Ziada Amal M, Hassan Mohammed O, Tahlilkar Khurram I, Inuwa Ibrahim M
Department of Physiology, College of Medicine, Sultan Qaboos University, Muscat, Sultanate of Oman.
J Hypertens. 2005 Jun;23(6):1233-40. doi: 10.1097/01.hjh.0000170387.61579.ab.
To investigate whether combined treatment with lisinopril, an angiotensin-converting enzyme (ACE) inhibitor and exercise training would have an additive effect in enhancing the capillary supply of the left ventricular (LV) myocardium in spontaneously hypertensive rats (SHR).
Twelve-week-old male SHR were divided into four groups (10-12 each): sedentary, sedentary treated with lisinopril (15-20 mg/kg per day by gavage), exercise trained, and exercise trained while treated with lisinopril. Exercise training consisted of 1 h a day/5 days a week of running on a treadmill.
After 10 weeks of experimental protocols, capillary surface density and length density were sterologically determined in 1 mum thick LV tissue samples from perfuse-fixed hearts.
Lisinopril significantly reduced systolic blood pressure (SBP) and LV mass in the sedentary with lisinopril and exercise trained with lisinopril groups but did not affect the heart rate (HR). Exercise training did not reduce SBP or LV mass, but significantly reduced HR in the exercise trained and exercise trained with lisinopril groups. Lisinopril treatment (sedentary with lisinopril), exercise training (exercise) and their combination (exercise trained with lisinopril) significantly increased myocardial capillary surface area density by 26, 38 and 65% and length density by 38, 48 and 67%, respectively.
Lisinopril administration and exercise training independently enhanced myocardial capillarization through a reduction of myocardial mass and stimulation of angiogenesis, respectively. A combination of the two treatments enhanced myocardial capillarization more than either intervention alone. This may aid in the restoration of the normal nutritional status of cardiac myocytes compromised by the hypertrophic state of hypertension.
研究血管紧张素转换酶(ACE)抑制剂赖诺普利与运动训练联合治疗是否会对自发性高血压大鼠(SHR)左心室(LV)心肌的毛细血管供应产生累加效应。
将12周龄雄性SHR分为四组(每组10 - 12只):久坐不动组、接受赖诺普利治疗的久坐不动组(每天经口灌胃15 - 20 mg/kg)、运动训练组以及接受赖诺普利治疗的运动训练组。运动训练包括每周5天、每天1小时在跑步机上跑步。
经过10周的实验方案后,对灌注固定心脏的1μm厚LV组织样本进行体视学测定,以确定毛细血管表面积密度和长度密度。
赖诺普利显著降低了接受赖诺普利治疗的久坐不动组和接受赖诺普利治疗的运动训练组的收缩压(SBP)和LV质量,但对心率(HR)无影响。运动训练未降低SBP或LV质量,但显著降低了运动训练组和接受赖诺普利治疗的运动训练组的HR。赖诺普利治疗(接受赖诺普利治疗的久坐不动组)、运动训练(运动训练组)及其联合治疗(接受赖诺普利治疗的运动训练组)分别使心肌毛细血管表面积密度显著增加26%、38%和65%,长度密度分别增加38%、48%和67%。
赖诺普利给药和运动训练分别通过减少心肌质量和刺激血管生成独立增强心肌毛细血管化。两种治疗方法联合使用比单独任何一种干预措施更能增强心肌毛细血管化。这可能有助于恢复因高血压肥厚状态而受损的心肌细胞的正常营养状态。