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  • Title: Isoflurane and halothane produce similar alterations in aortic distensibility and characteristic aortic impedance.
    Author: Hettrick DA, Pagel PS, Warltier DC.
    Journal: Anesth Analg; 1996 Dec; 83(6):1166-72. PubMed ID: 8942580.
    Abstract:
    The effects of volatile anesthetics on arterial mechanical properties in vivo are incompletely understood. The present investigation tested the hypothesis that isoflurane and halothane cause differential actions on the mechanical characteristics of the aorta in barbiturate-anesthetized dogs instrumented for measurement of aortic blood pressure, blood flow, and diameter. Aortic distensibility and characteristic aortic impedance were calculated from aortic diameter measurements. Oscillatory (Wo) and mean (Wm) hydraulic power were determined from aortic pressure and blood flow waveforms. Hemodynamics and aortic pressure, blood flow, and diameter were recorded before, during, and after 0.5, 0.75, and 1.0 minimum alveolar anesthetic concentration (MAC) (end-tidal) isoflurane (n = 7), or halothane (n = 8). Isoflurane and halothane caused significant (P < 0.05) and dose-related decreases in heart rate, mean arterial pressure, peak and end-diastolic aortic diameters, and aortic distensibility (e.g., from 0.16% +/- 0.03% during control to 0.24% +/- 0.04% mm Hg during 1.0 MAC isoflurane). Characteristic aortic impedance remained unchanged by either drug. In contrast to the findings with isoflurane, halothane increased the ratio of Wo to Wm (from 6.7 +/- 1.1 during control to 11.3 +/- 3.1 x 10(-2) during 1.0 MAC), suggesting that this drug decreases left ventricular mechanical efficiency. The results indicate that isoflurane and halothane do not alter characteristic aortic impedance and produce similar increases in aortic distensibility concomitant with reductions in aortic pressure. These findings support the contention that volatile anesthetic-induced alterations in aortic mechanical properties do not contribute to the differential effects of these drugs on left ventricular afterload in vivo.
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