充血性心力衰竭对犬肺静脉肌袖结构的影响

Effect of congestive heart failure on structure of myosleeve in canine pulmonary veins

目的探讨充血性心力衰竭(CHF)对犬肺静脉(PV)肌袖结构的影响。方法将16只杂种犬,随机等分为CHF组和对照组,CHF组以240次/min的频率在右室持续起搏4周,建立CHF模型;对照组埋置起搏器但不起搏;Burst刺激诱发心房颤动(AF)。分别取两组犬的PV肌袖组织,用天狼星红染色进行纤维化定量分析和胶原组成分析。用免疫组化染色法对缝隙连接蛋白43(Cx43)进行半定量分析。结果4周后,进行快速右室起搏的CHF组的所有犬均可诱发出稳定CHF。终止起搏后,CHF犬的持续AF(>15min)的诱发率为87.5%(7/8),显著高于对照犬(P<0.01)。CHF组PV肌袖纤维化的程度明显增加,总胶原的含量显著高于对照组的相应部位[(5.3±1.0)%vs(2.1±0.7)%,P<0.01]。CHF组Ⅲ型胶原的含量及Ⅲ型胶原与I型胶原含量的比值均显著高于对照组[(4.6±1.0)%vs(1.6±0.7)%和(7.9±3.2)vs(3.0±1.9),P<0.01];但I型胶原的含量与对照组无显著差异[(0.6±0.2)%vs(0.6±0.3)%]。CHF组PV肌袖内Cx43的水平显著高于对照组[(3.3±0.6)%vs(2.8±0.7)%,P<0.05];其PV肌袖内细胞侧侧连接处Cx43的分布较对照组增加。结论CHF对PV肌袖结构具有显著影响。

AIM To explore the effect of congestive heart failure （CHF） on the structure of myosleeve tissue of pulmonary veins （PVs） in canine. METHODS Sixteen hybrid dogs were divided into congestive heart failure （CHF） group （ n = 8） and normal control group （ n = 8） randomly. In the CHF group, right ventricular pacing was performed at a frequency of 240/min for 4 weeks to establish CHF model. Atrial fibrillation （AF） was induced by burst stimulation of atrial pacing. The degree of interstitial fibrosis and the composition of type Ⅰ and Ⅲ collagens in the pulmonary vein myosleeve tissue in two groups were analyzed by sirius red staining. Immunohistochemical staining was used to detect the expression and distribution of connexin 43 （Cx43）. RESULTS After 4 weeks, stable CHF was seen in all the dogs in CHF group. After the pacing came to a stop, the rate of inducing sustained AF （ 〉 15 minutes） in CHF group was significantly higher than that in control group （P 〈 0.01 ）. Interstitial fibrosis in the PV myosleeve tissue increased in CHF group compared with that in control group. The expressions of type Ⅰ and type Ⅲ collagens in CHF group were obviously higher than those in normal control group [ （5.3 ± 1. 0）% vs （2. 1 ±0. 7）% ,P 〈0. 01 ]. The expression of type IU collagen in CHF group was significantly higher than that in normal control group [ （4. 6 ± 1.0） % vs （ 1.6 ±0. 7） % ,P 〈0. 01 ]. No difference in expression of type I collagen was found between the two groups [ （0. 6 ± 0. 2 ） % vs （0. 6 ±0. 3 ） % ]. The ratio of type Ⅱ to type Ⅰ collagen in CHF group was higher than that in control group （7.9 ±3.2 vs 3.0 ± 1.9, P 〈0. 01 ）. The expression of CX43 in the PV myosleeve tissue in CHF group was increased compared with that in control group [ （ 3.3 ± 0. 6 ） % vs （ 2.8 ± 0. 7 ） %, P 〈 0. 05 ]. In addition, in CHF group, Cx43 distribution over the cellular lateral membrane in the PV myosleeve myocytes was distinctly wider than that in control group. CONCLUSION CHF can result in structural remodeling of canine PVs. The remodeling may be part of the AF mechanism in canine CHF model.