Direct energy delivery improves tissue perfusion after resuscitated shock.
Direct energy delivery improves tissue perfusion after resuscitated shock.
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直接能量输送可改善休克复苏后的组织灌注。
DOI：
10.1016/j.surg.2005.06.009
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Garrison,RNeal
中科院分区：
文献类型：
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作者：
Zakaria,ElRasheid;Ehringer,WilliamD;Tsakadze,Nina;Li,Na;Garrison,RNeal
出血性休克（HS）的常规复苏（CR）不能恢复肠血流量。无氧代谢的指标表明，细胞的能量生产也受到损害。我们假设，直接静脉内递送脂质包封的高能磷酸盐的细胞，提高HS和复苏（RES）过程中的肠灌注。方法MAP（MAP）在雄性大鼠（200 g）进行了监测，末端回肠微血管直径通过在体视频显微镜进行测量，并计算血流量（多普勒测速仪）。在RES期间通过静脉输注含有三磷酸腺苷（ATP; VitaSol）的融合单层脂质囊泡来实现细胞能量递送。我们的方案是HS至50%基线MAP 60分钟，RES 30分钟，并继续显微镜观察120分钟。实验组（每组n=8）是HS+CR（组I）; HS+CR+ VitaSol（组II）; HS+CR+媒介物，媒介物是不含镁ATP的磷脂囊泡（组III）; HS+ VitaSol（组IV）;假手术对照+VitaSol（组V）;和时间匹配的假手术对照（组VI）。在单独的完整动物实验中评价了作为辅助VitaSol复苏的函数的存活结果和来自湿重/干重比的总组织水。CR恢复了基线血流动力学，导致所有小动脉水平的肠微血管直径初步恢复。然而，随后在RES后120分钟，粘膜前血管出现进行性血管收缩和灌注不足（基线直径的−20.48% ± 2.95%）。相比之下，VitaSol + CR可增强粘膜前扩张（+34.27% ± 4.62%）和增加血流（+20.50% ± 10.70%），高于出血前基线。单独的囊泡没有效果，单独的VitaSol仅引起适度的扩张。CR中度HS（40%的基线MAP为60分钟，n=10）造成20%的死亡率，而辅助VitaSol复苏有100%的生存率和更少的组织水contains.CONCLUSIONSOUR的数据证实，CR导致进行性肠灌注不足。直接静脉能量输送的细胞复苏改善了CR后的肠道灌注，并导致生存率提高和组织水肿减少。
BACKGROUNDConventional resuscitation (CR) from hemorrhagic shock (HS) does not restore intestinal blood flow. Indicators of anaerobic metabolism suggest that cellular energy production also is compromised. We hypothesize that the direct intravenous delivery of lipid-encapsulated high-energy phosphates to cells improves intestinal perfusion during HS and resuscitation (RES).METHODSMAP (MAP) was monitored in male rats (200 g), terminal ileum microvessel diameters were measured by in vivo videomicroscopy, and blood flow (Doppler velocimetry) was calculated. Cellular energy delivery was accomplished by intravenous infusion during RES of fusogenic unilamellar lipid vesicles that contain adenosine triphosphate (ATP; VitaSol). Our protocol was HS to 50% baseline MAP for 60 minutes, 30 minutes of RES, and continued microscopy observation for 120 minutes. Experimental groups (n=8 each) were HS+CR (group I); HS+CR+ VitaSol (group II); HS+CR+Vehicle, Vehicle is the phospholipid vesicles without magnesium ATP, (group III); HS+ VitaSol (group IV); sham-operated control+VitaSol (group V); and a time-matched sham-operated control (group VI). The survival outcome and total tissue water from wet weight/dry weight ratio as a function of adjunct VitaSol resuscitation were evaluated in separate intact animal experiments.RESULTSHS caused a selective vasoconstriction of the intestinal inflow arterioles (100 μm), which was not seen in the smaller intestinal premucosal arterioles (7-15 μm). CR, which restored baseline hemodynamics, resulted in an initial restoration of intestinal microvascular diameters at all arteriolar levels. However, this was followed by a progressive vasoconstriction and hypoperfusion in premucosal vessels at 120 minutes after RES (−20.48% ± 2.95% from baseline diameters). In contrast, VitaSol with CR caused enhanced premucosal dilation (+34.27% ± 4.62%) and augmented flow (+20.50% ± 10.70%) above prehemorrhage baseline. Vesicles alone had no effect, and VitaSol alone caused only a modest dilation. CR of moderate HS (40% of baseline MAP for 60 minutes, n=10) caused 20% mortality, whereas adjunct VitaSol resuscitation had a 100% survival and less tissue water content.CONCLUSIONSOur data confirms that CR causes progressive intestinal hypoperfusion. Cellular resuscitation with direct intravenous energy delivery improves intestinal perfusion after CR and results in improved survival and less tissue edema.