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Titolo:
ETOMIDATE AND THIOPENTAL INHIBIT THE RELEASE OF ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR IN THE HUMAN RENAL-ARTERY
Autore:
KESSLER P; LISCHKE V; HECKER M;
Indirizzi:
UNIV GOTTINGEN,CTR PHYSIOL & PATHOPHYSIOL,HUMBOLDTALLEE 23 D-37073 GOTTINGEN GERMANY UNIV GOTTINGEN,CTR ANESTHESIOL & RESUSCITAT D-37073 GOTTINGEN GERMANY UNIV GOTTINGEN,CTR PHYSIOL,DEPT CARDIOVASC D-37073 GOTTINGEN GERMANY
Titolo Testata:
Anesthesiology
fascicolo: 6, volume: 84, anno: 1996,
pagine: 1485 - 1488
SICI:
0003-3022(1996)84:6<1485:EATITR>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
K+;
Keywords:
ANESTHETICS, INTRAVENOUS, ETOMIDATE, THIOPENTAL; ANESTHETICS, GASES, NITRIC OXIDE; ARTERIES, RENAL; HEART, ENDOTHELIUM, ENDOTHELIUM-DEPENDENT RELAXATION, ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR; ENZYMES, CYTOCHROME P450; NEUROTRANSMITTERS, ACETYLCHOLINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
12
Recensione:
Indirizzi per estratti:
Citazione:
P. Kessler et al., "ETOMIDATE AND THIOPENTAL INHIBIT THE RELEASE OF ENDOTHELIUM-DERIVED HYPERPOLARIZING FACTOR IN THE HUMAN RENAL-ARTERY", Anesthesiology, 84(6), 1996, pp. 1485-1488

Abstract

Background: Endothelium-derived hyperpolarizing factor is thought to be a cytochrome P450-derived arachidonic acid metabolite that hyperpolarizes vascular smooth muscle cells by opening Ca2+-activated K+ channels (K-Ca(+) channels), In the rabbit carotid artery both volatile andintravenous anesthetics inhibit the acetylcholine-stimulated release of endothelium-derived hyperpolarizing factor. Because the release of this factor may help to maintain vascular tone in humans under conditions of a failing nitric oxide synthesis, e.g,, in atherosclerosis, theeffects of two intravenous anesthetics, thiopental and etomidate, on the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine were investigated in human isolated renal artery segments, Methods: The segments were suspended in Krebs-Henseleit solution (37 degrees C) containing the cyclooxygenase inhibitor diclofenac(1 mu M) and preconstricted with norepinephrine (6 mu M). Relaxationscaused by acetylcholine (1 mu M) were compared in the presence and absence of the nitric oxide synthase inhibitor N-G-nitro-L-arginine (0.1mM) in control segments and in segments exposed to etomidate or thiopental (0.03-0.3 mM). In addition, the effects of the two anesthetics on the relaxant response to the nitric oxide donors glyceryl trinitrate(3 mu M) and sodium nitroprusside (0.1 mu M) were examined. Results: The relaxant response to acetylcholine, which was resistant to both nitric oxide synthase and cyclooxygenase blockade, was markedly reduced by the K-Ca(+) channel antagonist tetrabutyl ammonium (3 mM) and the cytochrome P450 inhibitor clotrimazole (30 mu M). Both etomidate and thiopental, at a concentration of 0.3 mM, selectively attenuated the relaxant response to acetylcholine in N-G-nitro-L-arginine-treated segments, but did not affect relaxations elicited by glyceryl trinitrate or sodium nitroprusside. Conclusions: Etomidate and thiopental inhibit the endothelium-derived hyperpolarizing factor-mediated relaxant response to acetylcholine in the human renal artery, an effect that appears to be attributable to the cytochrome P450-inhibiting properties of these anesthetics.

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Documento generato il 30/10/20 alle ore 00:54:54