Ischemia–Reperfusion-Induced Unmeasured Anion Generation and Glycocalyx Shedding: Sevoflurane versus Propofol Anesthesia

ABSTRACT

Introduction: 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. Methods: 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. Results: 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). Conclusions: 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.

Keywords: :

• propofol
• sevoflurane
• aortic clamp
• endothelium
• glycocalyx
• acid–base equilibrium
• metabolic acidosis

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ACKNOWLEDGMENTS

The authors gratefully acknowledge the support of the following persons: Johannes Hilberath, Korbinian Langer, and Susanne Kahr for helping in data acquisition and performing the original pig study; Mrs. Sylvia Münzing for outstanding technical assistance; Mrs. Alke Schropp for preparation of histological cross-sections; Mrs. Brigitte Blount and team for animal care (at the Walter Brendel Center of Experimental Medicine, LMU Munich); Gabriele Gröger (Department of Anesthesiology); and Dr. Peter Göhring (Institute for Clinical Chemistry, LMU Munich) for serum analyses. The work was supported by a grant from the Friedrich Baur Foundation (reg. no. 0053/2003) and a research grant (Förderung von Forschung und Lehre, reg. no. 388/2004) provided by the LMU Munich (to Thorsten Annecke).

Declaration of Interest: At the time of submission, but independent from the presented study, Thorsten Annecke received a research grant sponsored by Abbott, Germany. Peter Conzen held paid lectures for Abbott, Germany.