研究者業績
  1. 研究者検索結果一覧
  2. 永井 良三

永井 良三

ナガイ リョウゾウ  (Ryozo Nagai)

基本情報

所属
自治医科大学 自治医科大学 学長
学位
博士(医学)
J-GLOBAL ID
200901024033893870
researchmap会員ID
1000190318

研究キーワード

 4

研究分野

 1

委員歴

 5

受賞

 7
もっとみる

論文

 955
  • Yasuhiro Hitomi, Yasushi Imai, Masanari Kuwabara, Yusuke Oba, Tomoyuki Kabutoya, Kazuomi Kario, Hisaki Makimoto, Takahide Kohro, Eiichi Shiraki, Naoyuki Akashi, Hideo Fujita, Tetsuya Matoba, Yoshihiro Miyamoto, Arihiro Kiyosue, Kenichi Tsujita, Masaharu Nakayama, Ryozo Nagai
    IJC Heart & Vasculature 54 101507-101507 2024年10月  
  • Yusuke Oba, Tomoyuki Kabutoya, Takahide Kohro, Yasushi Imai, Kazuomi Kario, Hisahiko Sato, Kotaro Nochioka, Masaharu Nakayama, Naoyuki Akashi, Hideo Fujita, Yoshiko Mizuno, Arihiro Kiyosue, Takamasa Iwai, Yoshihiro Miyamoto, Yasuhiro Nakano, Masanobu Ishii, Taishi Nakamura, Kenichi Tsujita, Tetsuya Matoba, Ryozo Nagai
    Hypertension research : official journal of the Japanese Society of Hypertension 2024年9月19日  
    The Japanese Society of Hypertension have established a blood pressure (BP) target of 130/80 mmHg for patients with coronary artery disease (CAD). We evaluated the data of 8793 CAD patients in the Clinical Deep Data Accumulation System database who underwent cardiac catheterization at six university hospitals and the National Cerebral and Cardiovascular Center (average age 70 ± 11 years, 78% male, 43% with acute coronary syndrome [ACS]). Patients were divided into two groups based on whether or not they achieved the guideline-recommended BP of <130/80 mmHg. We analyzed the relationship between BP classification and major adverse cardiac and cerebral event (MACCE) separately in two groups: those with ACS and those with chronic coronary syndrome (CCS). During an average follow-up period of 33 months, 710 MACCEs occurred. A BP below 130/80 mmHg was associated with fewer MACCEs in both the overall (hazard ratio [HR] 0.83, 95% confidence interval [CI] 0.70-1.00, p = 0.048) and the ACS group (HR 0.67, 95%CI 0.51-0.88, p = 0.003). In particular, stroke events were also lower among those with a BP below 130/80 mmHg in both the overall (HR 0.69, 95%CI 0.53-0.90, p = 0.006) and ACS groups (HR 0.44, 95%CI 0.30-0.67, p < 0.001). In conclusion, the achievement of BP guidelines was associated with improved outcomes in CAD patients, particularly in reducing stroke risk among those with ACS.
  • So Ikebe, Masanobu Ishii, Yasuhiro Otsuka, Taishi Nakamura, Kenichi Tsujita, Tetsuya Matoba, Takahide Kohro, Yusuke Oba, Tomoyuki Kabutoya, Yasushi Imai, Kazuomi Kario, Arihiro Kiyosue, Yoshiko Mizuno, Kotaro Nochioka, Masaharu Nakayama, Takamasa Iwai, Yoshihiro Miyamoto, Hisahiko Sato, Naoyuki Akashi, Hideo Fujita, Ryozo Nagai
    International Journal of Cardiology: Cardiovascular Risk and Prevention 22 2024年9月  
    The authors regret that the original version of the article incorrectly stated the study period as “April 2014 to March 2020" in both the Abstract and the Methods section. The correct study period should have been “April 2013 to March 2019". The authors would like to apologise for any inconvenience caused.
  • Hiroshi Iwata, Katsumi Miyauchi, Ryo Naito, Satoshi Iimuro, Yukio Ozaki, Ichiro Sakuma, Yoshihisa Nakagawa, Kiyoshi Hibi, Takefui Hiro, Yoshihiro Fukumoto, Seiji Hokimoto, Yasushi Saito, Hisao Ogawa, Hiroaki Shimokawa, Hiroyuki Daida, Takeshi Kimura, Ryozo Nagai
    JACC: Advances 3(7) 2024年7月  
