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老年者本態性高血圧症例16名を対象とし4週間の休薬後,nilvadipin 2mg/日投与を8週間投与し,再び4週間の休薬後nilvadipine 8mg/日投与を8週間投与した.Nilvadipine2mg/日投与では血圧,心拍出量は変化を認めなかったが,nilvadipine 8mg/日投与では血圧は低下し,心拍出量は増加した.末梢局所血流についてはnilvadipine 2mg/日および8mg/日投与ともに総頸動脈血流,椎骨動脈血流は有意に増加したが,腹腔動脈,上腸間膜動脈,腎動脈,腹部大動脈終末部は有意な変化は認めなかった.Nilvadipine 8mg/日投与により心房性利尿ペプチド(ANP)は有意に増加し,noradrenalineは有意に低下したが,2mg/日投与ではともに変化しなかった.心拍出量の変化はANPの変化に対し有意な正相関を認め,noradrenalineの変化に対しては有意な逆相関を認めたことから,心臓前負荷増加に伴う心拍出量の増加と考えられた.
Hemodynamic and humoral responses to nilvadipine were assessed in 16 elderly hypertensives. A higher dose (8 mg/day) of nilvadipine reduced mean arterial pres-sure and increased cardiac output, whereas a lower dose (2 mg/day) of nilvadipine had no effect on mean arte-rial pressure or cardiac output. Both carotid and vertebral flows were increased irrespective of whether the dose of nilvadipine was high or low. There was no significant change in celiac, superior mesenteric, renal, or terminal aortic flow with either dose of nilvadipine. A lower dose of nilvadipine had no effect on any humor-al factor, while a higher dose of nilvadipine increased plasma atrial natriuretic peptide and decreased plasma noradrenaline. The relationship between changes in these humoral parameters and those in cardiac output suggest that an elevation of preload (venous return) may play a role in increasing cardiac output through a higher dose of nilvadipine.
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