Meybohm Patrick, Cavus Erol, Dörges Volker, Weber Bernd, Stadlbauer Karl-Heinz, Wenzel Volker, Scholz Jens, Steffen Martin, Bein Berthold
Department of Anaesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, Campus Kiel, Schwanenweg 21, 24105 Kiel, Germany.
Resuscitation. 2008 Mar;76(3):449-56. doi: 10.1016/j.resuscitation.2007.09.002. Epub 2007 Oct 31.
The present study was designed to evaluate the effect of conventional fluid resuscitation and small volume resuscitation alone and combined with arginine vasopressin (AVP) on cerebral perfusion pressure (CPP) and protein S100B during experimental haemorrhagic shock.
Thirty anaesthetised pigs underwent a penetrating liver trauma. Following haemodynamic decompensation, pigs received either (1) a combination of crystalloid (40 mL kg(-1)) and colloid (20 mL kg(-1)) solutions (fluid, n=10), (2) hypertonic-hyperoncotic solution (HHS; 4 mL kg(-1)) combined with normal saline (HHS+NS; n=10) or (3) HHS combined with AVP (0.2 U kg(-1) followed by an infusion of 2 U kg(-1)h(-1); HHS+AVP; n=10).
Compared to baseline, CPP decreased and S100B levels increased significantly at haemodynamic decompensation (S100B: fluid, 0.52+/-0.23 microg L(-1) vs. 0.85+/-0.37 microg L(-1), p<0.05; HHS+NS, 0.47+/-0.18 microg L(-1) vs. 0.90+/-0.33 microg L(-1), p<0.05; HHS+AVP, 0.53+/-0.18 microg L(-1) vs. 0.90+/-0.39 microg L(-1), p<0.01). During the initial 10 min of therapy, CPP of HHS+NS was significantly higher compared to the fluid group, increased more rapidly in the HHS+AVP group, but was not significantly different thereafter. S100B levels decreased close to baseline values (p<0.001), and did not differ between groups.
HHS+AVP resulted in higher CPP compared to fluid and HHS+NS in the initial phase of therapy, but did not differ thereafter. Haemorrhage-induced hypotension yielded increased S100B levels that were comparable in groups throughout the study period.
本研究旨在评估单纯常规液体复苏、小容量复苏以及联合精氨酸加压素（AVP）对实验性失血性休克期间脑灌注压（CPP）和蛋白S100B的影响。
30只麻醉猪接受穿透性肝损伤。血流动力学失代偿后，猪被分为三组，分别接受：（1）晶体液（40 mL·kg⁻¹）和胶体液（20 mL·kg⁻¹）联合输注（液体组，n = 10）；（2）高渗高胶溶液（HHS；4 mL·kg⁻¹）联合生理盐水（HHS + NS组，n = 10）；（3）HHS联合AVP（0.2 U·kg⁻¹静脉推注，随后以2 U·kg⁻¹·h⁻¹持续输注；HHS + AVP组，n = 10）。
与基线相比，血流动力学失代偿时CPP降低，S100B水平显著升高（S100B：液体组，0.52±0.23 μg·L⁻¹ 对比 0.85±0.37 μg·L⁻¹，p < 0.05；HHS + NS组，0.47±0.18 μg·L⁻¹ 对比 0.90±0.33 μg·L⁻¹，p < 0.05；HHS + AVP组，0.53±0.18 μg·L⁻¹ 对比 0.90±0.39 μg·L⁻¹，p < 0.01）。治疗最初10分钟内，HHS + NS组的CPP显著高于液体组，HHS + AVP组升高更快，但此后差异无统计学意义。S100B水平降至接近基线值（p < 0.001），且各组间无差异。
在治疗初始阶段，HHS + AVP组的CPP高于液体组和HHS + NS组，但此后差异无统计学意义。出血性低血压导致S100B水平升高，在整个研究期间各组相当。