    Background: The prognostic implications of persistent low-grade inflammation in patients with chronic coronary syndrome (CCS) are underexplored. The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy with Pitavastatin in Coronary Artery Disease) study demonstrated the benefit of higher intensity pitavastatin in Japanese patients with CCS. Objectives: This prespecified subanalysis of the REAL-CAD study aimed to assess the prognostic effect of the persistent low-grade inflammation represented by high-sensitivity C-reactive protein (hs-CRP) in CCS patients. Methods: The present analysis involved patients without events until 6 months after randomization and whose hs-CRP levels were available at baseline and 6 months (n = 10,460). The primary endpoint was the composite of cardiovascular mortality, myocardial infarction, stroke, and unstable angina hospitalization. Landmark analyses evaluated the prognostic impact of continuous inflammation in 4 groups based on the median levels of hs-CRP (0.5 mg/L for both) at baseline and 6 months. The 4 groups included patient with persistently low, elevated (increased), reduced, and persistently high hs-CRP. Results: Adjusted Cox proportional hazard analyses demonstrated an increased risk of the primary endpoint in the group with persistently high hs-CRP when compared to the group with persistently low hs-CRP as a reference (adjusted HR: 1.48, 95% CI: 1.18-1.89; P = 0.001), but with a similar risk in the group with elevated (HR: 1.07, 95% CI: 0.77-1.49, P = 0.68) and reduced (HR: 0.92; 95% CI: 0.66-1.27; P = 0.60) hs-CRP. Conclusions: The study shows that persistent low-grade inflammation is associated with poor outcomes and underscores the need to address residual inflammatory risk in CCS patients. (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease [REAL-CAD]; NCT01042730)
  • Hiroshi Iwata, Katsumi Miyauchi, Ryo Naito, Satoshi Iimuro, Yukio Ozaki, Ichiro Sakuma, Yoshihisa Nakagawa, Kiyoshi Hibi, Takefui Hiro, Yoshihiro Fukumoto, Seiji Hokimoto, Yasushi Saito, Hisao Ogawa, Hiroaki Shimokawa, Hiroyuki Daida, Takeshi Kimura, Ryozo Nagai
    JACC. Advances 3(7) 100996-100996 2024年7月  
    BACKGROUND: The prognostic implications of persistent low-grade inflammation in patients with chronic coronary syndrome (CCS) are underexplored. The REAL-CAD (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy with Pitavastatin in Coronary Artery Disease) study demonstrated the benefit of higher intensity pitavastatin in Japanese patients with CCS. OBJECTIVES: This prespecified subanalysis of the REAL-CAD study aimed to assess the prognostic effect of the persistent low-grade inflammation represented by high-sensitivity C-reactive protein (hs-CRP) in CCS patients. METHODS: The present analysis involved patients without events until 6 months after randomization and whose hs-CRP levels were available at baseline and 6 months (n = 10,460). The primary endpoint was the composite of cardiovascular mortality, myocardial infarction, stroke, and unstable angina hospitalization. Landmark analyses evaluated the prognostic impact of continuous inflammation in 4 groups based on the median levels of hs-CRP (0.5 mg/L for both) at baseline and 6 months. The 4 groups included patient with persistently low, elevated (increased), reduced, and persistently high hs-CRP. RESULTS: Adjusted Cox proportional hazard analyses demonstrated an increased risk of the primary endpoint in the group with persistently high hs-CRP when compared to the group with persistently low hs-CRP as a reference (adjusted HR: 1.48, 95% CI: 1.18-1.89; P = 0.001), but with a similar risk in the group with elevated (HR: 1.07, 95% CI: 0.77-1.49, P = 0.68) and reduced (HR: 0.92; 95% CI: 0.66-1.27; P = 0.60) hs-CRP. CONCLUSIONS: The study shows that persistent low-grade inflammation is associated with poor outcomes and underscores the need to address residual inflammatory risk in CCS patients. (Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease [REAL-CAD]; NCT01042730).
もっとみる

