Evans M A, Burnett J C, Redfield M M
Cardiorenal Laboratory, Mayo Clinic, Rochester, Minnesota 55905, USA.
J Am Coll Cardiol. 1995 May;25(6):1445-50. doi: 10.1016/0735-1097(95)00006-P.
This study examined the effect of low dose aspirin on cardiorenal and neurohumoral function and on the acute hemodynamic response to enalaprilat in a canine model of heart failure.
Low dose aspirin is frequently prescribed for patients with systolic dysfunction who also benefit from angiotensin-converting enzyme inhibition. Although high doses of potent cyclo-oxygenase inhibitors cause fluid retention and vaso-constriction and antagonize the effects of angiotensin-converting enzyme inhibitors, the effects of low dose aspirin in heart failure are unknown.
A model of heart failure was produced in 11 mongrel dogs by rapid ventricular pacing (250 beats/min for 12 to 14 days). Five dogs received 325 mg aspirin/day for the final 4 days of pacing before the acute experiment; six control dogs received no aspirin. Cardiorenal and neurohumoral function was measured during chloralose anesthesia. Hemodynamic and renal responses to enalaprilat were assessed.
Both groups demonstrated severe heart failure with decreased cardiac output; increased atrial pressures and systemic resistance; activation of plasma renin activity, aldosterone and atrial natriuretic factor; and sodium retention. Low dose aspirin had no detrimental effect on cardiorenal or neurohumoral function. Mean arterial pressure, pulmonary capillary wedge pressure and systemic vascular resistance decreased to a similar degree with enalaprilat in both groups. There was no difference between the groups with respect to renal response to enalaprilat.
The present study demonstrates that low dose aspirin has no adverse effect on hemodynamic, neurohumoral or renal function in heart failure. Furthermore, aspirin has no adverse effect on the acute response to enalaprilat. These findings suggest that there is no contraindication to concomitant treatment with low dose aspirin and angiotensin-converting enzyme inhibitors in humans with heart failure.
本研究在犬类心力衰竭模型中,考察了低剂量阿司匹林对心肾及神经体液功能以及对依那普利拉急性血流动力学反应的影响。
对于收缩功能障碍且能从血管紧张素转换酶抑制治疗中获益的患者,常开具低剂量阿司匹林。尽管高剂量强效环氧化酶抑制剂会导致液体潴留和血管收缩,并拮抗血管紧张素转换酶抑制剂的作用,但低剂量阿司匹林在心力衰竭中的作用尚不清楚。
通过快速心室起搏(250次/分钟,持续12至14天)在11只杂种犬中建立心力衰竭模型。5只犬在急性实验前起搏的最后4天接受325毫克/天的阿司匹林;6只对照犬未接受阿司匹林。在氯醛糖麻醉期间测量心肾及神经体液功能。评估对依那普利拉的血流动力学和肾脏反应。
两组均表现出严重心力衰竭,心输出量降低;心房压力和全身阻力增加;血浆肾素活性、醛固酮和心房利钠因子激活;以及钠潴留。低剂量阿司匹林对心肾或神经体液功能没有不利影响。两组中依那普利拉使平均动脉压、肺毛细血管楔压和全身血管阻力下降的程度相似。两组在对依那普利拉的肾脏反应方面没有差异。
本研究表明,低剂量阿司匹林对心力衰竭患者的血流动力学、神经体液或肾功能没有不良影响。此外,阿司匹林对依那普利拉的急性反应没有不良影响。这些发现表明,心力衰竭患者同时使用低剂量阿司匹林和血管紧张素转换酶抑制剂没有禁忌证。