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44 results on '"Arakawa, Naoshi"'

3. Peripheral resistance vessel dysfunction in Marfan syndrome

Author

Nakamura, Motoyuki, Itoh, Shigehiro, Makita, Shinji, Ohira, Atsushi, Arakawa, Naoshi, and Hiramori, Katsuhiko

Subjects
Marfan syndrome -- Physiological aspects, Endothelium -- Physiological aspects, Vascular resistance -- Abnormalities, Health
Published
2000

11. Renal, hormonal, and hemodynamic effects of low-dose infusion of atrial natriuretic factor in acute myocardial infarction

Author

Nakamura, Motoyuki, Arakawa, Naoshi, and Kato, Masataka

Subjects
Heart attack -- Physiological aspects, Natriuretic peptides -- Health aspects, Heart attack -- Care and treatment, Health
Abstract

In the body, water volume and sodium levels are linked and tightly regulated. One of the mechanisms that may regulate these important determinants of body function is the secretion of atrial natriuretic factor (ANF), a protein made by the atria, the upper heart chambers. ANF, secreted in response to increased blood pressure, stimulates urinary water and sodium excretion. Studies have suggested that ANF may be decreased or depleted after a heart attack (myocardial infarction; MI), causing water and sodium retention, which may lead to pulmonary (lung) congestion. It is possible that ANF treatment may benefit patients following MI, and this was investigated in a study of 12 patients (2 female). Treatment increased blood ANF levels five-fold, and urinary volume and sodium levels increased correspondingly. Levels of another hormone that regulates sodium balance, aldosterone, decreased during treatment. No significant changes in blood vessel functions were found as result of ANF therapy. Previous work suggested that in patients with MIs, elevated aldosterone levels were related to sodium and water retention, with ultimately harmful effects on heart function. This study suggests that ANF may prove to be useful in preventing these changes without affecting normal blood vessel function. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

24. Elevated Plasma Levels of Interleukin-1 Receptor Antagonist and Interleukin-10 in Patients with Acute Myocardial Infarction

Author

SHIBATA, MASASHI, primary, ENDO, SHIGEATSU, additional, INADA, KATSUYA, additional, KURIKI, SATOSHI, additional, HARADA, MASAKO, additional, TAKINO, TOSHIO, additional, SATO, NORIO, additional, ARAKAWA, NAOSHI, additional, SUZUKI, TOMOMI, additional, AOKI, HIDEHIKO, additional, SUZUKI, TOMOYUKI, additional, and HIRAMORI, KATSUHIKO, additional

Published
1997
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28. Impaired cholinergic peripheral vasodilation and its relationship to hyperemic calf blood flow response and exercise intolerance in patients with chronic heart failure

Author

Nakamura, Motoyuki, primary, Chiba, Makoto, additional, Ueshima, Kenji, additional, Arakawa, Naoshi, additional, Yoshida, Hiroaki, additional, Makita, Shinji, additional, Funakoshi, Tsutomu, additional, Hashimoto, Kohoya, additional, Ishikawa, Motoko, additional, and Hiramori, Katsuhiko, additional

Published
1995
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42. ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of l-arginine and B vitamins

Author

Sydow, Karsten, Schwedhelm, Edzard, Arakawa, Naoshi, Bode-Böger, Stefanie M., Tsikas, Dimitrios, Hornig, Burkhard, Frölich, Jürgen C., and Böger, Rainer H.

Subjects
ATHEROSCLEROSIS, NITRIC oxide
Abstract

Objectives: Hyperhomocyst(e)inemia is a risk factor for atherosclerotic vascular disease, and it is associated with endothelial dysfunction. Mechanisms responsible for endothelial dysfunction in hyperhomocyst(e)inemia may involve impaired bioavailability of NO, possibly secondary to accumulation of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) and increased oxidative stress. We investigated whether oral treatment with B vitamins or l-arginine normalizes endothelium-dependent, flow-dependent vasodilation (FDD) in patients with peripheral arterial occlusive disease (PAOD) and hyperhomocyst(e)inemia. Methods: 27 patients with PAOD and hyperhomocyst(e)inemia were assigned to oral treatment with combined B vitamins (folate, 10 mg; vitamin B-12, 200 μg; vitamin B-6, 20 mg/day), l-arginine (24 g/day) or placebo, for 8 weeks in a double-blind fashion. FDD was determined by high-resolution ultrasound in the radial artery. Results: Vitamin B supplementation significantly lowered plasma homocyst(e)ine concentration from 15.8±1.8 to 8.7±1.1 μmol/l (P<0.01). However, B vitamins had no significant effect on FDD (baseline, 7.8±0.7%, B vitamins, 8.3±0.9%, placebo 8.9±0.7%; P=n.s.). In contrast, l-arginine treatment did not affect homocyst(e)ine levels, but significantly improved FDD (10.2±0.2%), probably by antagonizing the impact of elevated ADMA concentration (3.8±0.3 μmol/l) and reducing the oxidative stress by lowering urinary 8-iso-prostaglandin F2α (baseline, 76.3±7.1 vs. 62.7±8.3 pmol/mmol creatinine after 8 weeks). Conclusions: Oral supplementation with combined B vitamins during 8 weeks does not improve endothelium-dependent vasodilation in PAOD patients with hyperhomocyst(e)inemia, whereas l-arginine significantly improved endothelial function in these patients. Thus, accumulation of ADMA and increased oxidative stress may underlie endothelial dysfunction under hyperhomocyst(e)inemic conditions. These findings may have importance for evaluation of homocyst(e)ine-lowering therapy. [Copyright &y& Elsevier]

Published
2003
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43. Increased Plasma Group II Phospholipase A[sub 2] Concentrations in Patients with Acute Myocardial Infarction: Correlation with Tumor Necrosis Factor-Alpha.

Author

Arakawa, Naoshi, Endo, Shigeatsu, Nakamura, Motoyuki, Saito, Seiichi, Inada, Katsuya, Ogawa, Michio, and Hiramori, Katsuhiko

Subjects
*MYOCARDIAL infarction treatment, *PHOSPHOLIPASE A2, *TUMOR necrosis factors, *INTERLEUKIN-12, *CYTOKINES, *ISCHEMIA
Abstract

Aims: Group II phospholipase A[sub 2] (PLA[sub 2] ) is thought to play an important role in inflammation and tissue injury. It has been suggested that the inflammatory process is important in the setting and progression of myocardial ischemia or reperfusion. We measured plasma PLA[sub 2] as well as inflammatory cytokines in patients in the acute stage of myocardial infarction. Methods and Results: In 48 patients with acute myocardial infarction, blood samples were taken to measure plasma PLA[sub 2] , tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) 36–48 h after onset. Serial changes in plasma PLA[sub 2] were also examined in 15 consecutive patients in this group. Plasma PLA[sub 2] levels were significantly higher in complicated patients (Killip’s class ≥ II) than in uncomplicated patients (Killip’s class = I) (35.9 ± 11.9 vs. 5.3 ± 1.1 ng/ml, p < 0.01). Plasma PLA[sub 2] concentrations increased gradually over time during the first 3 days and at 36–48 h after onset were correlated with left-ventricular ejection fraction on admission (r = –0.42, p < 0.01), and with plasma TNF-α (r = 0.39, p < 0.01), but not with IL-1β. Conclusion: Plasma PLA[sub 2] concentrations rose during the acute stage of myocardial infarction, especially in severe cases mainly with heart failure. TNF-α may be associated with PLA[sub 2 ] activity as a potent stimulator in vivo. [ABSTRACT FROM AUTHOR]

Published
2000
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