MISC

 1913
  • M Aikawa, Y Sakomura, M Ueda, K Kimura, I Manabe, S Ishiwata, N Komiyama, H Yamaguchi, Y Yazaki, R Nagai
    Circulation 96(1) 82-90 1997年7月1日  査読有り
    BACKGROUND: The pathophysiology of phenotypic modulation of smooth muscle cells (SMCs) involved in restenosis after angioplasty is not well understood. Smooth muscle myosin heavy chain (SM MHC) isoforms (SM1 and SM2) are specific markers for SMC differentiation. In particular, SM2 is useful as a marker of mature SMCs. SMemb is a nonmuscle myosin heavy chain (NM MHC) whose expression is upregulated in immature or activated SMC. METHODS AND RESULTS: To determine SMC phenotypes in neointimal tissues after percutaneous transluminal coronary angioplasty (PTCA), we performed immunohistochemistry on human coronary arteries with antibodies against alpha-SM actin, SM1, SM2, and SMemb. Tissues were obtained from six autopsied patients and from atherectomy specimens from 16 patients who had undergone PTCA. Medial SMCs were positive for alpha-actin, SM1, and SM2. Expression of SM1 and SM2 in the neointima varied with the time after intervention, whereas alpha-actin was constitutively expressed in all cases studied. Neointimal cells at 16 and 20 days after PTCA contained alpha-actin but little or no SM1 or SM2, indicating that these cells modulated their phenotype to the immature state. Neointimal SMCs recovered SM MHC expression, first SM1 and then SM2, by 6 months after PTCA. Increased expression of SMemb was found in the neointima but without apparent relationship to the time after PTCA. CONCLUSIONS: Neointimal SMCs show features of an undifferentiated state, indicated by altered expression of SM MHC, and undergo redifferentiation in a time-dependent manner. The expression of SM MHC isoforms provides insight into the biology of healing after angioplasty and furnishes useful tools for the understanding of the roles of differentiation and phenotypic modulation of SMCs in human vascular lesions.
  • Tomono Shoichi, Kawazu Shoji, Hasegawa Akira, Nagai Ryozo, Murata Kazuhiko
    Japanese circulation journal 61(7) 612-612 1997年6月20日  
  • Ohyama Yoshio, Masuda Hiroaki, Okamoto Ei-ichi, Sakamoto Hironosuke, Nagai Ryozo, Simomura Yukio, Kuro-o Makoto, Kurabayashi Masahiko, Manabe Ichiro
    Japanese circulation journal 61(7) 574-575 1997年6月20日  
  • Saito Yuichiro, Nakamura Tetsuya, Sumino Hiroyuki, Mochida Manabu, Ohyama Yoshio, Hoshino Jin, Kato Tatsuya, Sato Kunio, Ono Zenpei, Sakamaki Tetsuo, Nagai Ryozo
    Japanese circulation journal 61(7) 582-583 1997年6月20日  
  • Saito Yuichiro, Nakamura Tetsuya, Sumino Hiroyuki, Mochida Manabu, Ohyama Yoshio, Hoshino Jin, Kato Tatsuya, Sato Kunio, Ono Zenpei, Sakamaki Tetsuo, Nagai Ryozo
    Japanese circulation journal 61(7) 556-557 1997年6月20日  
  • 中島 忠, 永井 良三
    医学のあゆみ 181(10) 906-910 1997年6月7日  
  • S Tomono, S Kawazu, T Ohno, T Utsugi, N Kato, Y Itoh, Y Ohyama, T Uchiyama, R Nagai
    DIABETOLOGIA 40 1765-1765 1997年6月  
  • Y von Kodolitsch, C A Nienaber, T Suzuki, R Nagai, Y Yazaki, T Meinertz
    Zeitschrift fur Kardiologie 86(6) 469-73 1997年6月  査読有り
    Despite the availability of diagnostic modalities such as transesophageal echocardiography, computed tomography or magnetic resonance imaging up to 30% of patients with acute aortic dissection remain undiagnosed before death. A novel immunoassay of serum smooth muscle myosin heavy chain was recently developed as a potential diagnostic tool for the detection of aortic dissection. The immunoassay was applied in two patients with an acute chest pain syndrome but no initial clinical suspicion of aortic disease. In both patients myocardial ischemia was ruled out by laboratory, electrocardiographic and echocardiographic examinations. In the first patient both dilation of the aorta and long-standing arterial hypertension were known; however, it was not before 48 h until dissection was suspected and a spiral-CT was performed demonstrating a localized ascending aortic dissection. At this time (48 h after onset of symptoms) the smooth muscle myosin heavy chain concentration in the serum was close to normal. In the other patient there was neither a suggestive history nor any clinical sign of aortic dissection. Widening of the abdominal aortic wall on an ultrasound examination was the key to the incidental diagnosis of a clinically unsuspected type B dissection. The serum test 12 h after onset of pain revealed elevated (diagnostic) serum levels of smooth muscle myosin heavy chains. Both cases exemplify important gaps in the diagnostic strategy for the detection of acute aortic dissection. A novel immunoassay for smooth muscle myosin heavy chains provides rapid and reliable diagnostic information especially in patients without clinically suspected aortic dissection and may avoid limitations in the diagnostic work-up of patients with acute aortic disease, if used early in the evaluation of patients with chest pain syndromes.
