Usefulness of circulating interleukin-18 concentration in acute myocardial infarction as a risk factor for late restenosis after emergency coronary angioplasty.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Motomaru Masutani.
Explore the source record for details and available documents.
BACKGROUND: Hepatocyte growth factor (HGF), a member of the endothelial-specific growth factors with the greatest mitogenic activity, may play a role in the protection and/or repair of vascular endothelial cells injured by atherosclerosis. As a result, plasma HGF concentration may increase in response to endothelial cell damage. To test this hypothesis, we measured plasma concentrations of HGF in patients with or without aorto-iliac artery atherosclerotic disease. METHODS: One hundred ten consecutive patients who underwent coronary angiography were enrolled in this study. Abdominal aortography was performed after coronary arteriography to determine whether aorto-iliac artery atherosclerotic disease was present. Peripheral venous blood samples were obtained to measure the plasma HGF concentration. RESULTS: Aortography revealed aorto-iliac atherosclerotic disease in 35 patients (32%). The plasma HGF concentration was significantly higher in patients with arteriosclerotic lesions (0.35 +/- 0.11 ng/mL) than in patients without atherosclerotic lesions (0.27 +/- 0.09 ng/mL, P =.0002). On the basis of multiple logistic regression analysis of the relationships between coronary risk factors, age, sex, severity of coronary artery disease, plasma HGF concentration, and the presence of arteriosclerotic lesions, plasma HGF concentration (P =.0005) and age (P =.035) were found to predict independently the presence of aorto-iliac arteriosclerosis. CONCLUSION: Plasma HGF concentration can be used to predict the presence of arteriosclerotic lesions in the region from the abdominal aorta to the femoral arteries.
We investigated the concentration of stimulatory GTP-binding protein (Gs protein) in the peripheral resistance arteries of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), and renovascular hypertensive rats (RHR). Changes in the function of Gs protein in SHR and WKY were also investigated by microcannulation techniques. The localization and abundance of Gs protein were determined immunohistochemically in 4-, 10- and 20-week-old SHR and age-matched WKY (control), as well as in RHR. Sections of the cremaster artery were stained with polyclonal antibodies to Gs protein. The concentration of Gs protein-like immunoreactivity in the cremaster artery was significantly lower in SHR at 4, 10, and 20 weeks of age, relative to that in age-matched WKY. In contrast, no significant differences were detected in the abundance of Gs between RHR and control rats. The dilatory response by isoproterenol in the presence of beta1-adrenoceptor blocker was lower in 4- and 10-week-old SHR than in age-matched WKY. The dilatory response by cholera toxin was also lower in SHR than in WKY for these two age groups. These results indicated that the amount and function of Gs protein in the peripheral resistance vessels in SHR was reduced. Since this change occurred before the onset of hypertension and no changes were seen in the secondary hypertensive rats, this change was not a secondary change due to hypertension. The impaired receptor-Gs protein-mediated signal transduction in the peripheral resistance arteries may be one of the possible mechanisms responsible for the pathogenesis of hypertension in SHR.