大鼠脑局灶性缺血再灌注后梗死体积变化与低分子肝素的保护效应

目的:观察低分子肝素对大鼠脑缺血再灌注后不同时间点脑梗死体积的影响。方法:实验于2005-03/2005-06在华北煤炭医学院动物实验中心完成。①选用雄性SD大鼠90只,体质量280～330g。应用随机数字表法将大鼠分为3组:假手术组、缺血再灌注组、低分子肝素组,每组30只。假手术组:只游离右侧颈总动脉、颈内动脉、颈外动脉。缺血再灌注组和低分子肝素组:均采用改良Longa法制作大鼠右侧大脑中动脉闭塞局灶性脑缺血再灌注模型。缺血2h后分别腹腔注射生理盐水1mL和皮下注射低分子肝素(200IU/kg)生理盐水稀释液1mL。2组均于缺血2.5h后开始再灌注3,6,12,24,48h,每个时间点取6只进行观察。②分别称重应用四氮唑红染色法染成白色的梗死组织与染成红色的正常组织,以梗死组织占全脑湿重的百分比表示脑梗死体积。③采用两样本均数的t检验对两组间数据进行分析。结果:大鼠90只均进入结果分析。缺血再灌注组大鼠脑缺血再灌注3,6,12,24,48h时脑梗死体积分别为(17.28±2.69)%,(22.66±2.16)%,(30.17±4.17)%,(38.83±4.54)%,(43.75±2.66)%,低分子肝素组分别为(12.54±1.35)%,(19.83±2.32)%,(23.83±3.19)%,(30.33±2.50)%,(36.25±2.54)%,假手术组均为0。随着缺血再灌注时间的延长,缺血再灌注组脑梗死体积逐渐增大,低分子肝素组梗死体积较缺血再灌注同一时间组明显缩小(t=-2.376,-2.191,-2.96,-4.019,-4.446,P<0.05)。结论:脑缺血再灌注损伤随再灌注时间延长而加重,低分子肝素能减少脑梗死体积,缩小梗死范围,对大鼠脑缺血再灌注损伤后具有保护作用。     

Influence of Different Atrioventricular and Interventricular Delays on Cardiac Output During Cardiac Resynchronization Therapy

Restoration of the atrioventricular (AVD) and interventricular (VVD) delays increases the hemodynamic benefit conferred by biventricular (BiV) stimulation. This study compared the effects of different AVD and VVD on cardiac output (CO) during three stimulation modes: BiV-LV = left ventricle (LV) preceding right ventricle (RV) by 4 ms; BiV-RV = RV preceding LV by 4 ms; LVP = single-site LV pacing. We studied 19 patients with chronic heart failure due to ischemic or idiopathic dilated cardiomyopathy, QRS ≥ 150 ms, mean LV end-diastolic diameter = 78 ± 7 mm, and mean LV ejection fraction = 21 ± 3%. CO was estimated by Doppler echocardiographic velocity time integral formula with sample volume placed in the LV outflow tract. Sets of sensed-AVDs (S-AVD) 90–160 ms, paced-AVDs (P-AVD) 120–160 ms, and VVDs 4–20 ms were used. BiV-RV resulted in lower CO than BiV-LV. S-AVD 120 ms and P-AVD 140 ms caused the most significant increase in CO for all three pacing modes. LVP produced a similar increase in CO as BiV stimulation; however, AV sequential pacing was associated with a nonsignificantly higher CO during LVP than with BiV stimulation. CO during BiV stimulation was the highest when LV preceded RV, and VVD ranged between 4 and 12 ms. The most negative effect on CO was observed when RV preceded LV by 4 ms. Hemodynamic improvement during BiV stimulation was dependent both on optimized AVD and VVD. LV preceding RV by 4–12 ms was the most optimal. Advancement of the RV was not beneficial in the majority of patients.