Ertl G, Alexander R W, Kloner R A
Basic Res Cardiol. 1983 Sep-Oct;78(5):518-33. doi: 10.1007/BF01906463.
Studies were carried out in 39 barbiturate-anesthetized dogs to determine whether the renin-angiotensin system is important in control of hemodynamics and coronary flow during myocardial ischemia. Plasma renin activity (PRA) was 2.2 +/- 0.4 ng x ml-l x hr-1 immediately before coronary artery occlusion (CAO) and increased to 3.8 +/- 0.5 (p less than .005) 15 minutes after CAO. In nephrectomized dogs, PRA was 0.76 +/- 0.14 ng x ml-l x hr-1 two hours after nephrectomy and remained unchanged after CAO. In contrast, hemodynamic changes following CAO were similar between nephrectomized and intact dogs: mean arterial pressure fell from 126 +/- 4 pre CAO to 116 +/- 4 mm Hg post CAO (p less than 0.005) in nephrectomized dogs and from 130 +/- 11 to 120 +/- 11 mm Hg (p less than 0.005) in intact dogs. Left atrial pressure rose from 5.4 +/- 0.9 pre CAO to 7.7 +/- 0.9 mm Hg (p less than 0.005) post CAO in nephrectomized from 5.4 +/- 0.9 pre CAO to 7.7 +/- 0.9 mm Hg (p less than 0.005) post CAO in nephrectomized dogs and 6.3 +/- 1.3 to 9.0 +/- 1.8 mm Hg (p less than 0.005) in intact dogs. Heart rate remained unchanged in both groups. In sham-operated dogs without CAO, neither the angiotensin II blocker Saralasin nor the converting enzyme inhibitor Captopril had significant effects on systemic (SVR) and coronary (CVR) vascular resistances. In contrast, in dogs with CAO, these drugs reduced CVR from 1.28 +/- 0.13 mm Hg x ml-1 x min x 100 g heart weight (resistance units = RU) to 0.85 +/- 0.08 RU (p less than 0.05) (Saralasin) 15 minutes after treatment and from 1.17 +/- 0.09 to 0.88 +/- 0.08 RU (p less than 0.025), (Captopril) respectively. However, only Captopril reduced SVR, from 10.7 +/- 1.13 to 8.2 +/- 0.8 RU (p less than 0.025). Both Captopril and Saralasin induced a significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significant increase in collateral blood flow. Nephrectomy, two hours prior to CAO, significantly reduced the effect of Captopril on CVR and collateral blood flow while the effect on SVR persisted. Thus the reduction in CVR appears to be an effect of inhibition of the renin-angiotensin system; this system participates in control of CVR during CAO and may limit coronary collateral blood flow.
在39只巴比妥类麻醉犬身上进行了研究，以确定肾素-血管紧张素系统在心肌缺血期间对血流动力学和冠状动脉血流的控制中是否重要。冠状动脉闭塞（CAO）前即刻血浆肾素活性（PRA）为2.2±0.4 ng·ml⁻¹·hr⁻¹，CAO后15分钟升至3.8±0.5（p<0.005）。在肾切除的犬中，肾切除术后2小时PRA为0.76±0.14 ng·ml⁻¹·hr⁻¹，CAO后保持不变。相比之下，肾切除犬和完整犬CAO后的血流动力学变化相似：肾切除犬的平均动脉压从CAO前的126±4降至CAO后的116±4 mmHg（p<0.005），完整犬从130±11降至120±11 mmHg（p<0.005）。肾切除犬的左心房压从CAO前的5.4±0.9升至CAO后的7.7±0.9 mmHg（p<0.005），完整犬从6.3±1.3升至9.0±1.8 mmHg（p<0.005）。两组心率均无变化。在未进行CAO的假手术犬中，血管紧张素II拮抗剂沙拉新和转化酶抑制剂卡托普利对全身血管阻力（SVR）和冠状动脉血管阻力（CVR）均无显著影响。相比之下，在CAO犬中，这些药物使CVR在治疗后15分钟从1.28±0.13 mmHg·ml⁻¹·min⁻¹·100 g心脏重量（阻力单位=RU）降至0.85±0.08 RU（p<0.05）（沙拉新），卡托普利则从1.17±0.09降至0.88±0.08 RU（p<0.025）。然而，只有卡托普利降低了SVR，从10.7±1.13降至8.2±0.8 RU（p<0.025）。卡托普利和沙拉新都使侧支血流显著增加。CAO前两小时肾切除显著增加了侧支血流。CAO前两小时肾切除显著降低了卡托普利对CVR和侧支血流的作用，而对SVR的作用持续存在。因此，CVR的降低似乎是肾素-血管紧张素系统受抑制的结果；该系统在CAO期间参与CVR的控制，并可能限制冠状动脉侧支血流。
