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首页> 外文期刊>European surgical research >Diaspirin cross-linked hemoglobin fails to improve left ventricular diastolic function after fluid resuscitation from hemorrhagic shock.
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Diaspirin cross-linked hemoglobin fails to improve left ventricular diastolic function after fluid resuscitation from hemorrhagic shock.

机译:失血性休克复苏液体后,diaspirin交联的血红蛋白无法改善左心室舒张功能。

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摘要

In severe hemorrhagic shock, left ventricular (LV) diastolic dysfunction is an early sign of cardiac failure due to compromised myocardial oxygenation. Immediate fluid replacement or, in particular, administration of a hemoglobin-based oxygen carrier (diaspirin cross-linked hemoglobin; DCLHb) improves myocardial oxygenation; therefore, positive effects on LV diastolic function could be expected. The effects of fluid resuscitation from severe hemorrhagic shock with DCLHb were investigated in 20 anesthetized domestic pigs. After generation of a critical left anterior descending coronary artery stenosis (narrowing of the artery until disappearance of reactive hyperemia after a 10-second complete vessel occlusion), hemorrhagic shock (mean arterial blood pressure 45 mm Hg) was induced within 15 min by controlled blood withdrawal and maintained for 60 min. Fluid resuscitation consisted of replacement of the plasma volume withdrawn during hemorrhage by infusion of either 10% DCLHb (DCLHb group, n = 10) or 8% human serum albumin (HSA) oncotically matched to DCLHb (HSA group, n = 10). After completion of resuscitation, an observation period of 60 min elapsed. Measurements of central hemodynamics, myocardial oxygenation, and LV diastolic function were performed at baseline, after induction of critical coronary artery stenosis, after 60 min of hemorrhagic shock, immediately after resuscitation, and 60 min later. While 5 out of 10 animals treated with HSA died within the first 20 min after fluid resuscitation from acute LV pump failure, all DCLHb-treated animals survived until the end of the protocol (p < 0.05). Despite superior myocardial oxygenation due to augmentation of the arterial O(2) content as well as of coronary perfusion pressure, no beneficial effects on LV diastolic function were observed after infusion of DCLHb. Peak velocity of LV pressure decrease (dp/dt(min)) did not reveal significant differences between the two groups. Immediately after completion of fluid resuscitation with DCLHb, the time constant of LV diastolic relaxation (tau) was prolonged when compared with HSA-treated animals (p < 0.05), indicating retardation of early LV diastolic relaxation. Our data suggest that DCLHb fails to improve LV diastolic function after fluid resuscitation from severe hemorrhagic shock. However, positive effects on myocardial perfusion and oxygenation result in a significant reduction of the mortality of severe hemorrhagic shock.
机译:在严重失血性休克中,由于心肌氧合受损,左心室舒张功能障碍是心力衰竭的早期征兆。立即补液或给予基于血红蛋白的氧气载体(diaspirin交联的血红蛋白; DCLHb)可改善心肌的充氧;因此,有望对LV舒张功能产生积极影响。在20头麻醉的家猪中研究了DCLHb对严重失血性休克进行液体复苏的效果。产生严重的左冠状动脉前降支狭窄(狭窄血管直至完全闭塞10秒后反应性充血消失)后,通过控制血液在15分钟内诱发失血性休克(平均动脉血压45 mm Hg)停药60分钟。液体复苏包括通过输注10%DCLHb(DCLHb组,n = 10)或8%经手法与DCLHb匹配的人血清白蛋白(HSA)(HSA组,n = 10)来替换出血期间抽取的血浆量。复苏完成后,经过60分钟的观察期。在诱发严重冠状动脉狭窄后,出血性休克后60分钟,复苏后立即和60分钟后,在基线时进行中心血流动力学,心肌氧合和LV舒张功能的测量。尽管在接受急性左室泵衰竭进行液体复苏后的头20分钟内,用HSA治疗的动物中有5只在死亡后的20分钟内死亡,但所有DCLHb治疗的动物都存活到实验方案结束(p <0.05)。尽管由于动脉O(2)含量的增加以及冠脉灌注压的增加而产生了优越的心肌氧合作用,但在输注DCLHb后未观察到对LV舒张功能的有益作用。左室压力降低的峰值速度(dp / dt(min))未显示两组之间的显着差异。与用HSA处理的动物相比,用DCLHb进行液体复苏完成后,LV舒张舒张时间常数(tau)随即延长(p <0.05),这表明早期LV舒张舒张的延迟。我们的数据表明,严重失血性休克复苏液体后,DCLHb无法改善左室舒张功能。然而,对心肌灌注和氧合的积极影响导致严重失血性休克的死亡率大大降低。

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