Effects of isoflurane and propofol on arterial mechanical properties.

Abstract

To the Editor: We read with great interest the recent article by Deryck et al. [1]. The authors state, "the effects of propofol on aortic elastance have not been studied previously." We have comprehensively examined and compared the effects of isoflurane and propofol on left ventricular (LV) afterload, including aortic mechanics, in chronically instrumented dogs [2,3]. The forces opposing LV ejection were quantified with aortic input impedance generated with power spectral analysis and interpreted using a three-element Windkessel model. Total arterial compliance was calculated directly from aortic pressure and blood flow wave forms. Total arterial compliance represents the energy storage component of the arterial system and is determined primarily by the mechanical characteristics of the aorta. We demonstrated that isoflurane and propofol cause dose-related decreases in total arterial resistance, which confirms that these drugs produce arteriolar vasodilation [2,3]. Isoflurane increased total arterial compliance and characteristic aortic impedance [2], effects that were related to decreases in aortic pressure. In contrast, propofol caused large increases in total arterial compliance and altered the relationship between compliance and aortic pressure. The actions of propofol were similar to those observed with sodium nitroprusside but distinctly different from those produced by volatile anesthetics [3,4]. Our results indicate that propofol produces direct actions on aortic mechanical properties that cannot be solely attributed to simultaneous reductions in aortic pressure and blood flow [3]. The present results of Deryck et al. [1] support our previous observations [2,3]. The reductions in LV afterload produced by isoflurane and propofol imply that these anesthetics may preserve or even enhance mechanical coupling between the LV and the arterial vasculature. Dercyk et al. [1] demonstrate that propofol (18 mg [centered dot] kg-1 [centered dot] h-1) reduces the ratio of oscillatory to total hydraulic power. These findings suggest that propofol improves LV mechanical efficiency by decreasing wasted LV energy. However, this beneficial effect may not occur at larger concentration doses. We have recently shown that both isoflurane [5] (>or=to0.9 minimum alveolar anesthetic, end-tidal concentration) and propofol [6] (>or=to50 mg [centered dot] kg-1 [centered dot] h-1) impair LV-arterial coupling and mechanical efficiency as evaluated using LV pressure-volume analysis in barbiturate-anesthetized dogs. Thus, our data indicate that larger concentrations of isoflurane and propofol do not enhance and may adversely affect energy transfer from the LV to the arterial circulation because these drugs cause significant direct negative inotropic effects that are greater in magnitude than the beneficial reductions in afterload. Douglas A. Hettrick, PhD Department of Anesthesiology; Medical College of Wisconsin; Zablocki Veterans Affairs Medical Center; Milwaukee, WI 53226 Paul S. Pagel, MD, PhD Department of Pharmacology and Toxicology; Medical College of Wisconsin; Zablocki Veterans Affairs Medical Center; Milwaukee, WI 53226 David C. Warltier, MD, PhD Department of Medicine; Medical College of Wisconsin; Zablocki Veterans Affairs Medical Center; Milwaukee, WI 53226