Myocardial protection in the failing heart: II. Effect of pulsatile cardioplegic perfusion under simulated left ventricular restoration.
Myocardial protection in the failing heart: II. Effect of pulsatile cardioplegic perfusion under simulated left ventricular restoration.
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DOI：
10.1016/j.jtcvs.2006.04.048
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发表时间：
2006-10
期刊：
影响因子：
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通讯作者：
G. Kassab;M. Kostelec;G. Buckberg;J. Covell;A. Sadeghi;J. Hoffman
中科院分区：
文献类型：
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作者：
G. Kassab;M. Kostelec;G. Buckberg;J. Covell;A. Sadeghi;J. Hoffman
目的研究心脏起搏诱导的实验性心力衰竭模型中的开放心室，以确定心脏停搏持续灌流和搏动性心脏停搏期间冠脉血流的范围和分布，并与心脏跳动中的全血比较。方法在5只心脏起搏诱导的心力衰竭动物和6只对照猪中，在(1)跳动、(2)非搏动性停搏液和(3)搏动性停搏液模式下，测量开放左心室的局部冠脉血流量(模拟暴露以恢复左心室)。平均灌流压维持在80 mm Hg。结果在开放的左心室中，对照和衰竭心脏的血流幅度和分布有所不同。在对照心脏中，非搏动性和搏动性血流(彼此相似)的跨室壁和心内膜停搏血流在左心室开放状态下分别比搏动血流多63%和70%。在心脏停搏分娩期间，衰竭心脏的跨壁和心内膜下血管阻力增加，导致在相同灌流压的非搏动性条件下心内膜下血流减少。心功能不全组心内膜下血流灌注状况在不停跳状态下无明显变化(对照组为0.89，开放不停跳状态为0.78 m L/min/g)，但非搏动性停搏流量显著减少154%，较不停跳状态减少32.2%(0.78 m L/m in/g)。相反，搏动性停搏液输送改善了开放衰竭心脏的心内膜血流，因为搏动性停搏液灌流比搏动流量多41%。在心力衰竭中，在相同的灌流压力下，来自不停跳心脏的搏动性(导致冠状动脉外在压迫)或在搏动性停搏灌流过程中的内在血管扩张比非搏动性停搏液更好地保存了心内膜灌注量。结论在衰竭的开放脑室(在心室恢复时模拟几何形状)，心内膜下血流维持在搏动状态，但在非搏动性停搏液灌流时明显低于对照组。相反，搏动性心脏停搏输注改善了开放的衰竭脑室的心内膜下血流。与非搏动性停跳分娩相比，搏动性分娩(无论是在跳动期间还是心脏停搏灌注期间)心内膜下血流灌注改善的这些发现可能对衰竭心脏的心肌保护有重要意义。
OBJECTIVEThe open ventricle was studied in pacing-induced experimental heart failure to determine the extent of coronary perfusion and distribution during either continuous or pulsatile cardioplegic perfusion compared with whole blood in the beating heart.METHODSIn 5 animals that underwent pacing-induced heart failure and in 6 control swine, regional coronary blood flows were measured on bypass in the open left ventricle (simulating exposure for left ventricle restoration) during (1) beating, (2) nonpulsatile cardioplegia, and (3) pulsatile cardioplegia modalities. Mean perfusion pressure was maintained at 80 mm Hg.RESULTSFlow magnitude and distribution differed in control and failing hearts in the open left ventricle. In control hearts, transmural and endocardial cardioplegic flow of nonpulsatile and pulsatile flow (which were similar to each other) exceeded beating flow by 63% and 70%, respectively, in the open left ventricle condition. Transmural and subendocardial vascular resistance increased in failing hearts during cardioplegic delivery, resulting in lower subendocardial flow under nonpulsatile conditions for the same perfusion pressure. In failing hearts, subendocardial perfusion conditions did not change in the beating state (0.89 vs 0.78 mL/min/g in control and failing open beating states, respectively), but nonpulsatile cardioplegic flow was significantly reduced by 154%, and became lower than beating flow by 32.2% (0.78 vs 0.59 mL/min/g). Conversely, pulsatile cardioplegic delivery improved endocardial flow in the open failing hearts, as cardioplegic perfusion with pulsatility exceeded beating flow by 41%. In heart failure, pulsatility from either the beating heart, which causes extrinsic compression of coronary vessels, or intrinsic vessel distension during pulsatile cardioplegic perfusion preserved endocardial perfusion better than nonpulsatile cardioplegia at the same perfusion pressure.CONCLUSIONIn the failing open ventricle (simulated geometry during ventricular restoration), subendocardial blood flow was maintained in the beating state, but decreased significantly from control values during nonpulsatile cardioplegic perfusion. Conversely, pulsatile cardioplegic delivery improved subendocardial perfusion of the open failing ventricle. These findings of improved subendocardial perfusion during pulsatile delivery (either during beating or cardioplegic perfusion) compared with nonpulsatile cardioplegic delivery may have important implications for myocardial protection in failing hearts.