Fisher Naomi D L, Hollenberg Norman K
Department of Medicine, Harvard Medical School and the Brigham and Women's Hospital, Boston, Massachusetts, USA.
J Hypertens. 2006 Aug;24(8):1575-80. doi: 10.1097/01.hjh.0000239293.40507.2a.
Strong evidence has secured aging as a powerful predictor of both cardiovascular risk and endothelial dysfunction, yet specific treatment is not available. We tested the hypothesis that vascular responsiveness to flavanol-rich cocoa increases with advancing age. We have previously shown that flavanol-rich cocoa induced peripheral vasodilation, improving endothelial function via a nitric oxide (NO)-dependent mechanism.
We studied blood pressure and peripheral arterial responses to several days of cocoa in 15 young (< 50 years) and 19 older (> 50) healthy subjects.
The nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine-methyl-ester (L-NAME) induced significant pressor responses following cocoa administration only among the older subjects: systolic blood pressure (SBP) rose 13 +/- 4 mmHg, diastolic blood pressure (DBP) 6 +/- 2 mmHg (P = 0.008 and 0.047, respectively); SBP was significantly higher in the older subjects (P < 0.05). Flow-mediated vasodilation, measured by tonometry in the finger, was enhanced with flavanol-rich cocoa in both groups, but significantly more so among the old (P = 0.01). Finally, basal pulse wave amplitude (PWA) followed a similar pattern. Four to six days of flavanol-rich cocoa caused a rise in PWA in both groups. At peak vasodilation following acute cocoa intake on the final day, both groups showed a further, significant rise in PWA. The response in the older subjects was more robust; P < 0.05. L-NAME significantly reversed dilation in both groups.
Flavanol-rich cocoa enhanced several measures of endothelial function to a greater degree among older than younger healthy subjects. Our data suggest that the NO-dependent vascular effects of flavanol-rich cocoa may be greater among older people, in whom endothelial function is more disturbed.
有力证据已证实衰老可作为心血管风险和内皮功能障碍的有力预测指标,但尚无特效治疗方法。我们检验了这样一个假设,即随着年龄增长,血管对富含黄烷醇的可可的反应性会增强。我们之前已经表明,富含黄烷醇的可可可诱导外周血管舒张,通过一氧化氮(NO)依赖性机制改善内皮功能。
我们研究了15名年轻(<50岁)和19名年长(>50岁)健康受试者在连续几天饮用可可后血压和外周动脉的反应。
一氧化氮合酶(NOS)抑制剂N(ω)-硝基-L-精氨酸甲酯(L-NAME)仅在年长受试者饮用可可后诱导出显著的升压反应:收缩压(SBP)升高13±4 mmHg,舒张压(DBP)升高6±2 mmHg(分别为P = 0.008和0.047);年长受试者的SBP显著更高(P < 0.05)。通过手指张力测量法测得的血流介导的血管舒张在两组中均因富含黄烷醇的可可而增强,但在年长组中增强更为显著(P = 0.01)。最后,基础脉搏波振幅(PWA)呈现类似模式。连续四至六天饮用富含黄烷醇的可可使两组的PWA均升高。在最后一天急性摄入可可后达到血管舒张峰值时,两组的PWA均进一步显著升高。年长受试者的反应更为强烈;P < 0.05。L-NAME显著逆转了两组的血管舒张。
在健康受试者中,富含黄烷醇的可可对内皮功能的多项指标的增强作用在年长组比年轻组更大。我们的数据表明,富含黄烷醇的可可对血管的NO依赖性作用在年长人群中可能更大,因为他们的内皮功能受到的干扰更大。