Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.
Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria.
J Cardiovasc Pharmacol. 2018 Nov;72(5):242-251. doi: 10.1097/FJC.0000000000000620.
Hypertension is a major cause of left ventricular (LV) diastolic dysfunction. Although β-adrenergic receptor (β-AR) blockers are often used to manage hypertension, the impact of β-AR activation on LV lusitropic effects and hence filling pressures in the hypertensive heart with LV diastolic dysfunction is uncertain.
Using tissue Doppler imaging and Speckle tracking software, we assessed LV function in isoflurane anesthetised spontaneously hypertensive (SHR) and Dahl salt-sensitive (DSS) rats before and after β-AR activation [isoproterenol (ISO) administration].
As compared to normotensive Wistar Kyoto control rats, or DSS rats not receiving NaCl in the drinking water, SHR and DSS rats receiving NaCl in the drinking water had a reduced myocardial relaxation as indexed by lateral wall e' (early diastolic tissue velocity at the level of the mitral annulus) and an increased LV filling pressure as indexed by E/e'. However, LV ejection fraction and deformation and motion were preserved in both SHR and DSS rats. The administration of ISO resulted in a marked increase in ejection fraction and decrease in LV filling volumes in all groups, and an increase in e' in SHR, but not DSS rats. However, after ISO administration, although E/e' decreased in DSS rats in association with a reduced filling volume, E/e' in SHR remained unchanged and SHR retained greater values than Wistar Kyoto control.
The hypertensive heart is characterized by reductions in myocardial relaxation and increases in filling pressures, but β-AR activation may fail to improve myocardial relaxation and when this occurs, it does not reduce LV filling pressures.
高血压是左心室（LV）舒张功能障碍的主要原因。虽然β-肾上腺素能受体（β-AR）阻滞剂通常用于治疗高血压，但β-AR 激活对 LV 松弛效应以及高血压伴 LV 舒张功能障碍心脏的充盈压的影响尚不确定。
在异氟烷麻醉的自发性高血压（SHR）和盐敏感型（DSS）大鼠中，使用组织多普勒成像和斑点追踪软件，在β-AR 激活[异丙肾上腺素（ISO）给药]前后评估 LV 功能。
与正常血压的 Wistar Kyoto 对照大鼠或未在饮水中接受 NaCl 的 DSS 大鼠相比，在饮水中接受 NaCl 的 SHR 和 DSS 大鼠的心肌松弛性降低，以侧壁 e'（二尖瓣环水平的早期舒张组织速度）为指标，LV 充盈压升高，以 E/e'为指标。然而，LV 射血分数和变形与运动在 SHR 和 DSS 大鼠中均得到保留。ISO 的给药导致所有组的射血分数明显增加，LV 充盈量减少，以及 SHR 的 e'增加，但 DSS 大鼠的 e'没有增加。然而，ISO 给药后，尽管 DSS 大鼠的 E/e'降低与充盈量减少有关，但 SHR 的 E/e'保持不变，且 SHR 的 E/e'值仍高于 Wistar Kyoto 对照大鼠。
高血压心脏的特征是心肌松弛性降低和充盈压升高，但β-AR 激活可能无法改善心肌松弛性，当这种情况发生时，它不会降低 LV 充盈压。
