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The vascular relaxing effects of sevoflurane and isoflurane are more important in hypertensive than in normotensive rats

[Les effets vasculaires décontractants du sévoflurane et de l’isoflurane sont plus importants chez les rats hypertendus comparés aux normotendus]

Jingui Yu, MD^*, Koji Ogawa, MD, Yasuyuki Tokinaga, MD^*, Shizue Iwahashi, MD^* and Yoshio Hatano, MD^*

^* From the Department of Anesthesiology, and
the Surgical Operating Center, Wakayama Medical University, Wakayama City, Japan.

Address correspondence to: Dr. Yoshio Hatano, Department of Anesthesiology, Wakayama Medical University, 811 – 1 Kimiidera, Wakayama City 641–0012, Japan. Phone: 81-73-441-0610; Fax: 81-73-447-0051; E-mail: yhatano{at}wakayama-med.ac.jp

Purpose: The vascular response to anesthetics is altered in hypertensive patients since the functional and structural integrities of vascular smooth muscle and endothelium are deranged. The effects of anesthetics on angiotensin II (Ang II)-induced changes in vascular tone are not well understood. We investigated the effects of sevoflurane and isoflurane on Ang II-induced vasoconstriction in spontaneously hypertensive rats (SHR).

Methods: The dose-dependent effects of sevoflurane and isoflurane on the Ang II-induced contraction of aortic rings, in the presence and absence of an intact endothelium, were investigated in normotensive Wistar-Kyoto rats (WKY) and SHR and compared using isometric force transducers.

Results: Ang II (10^–9–10^–6 M) induced a similar transient phasic contraction of endothelium-intact rings from the two rat strains in a dose-dependent manner. Removal of the endothelium augmented the Ang II-elicited phasic contraction, to a greater extent in the SHR group than in the WKY group. Sevoflurane and isoflurane (1–3 minimum alveolar concentration) concentration-dependently inhibited the Ang II-induced contraction of endothelium-intact rings from WKY; an effect that was greatly enhanced following removal of the endothelium. A greater degree of attenuation of the Ang II-induced contraction of both endothelium-intact and -denuded rings by the two anesthetics was observed in the SHR group. The inhibitory effects of isoflurane on the Ang II-induced contraction of aortic rings from both strains appeared to be stronger than that of sevoflurane at equipotent concentrations.

Conclusion: Our finding that the inhibitory effects of isoflurane and sevoflurane on Ang II-induced vasoconstriction are enhanced in SHR may, at least in part, account for the anesthesia-induced systemic hypotension frequently seen in hypertensive patients.

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