  • N Suzuki, K Kimura, R Nagai, S Ohba, N Mise, J Hiroi, A Tojo, Y Hirata, A Nagaoka, A Goto, M Omata
    NEPHROLOGY 3(3) 251-259 1997年6月  
    The aim of this study was to determine the phenotypic modulation in preglomerular vascular smooth muscles and glomerular cells in hypertension. Eight-week-old stroke-prone spontaneously hypertensive rats (SHRSP) fed high sodium pellets (3%) were untreated or treated with a calcium antagonist, manidipine HCl (2 mg/kg per day), for 8 weeks. The expression of myosin heavy chain isoforms (MHC), SM2 (muscle-type) and SMemb (non-muscle-type) or alpha-actin was examined by the immunohistochemical technique. In normotensive Wistar-Kyoto rats, both SM2 and alpha-actin were expressed equally in the smooth muscles of preglomerular vessels, and SMemb was expressed slightly in the glomerular epithelial cells. In the SHRSP, however, the expression of SM2 and alpha-actin was significantly decreased or disappeared in the afferent arterioles, depending on the degree of vascular damage. In damaged glomeruli, SMemb and alpha-actin were newly expressed in mesangial cells. Manidipine HCl attenuated the renal damage and restored the expression of alpha-actin in the afferent arterioles. There was a significant correlation between the glomerular damage and the attenuation of SM2 expression (r=0.87). In conclusion, phenotypic modulation of vascular smooth muscles occurred in hypertensive renal damage and was correlated with the glomerular damage, where the phenotypic modulation also took place in the mesangial cells. These results indicate that the phenotypic modulations revealed by the expression of myosin isoforms might play an important role in the development of hypertensive renal damage.
  • T Suzuki, T Kanda, H Nagaoka, S Kubota, T Iizuka, R Nagai, I Kobayashi
    Angiology 48(6) 497-502 1997年6月  査読有り
    The objective of this study was to determine noninvasively the likelihood of recovery of the left ventricular ejection fraction (LVEF) in patients with dilated cardiomyopathy (DCM) verified by radionuclide ventriculography. Twenty patients with DCM were classified into two groups according to the LVEF by M-mode echocardiographic findings two years after ventriculographic examination. The LVEF recovered to > or = 50% in 10 patients (Group A), while it was sustained at < 50% in 10 patients (Group B). The clinical features of each group were compared, based on results of physical examination, radionuclide ventriculography, and other diagnostic tests performed on their referral to hospital. Only the systolic blood pressure differed significantly between the two groups, being slightly, but significantly, increased in Group A over that in Group B (P < 0.05). LVEF at rest by radionuclide did not differ (Group A: 31.5 +/- 10.3% vs Group B: 26.5 +/- 9.4%). Peak exercise EF-EF at rest (peak delta EF) in Group A was apparently increased (3.4 +/- 4.0%), while that in Group B was decreased (-4.4 +/- 5.2%). The positive peak delta EF had a highly predictive value of 90% for patients with DCM whose LVEF will recover to more than 50%. The recovery EF-EF at rest did not differ significantly between groups (Group A: 8.4 +/- 4.7 vs Group B: 3.9 +/- 2.3, P < 0.05). Other clinical parameters such as functional class, cardiothoracic ratio, LVEF by echocardiography, cardiac index by Swan-Ganz catheter examination, and histologic examination of biopsied endocardium were indistinguishable in the two groups. The authors conclude that peak delta EF of radionuclide ventriculography on exercise indicates a preservation of LVEF and predicts a good clinical recovery in patients with DCM.
  • 奥村 渉, 宇都木 敏浩, 石井 主税, 須賀 達夫, 佐藤 秀樹, 関口 賢一, 中村 哲也, 伴野 祥一, 河津 捷二, 永井 良三, 児島 高寛, 長町 幸雄, 桜井 信司, 福里 利夫
    糖尿病 40(5) 285-291 1997年5月30日  
  • Y Ohyama, T Utsugi, T Ohno, T Suga, T Uchiyama, M KuroO, Y Nabeshima, R Nagai
    DIABETES 46 1161-1161 1997年5月  
  • T Utsugi, T Kanda, Kobayashi, I, N Katoh, A Tanaka, S Tomono, S Kawazu, R Nagai
    DIABETES 46 151-151 1997年5月  
  • N Akuzawa, T Nakamura, A Tanaka, S Ikeda, T Fukuda, T Sakamaki, R Nagai
    INTERNAL MEDICINE 36(4) 289-292 1997年4月  
    A 29-year-old man with von Recklinghausen's disease suddenly developed severe epigastric pain and was admitted to hospital, Physical examination revealed elevated blood pressure (200/130 mmHg) and tachycardia (162 bpm),Initially, he was suspected to have appendicitis, and appendectomy was performed immediately; however, appendicitis was not demonstrable pathologically, Retroperitoneal hematoma was found incidentally during the operation, Further clinical and laboratory examination demonstrated a marked increase in the urinary excretion of catecholamines, There was no evidence of pheochromocytoma on computed tomography or magnetic resonance imaging; however, these imaging studies simply showed a hematoma at the right adrenal gland, Transient hypertension and tachycardia, resembling pheochromocytoma, was caused by adrenal hemorrhage.
