非甾体类抗炎药和对乙酰氨基酚对血压和高血压的影响
- Authors
- Norman M Kaplan, MD
Norman M Kaplan, MD
- Editor-in-Chief — Nephrology
- Section Editor — Hypertension
- Clinical Professor of Internal Medicine
- University of Texas Southwestern Medical Center
- Raymond R Townsend, MD
Raymond R Townsend, MD
- Professor of Medicine
- Perelman School of Medicine
- University of Pennsylvania
- Section Editors
- Richard H Sterns, MD
Richard H Sterns, MD
- Editor-in-Chief — Nephrology
- Section Editor — Fluid and Electrolytes
- Professor Emeritus
- University of Rochester School of Medicine and Dentistry
- George L Bakris, MD
George L Bakris, MD
- Editor-in-Chief — Nephrology
- Section Editor — Hypertension
- Professor of Medicine
- The University of Chicago
- Deputy Editor
- John P Forman, MD, MSc
John P Forman, MD, MSc
- Senior Deputy Editor — UpToDate
- Deputy Editor — Nephrology
- Assistant Professor of Medicine
- Harvard Medical School
- Translators
- 王毅, 主任医师
王毅, 主任医师
- 上海交通大学附属第一人民医院心内科
引言
非甾体类抗炎药(nonsteroidal anti-inflammatory drug, NSAID)有多种不良反应。从心血管的角度来看，NSAID既可升高血压，也可影响总体心血管风险。
本文将总结NSAID和对乙酰氨基酚对血压及高血压发展的影响。NSAID的心血管作用及其在慢性肾脏病患者中的不良反应将单独讨论。 (参见“非选择性非甾体类抗炎药的心血管不良反应”和“选择性COX-2抑制剂的心血管不良反应”和“非甾体类抗炎药：急性肾损伤(急性肾衰竭)”)
NSAID对血压的影响
对于血压正常和高血压患者，所有NSAID在其剂量足以减轻炎症和疼痛时，均能升高血压[1]。血压平均升高3/2mmHg，但差异非常大[2-4]。这些影响可能促进了选择性环氧合酶-2(cyclooxygenase-2, COX-2)抑制剂有关的心血管风险升高[5]。 (参见“选择性COX-2抑制剂的心血管不良反应”)
此外，使用NSAID可减弱所有降压药的效果，但钙通道阻滞剂除外[6]。另外，一项小型研究纳入开始降压治疗的日本患者，发现使用NSAID对β受体阻滞剂有效性的影响也可能非常小[7]；该研究中，在364例接受β受体阻滞剂的患者中，NSAID使用者与非使用者相比，两组患者收缩压降低值的均数差值仅为0.4mmHg。
NSAID的致高血压作用呈剂量依赖性，而且可能涉及抑制肾脏中的COX-2，这种抑制作用会减少钠排泄并增加血管内容量[6]。小剂量阿司匹林没有COX-2抑制作用和致高血压作用。例如，在高血压最佳治疗(Hypertension Optimal Treatment, HOT)研究的18,790例患者中，与安慰剂组相比，75mg/d阿司匹林没有干扰降压治疗[8]。然而，这些结论不能扩展至更大剂量的阿司匹林。
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