Endothelin-1 limits increases in blood flow to native and collateral-dependent myocardium.
Endothelin-1 limits increases in blood flow to native and collateral-dependent myocardium.
复制标题
内皮素-1 限制流向天然心肌和侧支依赖性心肌的血流量增加。
DOI：
10.1152/ajpregu.1997.273.1.r41
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Longhurst,JC
中科院分区：
文献类型：
--
作者：
Symons,JD;Rendig,SV;Fu,LW;Longhurst,JC
我们假设内皮素（ET）A受体的拮抗作用改善了侧支和非侧支心肌的血流。通过在11只猪的左回旋支冠状动脉（LCx;侧支区域）周围放置ameroid缩窄器来刺激冠状动脉侧支的发育。35 +/-2天后，使用来自股动脉的血液在恒定压力下对左前降支冠状动脉（LAD;非侧支区域）进行自动灌注。在第1组（n = 6）中，在LAD、LCx和边缘区域（即，LAD和LCx之间的面积），同时将载体（磷酸盐缓冲盐水）注入LAD冠状动脉（起搏1）。约55分钟后，在存在ETA受体拮抗剂（BQ-123; 5 mg.ml-1.min-1 ic）的情况下进行第二次起搏（起搏2）。在时间对照组（第2组，n = 5）中，在两个起搏期间均输注溶媒。各组起搏1和起搏2的心肌需氧量指标相似。与第一个起搏周期相比，在ETA受体拮抗期间，跨壁血流量（ml.100 g-1.min-1）较高（P < 0.05）（即，第1组中LAD（105 +/- 8 vs. 139 +/- 9）、边界（51 +/- 5 vs. 83 +/- 7）和LCx区域（分别为22 +/- 3 vs. 41 +/- 4）的起搏2）。在第2组中，虽然第1次起搏和第2次起搏的边界（98 +/- 17 vs. 103 +/- 16）和LCx区域（19 +/- 4 vs. 27 +/- 6）的灌注相似，但在第二次起搏期间，LAD跨壁血流更大（134 +/- 9 vs. 160 +/- 13; P < 0.05）。然而，第1组（39 +/- 6%）与第2组（20 +/- 7%）相比，第1步与第2步相比，LAD血流增加百分比更大（P < 0.05）。这些数据表明，在起搏应激期间，在存在ETA受体阻滞剂的情况下，流向侧支化和非侧支化心肌的血流得到改善。
We hypothesized that blood flow to collateralized and noncollateralized myocardium is improved by antagonism of endothelin (ET) A receptors. Coronary collateral development was stimulated by placing an ameroid constrictor around the left circumflex coronary artery (LCx; collateralized region) in 11 swine. After 35 +/- 2 days, the left anterior descending coronary artery (LAD; noncollateralized region) was autoperfused at constant pressure using blood from a femoral artery. In group 1 (n = 6) transmural blood flow was measured using radioactive microspheres in the LAD, LCx, and border regions (i.e., area between LAD and LCx) during pacing stress while vehicle (phosphate-buffered saline) was infused into the LAD coronary artery (pace 1). Approximately 55 min later, a second period of pacing (pace 2) was performed in the presence of ETA receptor antagonism (BQ-123; 5 mg.ml-1.min-1 ic). In the time control group (group 2, n = 5) vehicle was infused during both pacing periods. Indexes of myocardial oxygen demand were similar between paces 1 and 2 in each group. Compared with the first pacing period, transmural blood flow (ml.100 g-1.min-1) was higher (P < 0.05) during ETA receptor antagonism (i.e., pace 2) in the LAD (105 +/- 8 vs. 139 +/- 9), border (51 +/- 5 vs. 83 +/- 7), and LCx regions (22 +/- 3 vs. 41 +/- 4, respectively) in group 1. In group 2, while perfusion in the border (98 +/- 17 vs. 103 +/- 16) and LCx regions (19 +/- 4 vs. 27 +/- 6) was similar in paces 1 and 2, LAD transmural flow was greater (134 +/- 9 vs. 160 +/- 13; P < 0.05) during the second pacing period. However, the percent increase in LAD flow comparing pace 1 with 2 was greater (P < 0.05) in group 1 (39 +/- 6%) compared with group 2 (20 +/- 7%). These data suggest that during the stress of pacing blood flow to collateralized and noncollateralized myocardium is improved in the presence of ETA receptor blockade.