  • T Nakamura, Y Ohyama, H Masuda, T Kurashina, Y Saito, T Kato, H Sumino, K Sato, T Sakamaki, A Sasaki, R Nagai
    JOURNAL OF HYPERTENSION 15(4) 373-381 1997年4月  
    Objectives Our objective was to determine the effect of nitric oxide (NO) inhibition on renal synthesis of endothelin-l (ET-1) in vivo. Design and methods Rats were administered 500 mg/l N-G-nitro-L-arginine methyl ester (L-NAME) in their drinking water or its vehicle for 2 weeks (PW-L-NAME, n=10; SW-CONT, n=10) or for 6 weeks (6W-L-NAME, n=13; 6W-CONT, n=11). We measured the levels of albumin, NO metabolites and ET-1 both in their blood and in 24 h urine samples, and determined the expression of preproET-1 messenger RNA in the renal cortex and the inner medulla. We also examined renal histology, Results L-NAME administration for 6 weeks reduced NO metabolites both in serum (21.5 versus 3.66 nmol/ml in 6W-CONT) and in urine (5.72 Versus 22.53 nmol/24 h in 6W-CONT), raised the systolic blood pressure (228 versus 162 mmHg in 6W-CONT), and the increased urinary excretion of albumin (24.29 +/- 11.66 versus 0.60 +/- 0.08 mg/day in 6W-CONT) and of ET-1 (112.0 +/- 38.3 versus 35.8 +/- 4.4 pg/day in 6W-CONT), There were no significant differences between the plasma levels of ET-1 in the control and L-NAME groups. Expression of preproET-1 messenger RNA increased in the renal cortex but not in the inner medulla in the 6W-L-NAME group, Bleeding and marked arteriolar narrowing were observed in the renal cortex of the 6W-L-NAME group. Conclusions Prolonged inhibition of NO synthesis increases urinary excretion of ET-1 and albumin without having any effect on plasma ET-1 levels. These results do not support the hypothesis that NO plays an inhibitory role in the regulation of ET-1 in the systemic circulation, although it is possible that such a role could exist in renal tissue. However, in view of the albuminuria, a more likely explanation is that increased urinary ET-l is secondary to L-NAME-induced renal hyperfiltration injury.
  • 斎藤 勇一郎, 中村 哲也, 角野 博之, 持田 学, 星野 仁, 加藤 達也, 佐藤 邦雄, 小野 善平, 酒巻 哲夫, 永井 良三
    Japanese circulation journal 61 332-332 1997年3月5日  
  • 鈴木 淳一, 磯部 光章, 山崎 論, 関口 守衛, 川内 基裕, 古瀬 彰, 永井 良三
    Japanese circulation journal 61 508-508 1997年3月5日  
  • 角野 博之, 佐藤 邦雄, 増田 浩明, 斎藤 勇一郎, 星野 仁, 坂本 浩之助, 大山 良雄, 加藤 達也, 中村 哲也, 小野 善平, 酒巻 哲夫, 永井 良三, 神田 享勉
    Japanese circulation journal 61 377-377 1997年3月5日  
  • 渡辺 徳, 倉林 正彦, 相原 康, 海老原 文, 渡辺 昌文, 鈴木 享, 矢崎 義雄, 永井 良三, 磯部 光章
    Japanese circulation journal 61 219-219 1997年3月5日  
  • 坂本 浩之助, 酒巻 哲夫, 神田 享勉, 大山 良雄, 原沢 充子, 永井 良三, 清籐 勉
    Japanese circulation journal 61 224-224 1997年3月5日  
  • 星野 仁, 中村 哲也, 斎藤 勇一郎, 角野 博之, 酒巻 哲夫, 永井 良三
    Japanese circulation journal 61 285-285 1997年3月5日  
  • 大山 良雄, 増田 浩明, 岡本 栄一, 坂本 浩之助, 永井 良三, 下村 行生, 黒尾 誠, 倉林 正彦, 真鍋 一郎
    Japanese circulation journal 61 293-293 1997年3月5日  
  • 山岸 高宏, 中村 哲也, 大山 良雄, 須賀 達夫, 岡本 栄一, 斉藤 勇一郎, 星野 仁, 宇都木 敏浩, 酒巻 哲夫, 永井 良三, 松村 穣, 相澤 宏樹, 黒尾 誠, 鍋島 陽一
    Japanese circulation journal 61 295-295 1997年3月5日  
  • 伴野 祥一, 河津 捷二, 長谷川 昭, 永井 良三, 村田 和彦
    Japanese circulation journal 61 476-476 1997年3月5日  
  • 馬場 俊曉, 神田 享勉, 中野 正幸, 永井 良三
    Japanese circulation journal 61 473-473 1997年3月5日  
  • 神田 享勉, 瀬田 享博, 関口 賢一, 金子 克己, 井上 雅浩, 横山 知行, 岩崎 勉, 永井 良三, 鈴木 忠
    Japanese circulation journal 61 461-461 1997年3月5日  
  • 渡辺 昌文, 倉林 正彦, 海老原 文, 相原 康, 鈴木 亨, 矢崎 義雄, 迫村 泰成, 永井 良三
    Japanese circulation journal 61 370-370 1997年3月5日  
  • 金古 善明, 谷口 靖広, 中島 忠, 間仁田 守, 伊藤 敏夫, 永井 良三
    Japanese circulation journal 61 187-187 1997年3月5日  
  • 斎藤 勇一郎, 中村 哲也, 角野 博之, 持田 学, 星野 仁, 加藤 達也, 佐藤 邦雄, 小野 善平, 酒巻 哲夫, 永井 良三
    Japanese circulation journal 61 196-196 1997年3月5日  
  • 鈴木 亨, 倉林 正彦, 矢崎 義雄, 永井 良三
    Japanese circulation journal 61 231-231 1997年3月5日  
  • 栗原 由紀子, 栗原 裕基, 鈴木 亨, 矢崎 義雄, 永井 良三
    Japanese circulation journal 61 231-231 1997年3月5日  
  • 渡辺 昌文, 倉林 正彦, 相原 康, 海老原 文, 鈴木 亨, 矢崎 義雄, 真鍋 一郎, 永井 良三
    Japanese circulation journal 61 229-229 1997年3月5日  
  • 佐藤 秀樹, 外山 卓二, 金古 善明, 太田 直樹, 金沢 紀雄, 鈴木 忠, 永井 良三, 井上 登美夫, 遠藤 啓吾
    Japanese circulation journal 61 234-234 1997年3月5日  
  • 木村 彰方, 原田 晴仁, 広井 知歳, 佐藤 真夏, 笹岡 大史, 高橋 めぐみ, 大渕 信二, 中村 剛之, 西 宏文, 小柳 毅, 中田 真詩, 今泉 勉, 古賀 義則, 戸嶋 裕徳, 永井 良三, 廣江 道昭, 和泉 徹, 沼野 藤夫, 河村 慧四郎, 横田 慶之, 横山 光宏, 矢崎 義雄, 坂本 二哉
    Japanese circulation journal 61 83-83 1997年3月5日  
  • 田中 敏博, 永井 良三, 矢崎 義雄, 中村 祐輔
    Japanese circulation journal 61(SupplementI) 1997年3月5日  
  • 鈴木 亨, 林 同文, 山崎 力, 水野 健彦, 小室 一成, 倉林 正彦, 山沖 和秀, 矢崎 義雄, 永井 良三
    Japanese circulation journal 61 1997年3月5日  
  • H Nagaoka, N Isobe, S Kubota, T Iizuka, S Imai, T Suzuki, R Nagai
    CARDIOLOGY 88(2) 180-188 1997年3月  
