临界血细胞比容时的高氧通气：对心肌灌注和功能的影响。

Hyperoxic ventilation at the critical hematocrit: effects on myocardial perfusion and function.

作者信息

Kemming G I, Meisner F G, Meier J, Tillmanns J, Thein E, Eriskat J, Habler O P

机构信息

Institute for Surgical Research, Ludwig-Maximilians-University Munich, Germany.

出版信息

Acta Anaesthesiol Scand. 2004 Sep;48(8):951-9. doi: 10.1111/j.0001-5172.2004.00460.x.

DOI:10.1111/j.0001-5172.2004.00460.x

PMID:15315611

Abstract

BACKGROUND

Hemodilution reduces hematocrit (Hct) and blood oxygen content. Tissue oxygenation is mainly preserved by increased cardiac output. As myocardial O2-demands increase, coronary vasodilatation becomes necessary to increase myocardial blood flow. Myocardial ischemia occurs at a critical Hct-value (Hctcrit), with accompanying exhaustion of coronary reserve. Hyperoxic ventilation is known to both reverse peripheral tissue hypoxia at Hctcrit and also to induce coronary vasoconstriction. This study aimed to determine whether hyperoxic ventilation at Hctcrit further exacerbates myocardial ischemia and dysfunction.

METHODS

Nine anesthetized pigs ventilated on room air were hemodiluted by 1:1 exchange of blood with pentastarch (6%HES) to Hctcrit, defined as onset of myocardial ischemia (ECG changes). At Hctcrit, hyperoxic ventilation was started. Measurements were performed at baseline, at Hctcrit, and after 15 min of hyperoxic ventilation. We determined myocardial blood flow (microsphere method), arterial O2-content, subendocardial O2-delivery and myocardial function (left ventricular pressure increase).

RESULTS

At Hctcrit 7 (6;8)%, O2-content was reduced [3.7 (3.1;3.9) ml dl(-1)]. Despite a compensatory increase of myocardial blood flow [531 (449;573), ml min(-1)100 g(-1)], all pigs displayed myocardial ischemia and compromised myocardial function (P < 0.05). Hyperoxic ventilation produced increased coronary vascular resistance secondary to vasoconstriction, and reduced myocardial blood flow [426 (404;464), ml min(-1)100 g(-1); P < 0.05]. Myocardial oxygenation was found to be maintained by increased O2-content [4.4 (4.2;4.8), ml dl(-1); P < 0.05], the contribution of dissolved O2 to subendocardial O2-delivery increased (32 vs. 8%; P < 0.05), which preserved myocardial function.

CONCLUSION

Hyperoxic ventilation at Hctcrit is followed by coronary vasoconstriction and reduction of coronary blood flow. However, myocardial oxygenation and function is maintained, as increased O2-content (in particular dissolved O2) preserves myocardial oxygenation.

摘要

背景

血液稀释会降低血细胞比容（Hct）和血氧含量。组织氧合主要通过心输出量增加得以维持。随着心肌需氧量增加，冠状动脉扩张对于增加心肌血流量变得必要。心肌缺血发生在临界血细胞比容值（Hctcrit）时，同时伴有冠状动脉储备耗竭。已知高氧通气既能在Hctcrit时逆转外周组织缺氧，也能诱发冠状动脉收缩。本研究旨在确定在Hctcrit时进行高氧通气是否会进一步加重心肌缺血和功能障碍。

方法

对9只吸入室内空气进行麻醉的猪，通过用羟乙基淀粉（6%HES）以1:1比例交换血液将其血液稀释至Hctcrit，定义为心肌缺血发作（心电图改变）。在Hctcrit时开始高氧通气。在基线、Hctcrit时以及高氧通气15分钟后进行测量。我们测定了心肌血流量（微球法）、动脉血氧含量、心内膜下氧输送以及心肌功能（左心室压力升高）。

结果

在Hctcrit为7（6；8）%时，血氧含量降低[3.7（3.1；3.9）ml dl⁻¹]。尽管心肌血流量有代偿性增加[531（449；573），ml min⁻¹100 g⁻¹]，但所有猪均出现心肌缺血且心肌功能受损（P < 0.05）。高氧通气由于血管收缩导致冠状动脉血管阻力增加，心肌血流量减少[426（404；464），ml min⁻¹100 g⁻¹；P < 0.05]。发现通过增加血氧含量[4.4（4.2；4.8），ml dl⁻¹；P < 0.05]可维持心肌氧合，溶解氧在心内膜下氧输送中的贡献增加（32%对8%；P < 0.05），从而维持了心肌功能。