Sevoflurane but not isoflurane can reduce prostacyclin production of endothelial cells

被引:3
作者
Heindl, B
Reichle, E
Becker, BF
机构
[1] Univ Munich, Dept Anaesthesiol, D-80336 Munich, Germany
[2] Univ Munich, Dept Physiol, D-80336 Munich, Germany
关键词
anaesthetics; inhalation; isoflurane; sevoflurane; blood vessels; endothelium; vascular; prostaglandins; prostacyclin;
D O I
10.1097/00003643-200302000-00006
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background and objective: Little is known about the interaction of newer volatile anaesthetics with endothelial eicosanold 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 mumol or histamine 0.1 mumol in the absence and presence of I 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 I 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.
引用
收藏
页码:116 / 119
页数:4
相关论文
共 15 条
[1]  
BARNES SD, 1992, ANESTH ANALG, V75, P1007
[2]   SYNTHESIS AND RELEASE OF PLATELET-ACTIVATING-FACTOR AND EICOSANOIDS IN HUMAN ENDOTHELIAL-CELLS INDUCED BY DIFFERENT AGONISTS [J].
CABRE, F ;
TOST, D ;
SUESA, N ;
GUTIERREZ, M ;
UCEDO, P ;
MAULEON, D ;
CARGANICO, G .
AGENTS AND ACTIONS, 1993, 38 (3-4) :212-219
[3]   Rate of vasoconstrictor prostanoids released by endothelial cells depends on cyclooxygenase-2 expression and prostaglandin I synthase activity [J].
Camacho, M ;
Löpez-Belmonte, J ;
Vila, L .
CIRCULATION RESEARCH, 1998, 83 (04) :353-365
[4]  
GERRITSEN ME, 1987, FASEB J, V46, P47
[5]  
Goulielmos NV, 1995, CARDIOVASC RES, V30, P788, DOI 10.1016/S0008-6363(95)00118-2
[6]   Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils [J].
Heindl, B ;
Reichle, FM ;
Zahler, S ;
Conzen, PF ;
Becker, BF .
ANESTHESIOLOGY, 1999, 91 (02) :521-530
[7]   Sevoflurane and isoflurane do not enhance the pre- and postischemic eicosanoid production in guinea pig hearts [J].
Heindl, B ;
Becker, BF .
ANESTHESIA AND ANALGESIA, 2000, 90 (01) :17-24
[8]   Volatile anaesthetics reduce adhesion of blood platelets under low-flow conditions in the coronary system of isolated guinea pig hearts [J].
Heindl, B ;
Becker, BF ;
Zahler, S ;
Conzen, PF .
ACTA ANAESTHESIOLOGICA SCANDINAVICA, 1998, 42 (08) :995-1003
[9]   Sevoflurane inhibits human platelet aggregation and thromboxane A(2) formation, possibly by suppression of cyclooxygenase activity [J].
Hirakata, H ;
Ushikubi, F ;
Toda, H ;
Nakamura, K ;
Sai, S ;
Urabe, N ;
Hatano, Y ;
Narumiya, S ;
Mori, K .
ANESTHESIOLOGY, 1996, 85 (06) :1447-1453
[10]  
HOHLFELD T, 1993, J PHARMACOL EXP THER, V264, P397