Effects of Isoflurane and Propofol on Arterial Mechanical Properties

Abstract

In Response: Hettrick and collegues are correct that we should have quoted their study published in 1995 [1], which somehow escaped our attention when finishing the first version of our article. Their subsequent studies on isoflurane and propofol were published when our article was in the process of revision and printing [2,3]. This being said, there are methodological differences between their studies and ours. To assess aortic input impedance, we measured pressure in the aortic root and used a micromanometer-tipped catheter to record the "true" pressure wave [4]. Hettrick et al. measured pressure in the descending aorta using a fluid-filled catheter and thus had to correct the signal mathematically to reconstruct the pressure wave of the proximal aorta [1,2]. The procedure implies assumptions on aortic mechanical properties, assumptions that may be incorrect because these properties were shown to be affected by the drugs being tested. We presented our results as complete impedance spectra. They interpreted their results using a Windkessel model, which is widely used but is limited mainly by not taking wave reflexions into account [5]. We investigated isoflurane and propofol in the same animals at the single equipotent dose of 1 minimum alveolar anesthetic concentration (MAC) and 18 mg [centered dot] kg-1 [centered dot] h-1, respectively. Compared with isoflurane, propofol yielded higher aortic pressure and compliance, lower elastance and oscillatory work, and better ventriculoarterial coupling. At doses of 1.25 MAC and 25 mg [centered dot] kg-1 [centered dot] hr-1, respectively, but in separate dogs, Hettrick and colleagues only reported a decreased resistance with isoflurane. At doses of 1.75 MAC and 50 mg [centered dot] kg-1 [centered dot] hr-1, respectively, isoflurane further decreased resistance and propofol increased compliance. Propofol also increased characteristic impedance due to low aortic pressure. These results are in agreement with ours but were only obtained at higher doses, maybe because of the methodological differences. Isoflurane deteriorated ventriculo-arterial coupling at low doses (0.9 MAC) and propofol only at large doses (>or=to50 mg [centered dot] kg-1 [centered dot] hr-1), which confirms our conclusions that propofol better preserves ventriculo-arterial matching at clinically relevant equipotent doses. All these studies thus are consistent, and complementary in that Hettrick and colleagues investigated several doses in different animals whereas we compared single but equipotent doses in the same animals. We hope that the present discussion will further stimulate the use of methods that take into account the pulsatility of the circulation for investigations on the cardiovascular effects of anesthetic agents. S. Brimioulle, MD, PhD Y. Deryck, MD R. Naeije, MD, PhD Laboratory of Cardiorespiratory Physiology; Free University of Brussels; Brussels, Belgium, B-1070