Annecke Thorsten, Rehm Markus, Bruegger Dirk, Kubitz Jens C, Kemming Gregor I, Stoeckelhuber Mechthild, Becker Bernhard F, Conzen Peter F
Department of Anesthesiology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
J Invest Surg. 2012 Jun;25(3):162-8. doi: 10.3109/08941939.2011.618524.
Vascular leakage after ischemia-reperfusion (IR) is largely attributed to the destruction of the endothelial barrier and its associated negatively charged glycocalyx. In vitro, sevoflurane attenuates these changes. Therefore, we compared sevoflurane with propofol with regard to the protection of the glycocalyx and the release of negatively charged substances in vivo.
After surgical preparation under midazolam-fentanyl, nine pigs each received either propofol or sevoflurane. Ischemia of 90 min was induced by a balloon catheter in the thoracic aorta. After 120 min of reperfusion, the anesthetics were changed back to midazolam-fentanyl. Five animals, each without aortic occlusion, served as time controls. Blood electrolyte parameters were measured, from which the strong ion gap (SIG) was calculated. Serum heparan sulfate concentrations and immunohistology served as a marker of glycocalyx destruction.
Immediately after reperfusion, SIG increased significantly only in the propofol group (+6.7 mEq/l versus baseline; p < .05), remaining stable in sevoflurane and both time-controlled groups. Initially, heparan sulfate concentration increased comparably in both experimental groups, but after 120 min, it became stable in sevoflurane-anesthetized animals, while increasing further in the propofol group (p < .05).
Unmeasured anions, predictive of negative outcome in previous studies, did not increase significantly in sevoflurane-anesthetized animals. Additionally, there was less heparan sulfate shedding over time, signaling less destruction of the glycocalyx. Therefore, in this in-vivo situation, sevoflurane proves to be superior to propofol in protecting the endothelium from IR injury.
缺血再灌注（IR）后的血管渗漏很大程度上归因于内皮屏障及其相关的带负电荷糖萼的破坏。在体外，七氟醚可减轻这些变化。因此，我们在体内对七氟醚和丙泊酚在保护糖萼及带负电荷物质释放方面进行了比较。
在咪达唑仑 - 芬太尼麻醉下进行手术准备后，9只猪分别接受丙泊酚或七氟醚麻醉。通过胸主动脉内的球囊导管诱导90分钟的缺血。再灌注120分钟后，将麻醉剂换回咪达唑仑 - 芬太尼。5只未进行主动脉阻断的动物作为时间对照组。测量血液电解质参数，并计算强离子间隙（SIG）。血清硫酸乙酰肝素浓度和免疫组织学作为糖萼破坏的标志物。
再灌注后即刻，仅丙泊酚组的SIG显著升高（相对于基线增加6.7 mEq/l；p <.05），七氟醚组和两个时间对照组保持稳定。最初，两个实验组的硫酸乙酰肝素浓度升高程度相当，但120分钟后，七氟醚麻醉的动物中该浓度趋于稳定，而丙泊酚组则进一步升高（p <.05）。
在先前研究中可预测不良结局的未测定阴离子，在七氟醚麻醉的动物中未显著增加。此外，随着时间推移，硫酸乙酰肝素的脱落较少，表明糖萼的破坏较少。因此，在这种体内情况下，七氟醚在保护内皮免受IR损伤方面优于丙泊酚。
