Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart
Progressive left ventricular remodeling and apoptosis late after myocardial infarction in mouse heart
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DOI：
10.1152/ajpheart.2000.279.1.h422
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发表时间：
2000-07-01
影响因子：
4.8
通讯作者：
Colucci, WS
中科院分区：
文献类型：
--
作者：
Sam, F;Sawyer, DB;Colucci, WS
我们检验了心肌梗死（MI）后晚期左心室（LV）重构与远离梗死区的心肌细胞凋亡相关，并与LV扩张和收缩功能障碍在时间上相关的假设。冠状动脉结扎引起心肌梗死后1、4和6个月，采用等容球囊-左心室Langendorff技术测定左心室容积和收缩功能。用末端脱氧核苷酸转移酶介导的缺口末端标记法（TUNEL）和Hoechst 33258染色法检测细胞凋亡和细胞核形态。MI后1-6个月的进行性LV扩张与LV峰发展压（LVDP）降低相关。在远离梗死区的心肌中，室壁厚度增加，心房利钠肽mRNA表达增加，与反应性肥大一致。心肌梗死后1至6个月，TUNEL阳性心肌细胞数量逐渐增加（6个月时增加2.9倍;与假手术组相比P< 0.001）。因此，MI后晚期的LV重构与远离缺血性损伤区域的心肌细胞凋亡增加有关。细胞凋亡的频率与左室功能障碍的严重程度有关。
We tested the hypothesis that left ventricular (LV) remodeling late after myocardial infarction (MI) is associated with myocyte apoptosis in myocardium remote from the infarcted area and is related temporally to LV dilation and contractile dysfunction. One, four, and six months after MI caused by coronary artery ligation, LV volume and contractile function were determined using an isovolumic balloon-in-LV Langendorff technique. Apoptosis and nuclear morphology were determined by terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) and Hoechst 33258 staining. Progressive LV dilation 1-6 mo post-MI was associated with reduced peak LV developed pressure (LVDP). In myocardium remote from the infarct, there was increased wall thickness and expression of atrial natriuretic peptide mRNA consistent with reactive hypertrophy. There was a progressive increase in the number of TUNEL-positive myocytes from 1 to 6 mo post-MI (2.9-fold increase at 6 mo; P< 0.001 vs. sham). Thus LV remodeling late post-MI is associated with increased apoptosis in myocardium remote from the area of ischemic injury. The frequency of apoptosis is related to the severity of LV dysfunction.