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Sevoflurane but not isoflurane can reduce prostacyclin production of endothelial cells

Published online by Cambridge University Press:  02 June 2005

B. Heindl ,
F. Reichle  and
B. F. Becker
B. Heindl
Affiliation:
Ludwig Maximilians University, Department of Anaesthesiology, Munich, Germany
F. Reichle
Affiliation:
Ludwig Maximilians University, Department of Anaesthesiology, Munich, Germany
B. F. Becker
Affiliation:
Ludwig Maximilians University, Department of Physiology, Munich, Germany
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Abstract

Summary

Background and objective: Little is known about the interaction of newer volatile anaesthetics with endothelial eicosanoid production. Sevoflurane may possibly reduce prostacyclin formation. Thus, we compared the influences of sevoflurane and isoflurane on endothelial prostacyclin production.

Methods: Production of prostacyclin of human umbilical vein endothelial cells was measured by the ELISA technique under basal conditions and after stimulation with calcium ionophore A 23187 10 μmol or histamine 0.1 μmol in the absence and presence of 1 and 2 minimal alveolar concentrations (MAC) of sevoflurane or isoflurane.

Results: The basal production of prostacyclin was unaffected by the volatile anaesthetics. Stimulation of endothelial cells increased prostacyclin formation 3–5-fold. Sevoflurane at 2 MAC, but not at 1 MAC, could reduce stimulated prostacyclin production by about half (P < 0.05). Isoflurane had no inhibitory effect. Inhibition of cyclo-oxygenase function by acetylsalicylic acid abolished the induced burst of prostacyclin formation completely.

Conclusions: Sevoflurane, but not isoflurane, can reduce stimulated endothelial prostacyclin production in a concentration-dependent manner. Because at least 2 MAC of sevoflurane were required, this effect should be of minor importance under clinical conditions of balanced anaesthesia.

Keywords

ANAESTHETICS, INHALATION, isoflurane, sevofluraneBLOOD VESSELS, endothelium, vascularPROSTAGLANDINS, prostacyclin
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 20 , Issue 2 , February 2003 , pp. 116 - 119
Copyright
2003 European Society of Anaesthesiology

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References

Goulielmos NV, Enayat ZE, Sheridan DJ, Cohen H, Flores NA. Nitric oxide and prostacyclin modulate the alterations in cardiac action potential duration mediated by platelets during ischaemia. Cardiovasc Res 1995; 30: 788–798.Google Scholar
Hohlfeld T, Strobach H, Schrör K. Stimulation of endogenous prostacyclin protects the reperfused pig myocardium from ischemic injury. J Pharmacol Exp Ther 1993; 264: 397–405.Google Scholar
Hirakata H, Ushikubi F, Toda H, et al. Sevoflurane inhibits human platelet aggregation and thromboxane A2 formation, possibly by suppression of cyclooxygenase activity. Anesthesiology 1996; 85: 1447–1453.Google Scholar
Heindl B, Becker BF. Sevoflurane and isoflurane do not enhance the pre- and postischemic eicosanoid production in guinea pig hearts. Anesth Analg 2000; 90: 17–24.Google Scholar
Jaffe E, Nachmann R, Becker C, Minick C. Culture of human endothelial cells derived from umbilical veins. Identification by morphologic and immunologic criteria. J Clin Invest 1973; 52: 2745–2756.Google Scholar
Radomski MW, Palmer RM, Moncada S. Endogenous nitric oxide inhibits human platelet adhesion to vascular endothelium. Lancet 1987; ii: 1057–1058.
Camacho M, Lopez BJ, Vila L. Rate of vasoconstrictor prostanoids released by endothelial cells depends on cyclooxygenase-2 expression and prostaglandin I synthase activity. Circ Res 1998; 83: 353–365.Google Scholar
Cabre F, Tost D, Suesa N, et al. Synthesis and release of platelet-activating factor and eicosanoids in human endothelial cells induced by different agonists. Agents Actions 1993; 38: 212–219.Google Scholar
Möbert J, Zahler S, Becker BF, Conzen PF. Inhibition of neutrophil activation by volatile anesthetics decreases adhesion to cultured human endothelial cells. Anesthesiology 1999; 90: 1372–1381.Google Scholar
Gerritsen ME. Eicosanoid production by the coronary microvascular endothelium. Fed Proc 1987; 46: 47–53.Google Scholar
McAdam BF, Catella-Lawson F, Mardini IA, Kapoor S, Lawso AJ. Systemic biosynthesis of prostacyclin by cyclooxygenase pharmacology of a selective inhibitor of COX-2. Proc Natl Acad Sci USA 1999; 96: 272–277.Google Scholar
Loeb AL, O'Brien DK, Longnecker DE. Halothane inhibits bradykinin-stimulated prostacyclin production in endothelial cells. Anesthesiology 1994; 81: 931–938.Google Scholar
Barnes SD, Martin LD, Wetzel RC. Halothane enhances pulmonary artery endothelial eicosanoid release. Anesth Analg 1992; 75: 1007–1013.Google Scholar
Heindl B, Becker BF, Zahler S, Conzen P. Halothane, sevoflurane and isoflurane reduce adhesion of blood platelets under low-flow conditions in the coronary system of isolated guinea pig hearts. Acta Anaesthesiol Scand 1998; 42: 995–1003.Google Scholar
Heindl B, Reichle FM, Zahler S, Conzen P, Becker BF. Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils. Anesthesiology 1999; 91: 521–530.Google Scholar