The effect of hypertension and left ventricular hypertrophy on the lower range of coronary autoregulation.
The effect of hypertension and left ventricular hypertrophy on the lower range of coronary autoregulation.
复制标题
高血压和左心室肥厚对冠状动脉自动调节范围较低的影响。
DOI：
10.1161/01.cir.77.5.1108
复制
发表时间：
1988
期刊：
影响因子：
37.8
通讯作者：
Marcus,ML
中科院分区：
文献类型：
--
作者：
Harrison,DG;Florentine,MS;Brooks,LA;Cooper,SM;Marcus,ML
进行这些研究是为了验证这样一种假设，即作为慢性高血压的并发症而出现的左心室肥厚与冠状动脉自身调节受损有关。12只高血压伴左室肥厚犬(一肾一夹模型)和11只正常犬在清醒状态下进行了研究。用冠状动脉内导管测量回旋压力，用放置在近端的液压封堵器将其调整为100、75和40毫米汞。在每个回旋压力下，用放射性微球测量心肌灌注。在此范围内降低回旋支压力不会显著改变心率、左房压力或动脉压。在正常犬中，降低回旋压力不会改变总的心肌灌注或跨壁心肌灌注的分布。相反，在患有高血压和左心室肥厚的狗中，当压力从100毫米汞柱降至40毫米汞时，回旋支心内膜下血流灌注减少46%(与正常相比p<0.05)。使用自动调节增益值(1=完全自动调节；0=没有自动调节)量化每三分之一心肌的自动调节。对于100-75毫米汞柱的压力变化，两组动物的所有心肌层的自动调节增益值几乎相同。当血压从75毫米汞柱降至40毫米汞柱时，正常组和高血压组的自动调节增益值分别为：心外膜下1+/-0.2(平均值+/-SE)比0.9+/-0.2(p=NS)，中壁0.8+/-0.2比0.5+/-0.2(p=NS)，心内膜下0.8+/-0.1比0.1+/-0.2(p<0.05)。
These studies were performed to test the hypothesis that left ventricular hypertrophy arising as a complication of chronic hypertension is associated with impaired coronary autoregulation. Twelve dogs with hypertension and left ventricular hypertrophy (one-kidney, one-clip model) and 11 normal dogs were instrumented and subsequently studied while conscious. Circumflex pressure, measured with an intracoronary catheter, was adjusted to 100, 75, and 40 mm Hg with a hydraulic occluder that was placed proximally. At each circumflex pressure, myocardial perfusion was measured with radioactive microspheres. Reduction of circumflex pressure over this range did not significantly alter heart rate, left atrial pressure, or arterial pressure. In normal dogs, reduction of circumflex pressure did not alter total myocardial perfusion or the transmural distribution of perfusion. In contrast, in dogs with hypertension and left ventricular hypertrophy, circumflex subendocardial perfusion decreased 46% when pressure was decreased from 100 to 40 mm Hg (p less than .05 compared with normal). Autoregulation was quantified for each third of myocardium with the use of autoregulatory gain values (1 = perfect autoregulation; 0 = the absence of autoregulation). For pressure changes of 100 to 75 mmHg, values for autoregulatory gain were near unity for all layers of myocardium in both groups of animals. When pressure was decreased from 75 to 40 mm Hg, values for autoregulatory gain among the normal and hypertensive groups were, respectively: for subepicardium 1 +/- 0.2 (mean +/- SE) vs 0.9 +/- 0.2 (p = NS), for the midwall 0.8 +/- 0.2 vs 0.5 +/- 0.2 (p = NS), and for the subendocardium 0.8 +/- 0.1 vs 0.1 +/- 0.2 (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)