Chronic reduction of myocardial ischemia does not attenuate coronary collateral development in miniswine.
Chronic reduction of myocardial ischemia does not attenuate coronary collateral development in miniswine.
复制标题
心肌缺血的慢性减少不会减弱小型猪的冠状动脉侧枝发育。
DOI：
10.1161/01.cir.86.2.660
复制
发表时间：
1992
期刊：
影响因子：
37.8
通讯作者：
Longhurst,JC
中科院分区：
文献类型：
--
作者：
Symons,JD;Pitsillides,KF;Longhurst,JC
心肌缺血被认为是冠状动脉侧支循环形成的可能刺激因素。因此，我们假设，慢性减少心肌耗氧量，以减轻缺血将衰减冠状动脉侧支发展超过8周的时间内使用左回旋支冠状动脉（LCx）ameroid诱导constriction in pigs.METHODS和numerTSCollateral的发展进行了评估，心肌血流量（放射性微球）和左心室局部功能（sonomicrometer尺寸计）。β-肾上腺素受体阻滞剂普萘洛尔（160或320 mg b.i.d.p.o.）在手术后1天在15只动物中开始。与16只未处理动物相比，通过1）异丙肾上腺素的药理学刺激，2）分级跑步机运动期间的生理学刺激，以及3）需氧量（心率和血压）和局部心肌功能的重复长期生物遥测记录，在处理组中记录了β-肾上腺素受体拮抗作用。除了β-阻滞的药理学和生理学验证外，生物遥测显示，与未经治疗的动物相比，普萘洛尔显著降低了代表心肌功能障碍的事件的每日数量、个体持续时间和严重程度。这表明，在β阻断组中，当侧支生长发生时，在整个前5周内几乎不存在任何缺血。术后31-38天（5周）和60-67天（8周），在静息和踏车运动（240次/分钟）期间测定左室心肌血流量（表示为左室心腔区与左室非闭塞区的血流比）和左室心腔区的收缩期室壁增厚。普萘洛尔停药前3天流量和功能测定，并恢复后立即测试。5周时，未治疗组（0.83 +/- 0.04至0.60 +/- 0.05，p <0.05）和β受体阻滞剂组（0.82 +/- 0.09至0.57 +/- 0.10，p <0.05）的血流比从休息到运动的下降相似。未治疗组（59 +/- 6%至38 +/-6%，p <0.05）和β-受体阻滞剂组（50 +/- 8%至30 +/-5%，p <0.05）从休息到运动的滑膜壁增厚程度相同。在两组中观察到类似的流量和功能的反应在8 weeks.CONCLUSIONSWe的结论是，在90%的最大心率的运动过程中测量功能的冠状动脉侧支循环的生长和发展是无关的心肌缺血的程度和持续时间在这个模型中。
BACKGROUNDMyocardial ischemia is considered to be a possible stimulus for development of the coronary collateral circulation. We therefore hypothesized that chronic reduction of myocardial oxygen demand to lessen ischemia would attenuate coronary collateral development over an 8-week period using left circumflex coronary artery (LCx) ameroid-induced constriction in pigs.METHODS AND RESULTSCollateral development was assessed by myocardial blood flow (radioactive microspheres) and left ventricular regional function (sonomicrometer dimension gauges). beta-Adrenoceptor blockade with propranolol (160 or 320 mg b.i.d.p.o.) was initiated in 15 animals 1 day after surgery. Compared with 16 untreated animals, beta-adrenoceptor antagonism was documented in the treated group by 1) pharmacological stimulation with isoproterenol, 2) physiological stimulation during graded treadmill exercise, and 3) repeated long-term biotelemetry recordings of oxygen demand (heart rate and blood pressure) and regional myocardial function. In addition to pharmacological and physiological verification of beta-blockade, biotelemetry showed that, compared with the untreated animals, propranolol significantly reduced the daily number, individual duration, and severity of events representing myocardial dysfunction. This suggests that in the beta-blocked group, little if any ischemia was present throughout the first 5 weeks when collateral growth occurs. Transmural myocardial blood flow (expressed as a ratio of flow in the LCx region to the nonoccluded region of the left ventricle) and systolic wall thickening in the LCx region were determined at rest and during treadmill exercise (240 beats per minute) 31-38 days (5 weeks) and 60-67 days (8 weeks) after surgery. Propranolol was withdrawn 3 days before flow and function determinations and was resumed immediately after testing. Blood flow ratios at 5 weeks decreased similarly from rest to exercise in the untreated (0.83 +/- 0.04 to 0.60 +/- 0.05, p less than 0.05) and beta-blockade group (0.82 +/- 0.09 to 0.57 +/- 0.10, p less than 0.05). Systolic wall thickening from rest to exercise was attenuated to the same degree in the untreated (59 +/- 6% to 38 +/- 6%, p less than 0.05) and beta-blockade group (50 +/- 8% to 30 +/- 5%, p less than 0.05). Similar flow and function responses were observed in both groups at 8 weeks.CONCLUSIONSWe conclude that growth and development of the coronary collateral circulation measured functionally during exercise at 90% of maximal heart rate is unrelated to the extent and duration of myocardial ischemia in this model.