Omvik P, Lund-Johansen P, Myking O
Medical Department, Haukeland Hospital, University of Bergen, School of Medicine, Norway.
J Cardiovasc Pharmacol. 1992;19 Suppl 1:S90-6. doi: 10.1097/00005344-199219001-00018.
Possible counterregulatory neurohumoral and hemodynamic responses to carvedilol (a new vasodilating nonselective beta-receptor blocker) were studied in 19 men with essential hypertension (age range, 34-59 years; mean age, 44 years). Intra-arterial pressure, cardiac output (Cardio-green), heart rate, and the vasoactive peptides norepinephrine, epinephrine, and atrial natriuretic peptide (ANP) were measured at rest supine and sitting and during 100-W bicycle exercise before and 2 h after administration of 25 mg carvedilol. The same protocol was followed after 9 months of chronic carvedilol treatment (mean dose, 52 mg/day). Carvedilol induced both acute and chronic reductions (at rest supine, 11%) in mean arterial pressure, due in part to reduction in cardiac output (5%) and in part to reduction in total peripheral resistance (5%). At rest supine, carvedilol induced a reduction in ANP (27%) that could be viewed as a counterregulatory response to decrease in cardiac output, preventing excessive blood pressure reduction. ANP decreased (18%) when the patient sat up from the supine position and increased (67%) during exercise, but no further change was seen after acute or chronic carvedilol treatment. With the patient in the sitting position, norepinephrine was 110% higher than at rest supine; during 100-W exercise, norepinephrine increased 368%. A further increase (38-86% in the three situations, respectively) was seen after the first dose of carvedilol. Epinephrine showed similar but less marked changes. Neither extracellular fluid volume nor plasma volume (isotope dilution techniques) changed significantly during the study, but the acute blood pressure response to carvedilol was directly related to changes in extracellular fluid volume.(ABSTRACT TRUNCATED AT 250 WORDS)
在19名原发性高血压男性患者(年龄范围34 - 59岁;平均年龄44岁)中,研究了对卡维地洛(一种新型血管舒张性非选择性β受体阻滞剂)可能产生的对抗调节性神经体液和血流动力学反应。在静息仰卧位、坐位以及进行100瓦自行车运动时,于服用25毫克卡维地洛之前和之后2小时测量动脉内压、心输出量(Cardio - green)、心率以及血管活性肽去甲肾上腺素、肾上腺素和心房利钠肽(ANP)。在卡维地洛慢性治疗9个月(平均剂量52毫克/天)后,遵循相同方案进行测量。卡维地洛导致平均动脉压急性和慢性降低(静息仰卧位时降低11%),部分原因是心输出量降低(5%),部分原因是总外周阻力降低(5%)。在静息仰卧位时,卡维地洛使ANP降低(27%),这可视为对心输出量降低的一种对抗调节反应,防止血压过度降低。患者从仰卧位坐起时ANP降低(18%),运动期间升高(67%),但在急性或慢性卡维地洛治疗后未见进一步变化。患者坐位时,去甲肾上腺素比静息仰卧位时高110%;在100瓦运动期间,去甲肾上腺素升高368%。首次服用卡维地洛后进一步升高(三种情况下分别升高38 - 86%)。肾上腺素显示出类似但不太明显的变化。在研究期间,细胞外液量和血浆量(同位素稀释技术)均无显著变化,但卡维地洛引起的急性血压反应与细胞外液量变化直接相关。(摘要截断于250字)