    The diagnostic values of adenosine, dobutamine, and exercise radionuclide ventriculography (RNVG) in the detection of coronary artery disease (CAD), and the characteristics of those patients who showed myocardial ischemia during the infusion of adenosine or dobutamine were assessed in 41 patients with suspected CAD. Sensitivity, specificity, and accuracy, respectively, for detecting patients with CAD were 35 (p &lt; 0.01 vs. exercise RNVG), 100 and 46% (p &lt; 0.01 vs. exercise RNVG) with adenosine RNVG, 74, 100 and 78% with dobutamine RNVG and 88, 71 and 85% with exercise RNVG. There was a significant difference in physiologic parameters during the provocation of ischemia by adenosine versus exercise RNVG, although these parameters were similar by dobutamine and exercise RNVG. Stepwise discriminant analysis revealed that the number of stenotic vessels was an important and independent predictor for the myocardial ischemia induced by each stress; the peak filling rate was the only predictor for adenosine-induced ischemia. Dobutamine induced myocardial ischemia in a way similar to that of exercise, and was more useful than adenosine for pharmacologic stress RNVG, The mechanism of the adenosine-induced ischemia seemed to differ from that of the ischemia induced by dobutamine or exercise, and to be closely associated with left ventricular diastolic function.
  • T Okazaki, H S Sharma, M Aikawa, A Yamataka, R Nagai, T Miyano, D Tibboel
    Journal of pediatric surgery 32(3) 391-4 1997年3月  査読有り
    Abnormalities of the pulmonary vasculature are well documented in cases of congenital diaphragmatic hernia (CDH). Vascular endothelial growth factor (VEGF), an angiogenic factor, is a recently described endothelial cell-specific growth factor. Myosin heavy chain (MHC) isoforms such as SMemb, SM1 and SM2 are important molecular markers used to study vascular smooth muscle cell differentiation. SMemb is predominantly expressed in immature smooth muscle cells (SMC), and SM2 is expressed in mature SMCs. The authors investigated the expression of VEGF and SMC differentiation in pulmonary vessels in CDH rat lungs and in controls. The lungs of nitrofen-induced CDH rat fetuses (n = 16, gestational age 16, 18, 20, and 22 days) were stained immunohistochemically using antibodies against VEGF, SMemb and SM2, while alpha-actin was used as a general marker of vascular smooth muscle cells. In the CDH group VEGF expression was negative in pulmonary vessels before birth, and in the control group VEGF was positive in smooth muscle cells in vessel walls from 20 days both in vessels at the hilum and in pulmonary parenchyma. In both control and CDH groups, SMemb expression was positive from 16 days' gestation. SM2 expression was negative in vessel walls during the prenatal period in both groups. Alpha-actin was localized in both lungs obtained from control and CDH groups in the lung hilum from 16 days and around peripheral vessels from 18 days. Differences in vascular smooth muscle cell differentiation were not observed between control and CDH lung. These findings suggest that differences in pulmonary vascular development exist between control and CDH rats for VEGF expression, and maturational differences in smooth muscle cell differentiation are not present. This role of altered endothelial cell growth might be related to the different pulmonary vascular reactivity present in CDH lungs.
  • T Nakajima, Y Kaneko, Y Taniguchi, K Hayashi, T Takizawa, T Suzuki, R Nagai
    European heart journal 18(3) 530-1 1997年3月  査読有り
  • T Tanaka, R Nagai, H Tomoike, S Takata, K Yano, K Yabuta, N Haneda, O Nakano, A Shibata, T Sawayama, H Kasai, Y Yazaki, Y Nakamura
    Circulation 95(3) 565-7 1997年2月4日  査読有り
    BACKGROUND: Familial long-QT syndrome (LQTS) is characterized by prolonged ventricular repolarization. Clinical symptoms include recurrent syncopal attacks, and sudden death may occur due to ventricular tachyarrhythmias. Three genes responsible for this syndrome (KVLQT1, HERG, and SCN5A) have been identified so far. We investigated mutations of these genes in LQTS families. METHODS AND RESULTS: Thirty-two Japanese families with LQTS were brought together for screening for mutations. Genomic DNA from each proband was examined by the polymerase chain reaction-single-strand conformation polymorphism technique followed by direct DNA sequencing. In four of the families, comprising 16 patients, mutations were identified in KVLQT1; five other families (9 patients) segregated mutant alleles of HERG. All 25 of these patients carried the specific mutations present in their respective families, and none of 80 normal individuals carried these alleles. Mutations were confirmed by endonuclease digestion or hybridization of mutant allele-specific oligonucleotides. No mutation in SCN5A was found in any family. CONCLUSIONS: We identified nine different mutations among 32 families with LQTS. Eight of these were novel and account for 25% of all types of mutations reported to date. Such a variety of mutations makes it difficult to screen high-risk groups using simple methods such as endonuclease digestion or mutant allele-specific amplification.
