before or after the T wave change. Cine-magnetic resonance imaging revealed focal apical hypertrophy after the appearance of the giant negative T wave. Although T wave inversions sometimes develop within a short period in patients with hypertrophic cardiomyopathy, they are rare in a patient without hypertension or chest pain.

DOI： 10.1007/BF01744991

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Apical hypertrophy associated with rapid T wave inversion on the electrocardiogram(共著)

Heart and Vessels 10 ( 4 ) 221 - 224 1995年

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