Schipke J D, Korbmacher B, Dorszewski A, Selcan G, Sunderdiek U, Arnold G
Institute of Experimental Surgery, Heinrich-Heine-University Düsseldorf, Germany.
Heart. 1996 Jan;75(1):55-61. doi: 10.1136/hrt.75.1.55.
To amplify the description of myocardial stunning.
Control versus 30 min after a 20 min no flow ischaemia.
15 isolated rabbit hearts perfused with erythrocyte suspension.
Left ventricular systolic function in terms of aortic flow, peak systolic pressure (LVPmax), dP/dtmax, and the end systolic pressure-volume relation (ESPVR); early relaxation from dP/dtmin and rate of left ventricular pressure decay (tau). Passive properties: ventricular and myocardial stiffness. Coronary resistance from coronary blood flow and perfusion pressure. Total myocardial oxygen consumption (MVo2tot). Total mechanical energy via pressure-volume area (PVA). Contractile efficiency (Econ) and MVo2 of the unloaded contracting heart (MVo2unl). External mechanical efficiency (Eext) from stroke work and MVo2tot.
Systolic variables in stunned myocardium were significantly decreased (mean (SD)): aortic flow: 38 (13) v 9 (11) ml/min; LVPmax: 112 (19) v 74 (18) mm Hg; dP/dtmax: 1475 (400) v 1075 (275) mm Hg/s. ESPVR was not significantly decreased, at 138 (73) v 125 (58) mm Hg/ml, but the volume axis intercept was shifted rightward: 0.30 (0.37) v 0.65 (0.25) ml. Likewise, early relaxation was impaired: dP/dtmin (-1275 (250) v -975 (250) mm Hg/s) and tau (37 (7) v 46 (10) ms). LVPed was significantly decreased at 19 (12) v 12 (7) mm Hg, and both the ventricular (end diastolic pressure-volume relation) and the myocardial stiffness (constant k) were increased by 75% and 31%, respectively. Coronary resistance increased non-significantly from 0.83 (0.31) to 1.04 (0.41) mm Hg/(ml/min/100 g). Decreases in PVA (570 (280) v 270 (200) mm Hg.ml/100 g), MVo2tot (40 (9) v 34 (8) microliters/beat/100 g), and MVo2unl (26 (9) v 22 (6) microliters/beat/100 g) did not reach significance, in contrast to significant decreases in Econ (31 (18) v 14 (7)%) and Eext (0.75 (0.29) v 0.18 (0.25) arbitrary units).
Ventricular systolic function is decreased after brief episodes of ischaemia. The decrease in diastolic function probably amplifies the systolic deterioration during myocardial stunning. Passive diastolic properties are also changed, shown by increases in both ventricular and myocardial stiffness. The increase in coronary resistance indicates stunning at the vascular level which could limit oxygen supply. With maintained MVo2tot during stunning, external efficiency is decreased. Possible candidates for this metabolic stunning are inadequate excitation-contraction coupling and disturbed O2 utilisation by the contractile apparatus.
扩展对心肌顿抑的描述。
对照组与20分钟无复流缺血后30分钟的对比。
15个用红细胞悬液灌注的离体兔心。
以主动脉流量、收缩压峰值(LVPmax)、dP/dtmax以及收缩末期压力-容积关系(ESPVR)衡量的左心室收缩功能;根据dP/dtmin和左心室压力衰减速率(tau)评估的早期舒张功能。被动特性:心室和心肌僵硬度。根据冠状动脉血流量和灌注压计算的冠状动脉阻力。总心肌耗氧量(MVo2tot)。通过压力-容积面积(PVA)计算的总机械能。收缩效率(Econ)和无负荷收缩心脏的MVo2(MVo2unl)。根据搏出功和MVo2tot计算的外在机械效率(Eext)。
顿抑心肌的收缩变量显著降低(均值(标准差)):主动脉流量:38(13)对9(11)ml/min;LVPmax:112(19)对74(18)mmHg;dP/dtmax:1475(400)对1075(275)mmHg/s。ESPVR未显著降低,分别为138(73)对125(58)mmHg/ml,但容积轴截距右移:0.30(0.37)对0.65(0.25)ml。同样,早期舒张功能受损:dP/dtmin(-1275(250)对-975(250)mmHg/s)和tau(37(7)对46(10)ms)。左心室舒张末压显著降低,分别为19(12)对12(7)mmHg,心室(舒张末期压力-容积关系)和心肌僵硬度(常数k)分别增加75%和31%。冠状动脉阻力从0.83(0.31)非显著增加至1.04(0.41)mmHg/(ml/min/100g)。PVA(570(280)对270(200)mmHg.ml/100g)、MVo2tot(40(9)对34(8)微升/搏/100g)和MVo2unl(26(9)对22(6)微升/搏/100g)的降低未达显著水平,与之形成对比的是Econ(31(18)对14(7)%)和Eext(0.75(0.29)对0.18(0.25)任意单位)显著降低。
短暂缺血发作后心室收缩功能降低。舒张功能降低可能会加剧心肌顿抑期间的收缩功能恶化。被动舒张特性也发生改变,表现为心室和心肌僵硬度增加。冠状动脉阻力增加表明血管水平存在顿抑,这可能会限制氧供应。在顿抑期间MVo2tot保持不变的情况下,外在效率降低。这种代谢性顿抑的可能原因是兴奋-收缩偶联不足以及收缩装置的氧利用紊乱。