Ishihara K, Zile M R, Nagatsu M, Nakano K, Tomita M, Kanazawa S, Clamp L, DeFreyte G, Carabello B A
Ralph H. Johnson Department of Veterans Affairs Medical Center, Charleston, S.C.
Circ Res. 1992 Dec;71(6):1472-81. doi: 10.1161/01.res.71.6.1472.
Abnormal coronary blood flow (CBF) in long-standing left ventricular (LV) pressure-overload hypertrophy has been associated with ischemia and LV dysfunction. Thus, goals of therapy in pressure overload are not only the relief of the overload itself but also regression in hypertrophy and subsequent improvement in CBF. However, little is known about CBF in humans or in large mammals after the relief of pressure overload, when the hypertrophy has regressed. This study was performed to test the hypothesis that, even 6 months after the relief of pressure overload in the dog, CBF would still be abnormal. Three groups of dogs were studied: 1) normal control dogs (NL group), 2) dogs with LV pressure-overload hypertrophy (LVH group), and 3) dogs that had developed LV pressure-overload hypertrophy but in whom the pressure overload was relieved 6 months before the final study (LVH Reg group). CBF was studied in conscious dogs by use of the radiolabeled microsphere technique at rest, during rapid atrial pacing, and during maximum coronary vasodilation produced by adenosine infusion. The ratio of LV weight (g) to body weight (kg) (LVBW) was 4.2 +/- 0.3 in the NL group, 7.1 +/- 0.6 in the LVH group, and 7.7 +/- 0.5 in the LVH Reg group before pressure-overload relief (p = NS, LVH versus LVH Reg). Six months after removal of the pressure overload, the LVBW in the LVH Reg group had fallen to 5.5 +/- 0.3 (p < 0.05), but this LVBW was still greater than that in the NL group (p < 0.05). During rapid atrial pacing, endocardial and epicardial CBF rose significantly in NL dogs. However, during rapid atrial pacing, endocardial CBF fell from 1.18 +/- 0.22 to 0.7 +/- 0.20 ml/min per gram in the LVH group (p < 0.05) and did not rise in the LVH Reg group. During adenosine infusion, endocardial blood flow increased in NL dogs from 1.63 +/- 0.13 to 4.0 +/- 0.3 ml/min per gram and increased to a similar level in the LVH Reg group. Although CBF increased during adenosine infusion in the LVH group, the increase was less than that in the NL or LVH Reg group (p < 0.05). Minimum coronary vascular resistance was similar in NL dogs (14 +/- 2 units) and LVH Reg dogs (18 +/- 3 units, p = NS) but was significantly elevated (32 +/- 10 units) in LVH dogs (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
长期左心室压力超负荷肥大时的异常冠状动脉血流（CBF）与心肌缺血和左心室功能障碍有关。因此，压力超负荷的治疗目标不仅是减轻超负荷本身，还包括使肥大消退并随后改善CBF。然而，对于人类或大型哺乳动物在压力超负荷解除后（此时肥大已消退）的CBF情况，人们了解甚少。本研究旨在验证以下假设：即使在狗的压力超负荷解除6个月后，CBF仍会异常。研究了三组狗：1）正常对照狗（NL组），2）患有左心室压力超负荷肥大的狗（LVH组），3）已发生左心室压力超负荷肥大但在最终研究前6个月压力超负荷已解除的狗（LVH Reg组）。通过使用放射性微球技术，在清醒的狗处于静息状态、快速心房起搏期间以及腺苷输注产生最大冠状动脉血管舒张期间，对CBF进行研究。在压力超负荷解除前，NL组的左心室重量（克）与体重（千克）之比（LVBW）为4.2±0.3，LVH组为7.1±0.6，LVH Reg组为7.7±0.5（p =无显著性差异，LVH组与LVH Reg组相比）。压力超负荷解除6个月后，LVH Reg组的LVBW降至5.5±0.3（p <0.05），但该LVBW仍高于NL组（p <0.05）。在快速心房起搏期间，NL组狗的心内膜和心外膜CBF显著升高。然而，在快速心房起搏期间，LVH组的心内膜CBF从1.18±0.22降至0.7±0.20毫升/分钟·克（p <0.05），而LVH Reg组未升高。在腺苷输注期间，NL组狗的心内膜血流从1.63±0.13增加至4.0±0.3毫升/分钟·克，LVH Reg组增加至相似水平。尽管LVH组在腺苷输注期间CBF增加，但增加幅度小于NL组或LVH Reg组（p <0.05）。NL组狗的最小冠状动脉血管阻力（14±2单位）与LVH Reg组狗（18±3单位，p =无显著性差异）相似，但LVH组显著升高（32±10单位）（p <0.05）。（摘要截短至400字）
