del Nido P J, Benson L N, Mickle D A, Kielmanowicz S, Coles J G, Wilson G J
Division of Cardiovascular Surgery, Hospital for Sick Children, Toronto, Ontario, Canada.
Circulation. 1987 Nov;76(5 Pt 2):V168-73.
Chronic right ventricular hypertrophy (RVH) has been shown to produce changes in left ventricular diastolic properties but minimal effects on left ventricular systolic function. We studied the effects of chronic pressure overload RVH on left ventricular systolic function before and after reversible hypothermic global ischemia. RVH was induced by pulmonary artery banding (PAB) in newborn piglets (5 to 7 days). At 2 months of age the PAB group (n = 6) and a control group (n = 8) were subjected to cardiac arrest on cardiopulmonary bypass with cold crystalloid cardioplegia (10 degrees C) for 2 hr and were reperfused for 1 hr. Left ventricular function was assessed by a conductance catheter in the left ventricle measuring the end-systolic pressure-volume relationship (Emax). Preischemic and postischemic Emax were the same in the control group (4.1 +/- 0.4 mm Hg/ml before vs 4.1 +/- 0.4 mm Hg/ml after ischemia), but significantly different in the PAB group (4.7 +/- 0.5 mm Hg/ml before vs 2.97 +/- 0.7 mm Hg/ml after ischemia, p less than .05). There also was a marked drop in ATP and phosphocreatine (CP) content in the PAB group during ischemia (ATP, 20 +/- 2 mmol/kg dry wt before vs 10 +/- 2 mmol/kg dry wt after ischemia, p less than .05; PC, 26 +/- 3 mmol/kg dry wt before vs 11 +/- 1 mmol/kg dry wt after ischemia, p less than .05). In the control group there was no change in ATP content and, although CP did drop by end-ischemia, there was complete recovery by 1 hr of reperfusion but minimal CP recovery in the PAB group.(ABSTRACT TRUNCATED AT 250 WORDS)
慢性右心室肥厚(RVH)已被证明会引起左心室舒张特性的改变,但对左心室收缩功能影响极小。我们研究了慢性压力超负荷性RVH对可逆性低温全心缺血前后左心室收缩功能的影响。通过对新生仔猪(5至7日龄)进行肺动脉环扎(PAB)诱导RVH。在2月龄时,PAB组(n = 6)和对照组(n = 8)在体外循环下使用冷晶体心脏停搏液(10℃)进行心脏停搏2小时,并再灌注1小时。通过置于左心室内的电导导管测量左心室功能,评估收缩末期压力-容积关系(Emax)。对照组缺血前和缺血后的Emax相同(缺血前4.1±0.4mmHg/ml,缺血后4.1±0.4mmHg/ml),但PAB组有显著差异(缺血前4.7±0.5mmHg/ml,缺血后2.97±0.7mmHg/ml,p<0.05)。在缺血期间,PAB组的ATP和磷酸肌酸(CP)含量也显著下降(ATP,缺血前20±2mmol/kg干重,缺血后10±2mmol/kg干重,p<0.05;PC,缺血前26±3mmol/kg干重,缺血后11±1mmol/kg干重,p<0.05)。对照组ATP含量无变化,虽然CP在缺血末期确实下降,但再灌注1小时后完全恢复,而PAB组CP恢复极少。(摘要截断于250字)