  • Y Fukumoto, H Shimokawa, A Ito, T Kadokami, Y Yonemitsu, M Aikawa, M K Owada, K Egashira, K Sueishi, R Nagai, Y Yazaki, A Takeshita
    Journal of cardiovascular pharmacology 29(2) 222-31 1997年2月  査読有り
    We recently developed a porcine model in which chronic, local treatment with interleukin-1 beta (IL-1 beta) causes coronary arteriosclerosis-like changes and hyperconstrictive responses. This study was designed to examine whether or not other major inflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) might also cause similar coronary responses and whether those responses are associated with alterations in the smooth-muscle phenotypes. A segment of the porcine coronary artery was aseptically wrapped with cotton mesh, absorbing IL-1 beta, TNF-alpha, and IL-1 alpha. Two weeks after the operation, coronary arteriography showed the development of mild stenotic lesions at the cytokine-treated sites, where hyperconstrictive responses were repeatedly induced by intracoronary serotonin or histamine. Histologically mild intimal thickening was noted at those cytokine-treated sites. Immunostaining and immunoblotting demonstrated that all three myosin heavy chain isoforms, SM1, SM2 (smooth-muscle type), and SMemb (nonmuscle type), were noted in the normal coronary segments, whereas in the segments treated with inflammatory cytokines, SM1 and SM2 were markedly reduced, and only SMemb was noted. These results indicate that inflammatory cytokines all have a similar ability to induce coronary arteriosclerosis-like changes and hyperconstrictive responses, which are associated with alterations in smooth-muscle phenotypes toward dedifferentiation.
  • A Hasegawa, M Hatori, M Amano, T Iijima, H Adachi, E Yamaguchi, T Fukuda, K Murata, R Nagai
    PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY 20(2) 307-312 1997年2月  
    Our objective was to determine the adequate pacing rate during exercise in ventricular pacing by measuring exercise capacity, cardiac output, and sinus node activity. Eighteen patients with complete AV block and an implanted pacemaker underwent cardiopulmonary exercise tests under three randomized pacing rates: fixed rate pacing (VVI) at 60 beats/min and ventricular rate-responsive pacing (VVIR) programmed to attain a heart rate of about 110 beats/min or 130 beats/min (VVIR 110 and VVIR 130, respectively) at the end of exercise. Compared with VVI and VVIR 130, VVIR 110 was associated with an increased peak oxygen uptake (VVIR 110: 20.3 +/- 4.5 vs VVI: 16.9 +/- 3.1; P &lt; 0.01; and VVIR 130: 19.0 +/- 4.1 mL/min per kg, respectively; P &lt; 0.05) and a higher oxygen uptake at anaerobic threshold (15.3 +/- 2.7, 12.7 +/- 1.9; P &lt; 0.01, and 14.6 +/- 2.6 mL/min per kg; P &lt; 0.05). The atrial rate during exercise expressed as a percentage of the expected maximal heart rate was lower in VVIR 110 than in VVI or VVIR 130 (VVIR 110: 75.9% +/- 14.6% vs VVI: 90.6% +/- 12.8%; P &lt; 0.01; VVIR 110 vs VVIR 130: 89.1% +/- 23.2%; P &lt; 0.05). There was no significant difference in cardiac output at peak exercise between VVIR 110 and VVIR 130. We conclude that a pacing rate for submaximal exercise of 110 beats/min may be preferable to that of 130 beats/min in respect to exercise capacity and sympathetic nerve activity.
  • 中川 純一, 金古 善明, 長沼 文雄, 長谷川 昭, 永井 良三
    Japanese circulation journal 60 719-719 1997年1月20日  
  • 直田 匡彦, 金古 善明, 天野 晶夫, 永井 良三
    Japanese circulation journal 60 708-708 1997年1月20日  
  • Y Sawada, M Inoue, T Kanda, T Sakamaki, S Tanaka, N Minamino, R Nagai, T Takeuchi
    FEBS letters 400(2) 177-82 1997年1月3日  査読有り
    We investigated the expression of the yeast Kex2 family endoproteases furin and PACE4, and brain natriuretic peptide (BNP) in the atrium and ventricle after infarction as well as the conversion of the BNP precursor gammaBNP to BNP-45. In a rat heart failure model, plasma BNP rose in two phases--first at day 3, and again at day 14. BNP mRNA, as measured by Northern blot analysis, increased strongly at day 3, then at days 14 and 28 less strongly in the atrium, and in the ventricle it increased weakly at day 3, then strongly at days 14 and 28. Furin mRNA showed the same pattern of expression as that of BNP message, whereas PACE4 message stayed unchanged after the infarction. Both furin and BNP were immunostained in the myocardium adjacent to the infarcted tissue. We suggest that after myocardial infarction, furin is co-expressed with BNP in both the atrium and ventricle, and that furin may be responsible for the conversion of gammaBNP to BNP-45.
  • H Sumino, T Kanda, I Kobayashi, H Sakamoto, K Sato, T Sakamaki, T Fukuda, S Ichikawa, R Nagai
    Journal of medicine 28(5-6) 319-24 1997年  査読有り
