Characterization of right ventricular function after monocrotaline-induced pulmonary hypertension in the intact rat
Characterization of right ventricular function after monocrotaline-induced pulmonary hypertension in the intact rat
复制标题
DOI：
10.1152/ajpheart.00369.2006
复制
发表时间：
2006-11-01
影响因子：
4.8
通讯作者：
van der Laarse, Arnoud
中科院分区：
文献类型：
--
作者：
Hessel, Marleen H. M.;Steendijk, Paul;van der Laarse, Arnoud
我们描述了野百合碱 (MCT) 诱导的肺动脉高压大鼠模型中血流动力学以及收缩和舒张右心室 (RV) 功能与结构变化的关系。大鼠接受 30 mg/kg 体重（MCT30，n = 15）和 80 mg/kg 体重（MCT80，n = 16）的 MCT 治疗，分别诱导代偿性 RV 肥大和 RV 衰竭。用盐水处理的大鼠作为对照（续，n = 13）。 4周后，将压力-电导导管引入右心室以评估压力-容积关系。随后，处死大鼠，快速解剖心脏和肺，对右心室、左心室（LV）和室间隔（IVS）进行称重并进行组织化学分析。 RV 与 (LV + IVS) 重量比在 Cont 中为 0.29 +/- 0.05，在 MCT30 中为 0.35 +/- 0.05，在 MCT80 中为 0.49 +/- 0.10（与 Cont 和 MCT30 相比，P < 0.001），证实了 MCT 诱导的 RV 肥大。对照组大鼠的 RV 射血分数为 49 +/- 6%，MCT30 大鼠为 40 +/- 12%（相对于对照组，P < 0.05），MCT80 大鼠为 26 < 6%（相对于对照组和 MCT30，P < 0.05）。 MCT30组大鼠心输出量保持不变，但右心室容量和充盈压较对照组显着增加（均P < 0.05），表明右心室重塑。 MCT80组大鼠右心室收缩压、容积和室壁应力峰值进一步升高，心输出量显着降低（均P < 0.05）。然而，右心室收缩末期和舒张末期僵硬度没有变化，与间质纤维化的存在一致。 MCT 引起的压力超负荷与剂量依赖性的右心室肥大发展相关。对 MCT 最明显的反应是 RV 收缩末期和舒张末期容量的过载依赖性增加，即使在非失败条件下也是如此。
We characterized hemodynamics and systolic and diastolic right ventricular ( RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with MCT at 30 mg/kg body wt (MCT30, n = 15) and 80 mg/kg body wt (MCT80, n = 16) to induce compensated RV hypertrophy and RV failure, respectively. Saline-treated rats served as control (Cont, n = 13). After 4 wk, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were killed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV), and interventricular septum (IVS) were weighed and analyzed histochemically. RV-to-(LV + IVS) weight ratio was 0.29 +/- 0.05 in Cont, 0.35 +/- 0.05 in MCT30, and 0.49 +/- 0.10 in MCT80 (P < 0.001 vs. Cont and MCT30) rats, confirming MCT-induced RV hypertrophy. RV ejection fraction was 49 +/- 6% in Cont, 40 +/- 12% in MCT30 (P < 0.05 vs. Cont), and 26 < 6% in MCT80 ( P < 0.05 vs. Cont and MCT30) rats. In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared with Cont ( all P < 0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes, and peak wall stress were further increased, and cardiac output was significantly decreased ( all P < 0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under nonfailing conditions.