    We report the unusual case of an 87-year-old woman with cardiac myxoma and adenomatous goiter. She exhibited slight elevations of serum interleukin-6 (IL-6), but levels of thyroid hormones such as T3, free T3 and free T4 were all abnormally low. Interleukin-6 may potentiate the alteration of thyroid metabolism.
  • C Ishii, S Kawazu, T Utsugi, Y Ito, T Ohno, N Kato, S Tomono, R Nagai, K Komeda
    HORMONE AND METABOLIC RESEARCH 29(1) 9-11 1997年1月  
    Plasma 1,5-anhydro-D-glucitol (AG) is a marker of the diabetic state and also reflects the glycosuria induced by hyperglycemia but not by renal pathology. To investigate the benefits of the AG determination in order to diagnose diabetes in BB/Wor//Tky rats, AG was measured in non-diabetic (n = 104) and diabetic (n = 113) BB/Wor//Tky rats. AG was significantly higher in non-diabetic rats than in diabetic rats (25.2 +/- 9.3 vs 4.1 +/- 7.4 mu g/ml, mean +/- SD, p &lt; 0.001). The best cut-off level for AG (8.5 mu g/ml, was highly specific (100 %) for ruling out diabetes and fairly sensitive (82.3 %) to detect diabetes. Based on the AG cutoff levels, 90 % of false-negative diabetic rats (18/20) were observed within 4 days after the onset of diabetes, which corresponded to 38.3 % in diabetic rats (18/47) at that time. The false-negative diabetic rats and positive rats could be effectively distinguished based on the cumulative points given according to the urinary glucose after the onset of diabetes, 1 point for each cross [+] indicating glycosuria using the Testape, i.e. 2 or less points false negative and 4 or more points for diabetic rats in the first 4 days. In conclusion, there is a close inverse relation between the level of plasma AG and the amount of glycosuria detected just after the onset of overt diabetes in BB/Wor//Tky rats.
  • Y Seta, T Kanda, T Yokoyama, I Kobayashi, T Suzuki, R Nagai
    Research communications in molecular pathology and pharmacology 95(1) 57-66 1997年1月  査読有り
    Management of acute viral myocarditis is still controversial. Amrinone, a noncatecholamine nonglycoside bipyridine agent, produces sustained improvement of cardiac function and symptomatology in congestive heart failure (CHF). Amrinone demonstrates phosphodiesterase inhibitory activity that is relatively selective for the major phosphodiesterase isozyme in cardiac muscles, PDE III, which specifically hydrolyzes cyclic 3'5' adenosine monophosphate (cAMP). We investigated the effects of amrinone in an animal model of acute CHF related to myocarditis caused by the encephalomyocarditis virus (EMCV). Female C3H mice were inoculated intraperitoneally (i.p.) with 500 plaque-forming units of EMCV in 0.1 ml of saline. A total of 96 mice were randomly assigned to four groups. Each animal was administered 0.2 ml of phosphate-buffered saline (PBS) containing amrinone at a concentration of 1, 10, or 50 mg/kg, or PBS as an infected control, injected i.p. once daily for 21 days, starting on day 1 after viral inoculation. Each group contains 20 to 30 mice. Infected untreated mice survived at 80% (n = 16), however, only 13% (n = 16) of mice treated with amrinone (50 mg/kg) survived (p < 0.01). Downregulation of cardiac cAMP occurred 1 day after the viral infection. Although amrinone (10 and 50 mg/kg) treatment significantly (p < 0.05) increased the cardiac cAMP content and the dose of 10 mg/kg could potentially retard death from CHF due to viral myocarditis. The higher (50 mg/kg) doses of amrinone may produce unfavorable effects when used to treat mammals with viral myocarditis and CHF.
  • Nephrology 3(Supple) A15-16 1997年  
  • S Hasegawa, M Nakano, K Hamana, Y Taniguchi, T Iwasaki, T Kanda, T Suzuki, R Nagai
    Life sciences 60(19) 1643-50 1997年  査読有り
    Cardiac polyamines are thought to protect the myocardium against harmful stimuli and to be regulated by sympathetic nerve activation. In the present study, polyamines concentrations in non-infarcted myocardium were investigated. Myocardial polyamines contents decreased significantly in the non-infarcted regions by day 3 in rats with myocardial infarction compared with sham-operated rats and with the untreated control rats. The cardiac catecholamine concentration decreased by day 1 after myocardial infarction. Myocardial ornithine decarboxylase activity also decreased in the non-infarcted regions; suggesting that the decrease in cardiac polyamines contents relate to an insufficiency of the ornithine decarboxylase activity in rats with myocardial infarction. These results suggest that the decrease in polyamines concentrations after myocardial infarction is associated with functional sympathetic nerve denervation and that the vulnerability of the heart after myocardial infarction may be due to a decrease in polyamine concentrations in the non-infarcted region.

書籍等出版物

 21
もっとみる

所属学協会

 5

共同研究・競争的資金等の研究課題

 91
もっとみる
一覧へ戻る