We read with interest the recent review of aortic biomechanics and their clinical applications by Gregory et al.1  The authors should be congratulated for addressing this important but often underappreciated subject. Nevertheless, we are obligated to mention that the authors did not acknowledge or discuss a series of pertinent studies conducted in chronically instrumented dogs describing the effects of anesthetics on aortic biomechanics. This canine model is highly relevant to the review,1  because the cardiovascular effects of anesthetics are virtually identical in dogs and humans. We and others used aortic input impedance spectra in the frequency domain2  that were interpreted with a three-element Windkessel model of the arterial circulation, incorporating aortic mechanical properties,3  to quantify the effects of anesthetics on left ventricular afterload.4–13  We first demonstrated that isoflurane reduces total arterial resistance in a concentration-dependent manner and modestly increases total arterial compliance (primarily determined by the aorta and proximal great vessels14 ), but does not affect characteristic aortic impedance (the resistance of the aorta itself).4  In contrast, the potent vasodilator sodium nitroprusside decreased total arterial resistance and markedly increased total arterial compliance when the drug was administered at infusion rates that resulted in levels of hypotension equivalent to those observed during the administration of isoflurane. The findings with sodium nitroprusside confirmed previous observations in dogs15  and humans.16,17  Taken together, these data indicated that the primary effect of isoflurane on the determinants of left ventricular afterload was related to its well-known actions on arteriolar resistance vessels and not on the aorta itself, whereas sodium nitroprusside altered left ventricular afterload through its effects on both arteriolar vasomotor tone and the mechanical properties of the aorta. Similar findings with isoflurane were also reported in an acutely instrumented open-chest swine model.13  We further showed that desflurane also reduces total arterial resistance but does not substantially affect total arterial compliance and characteristic aortic impedance, actions that were indistinguishable from those of isoflurane.6  However, sevoflurane did not affect total arterial resistance but caused small increases in total arterial compliance and characteristic aortic impedance,6  observations that mirrored those seen with the obsolete volatile anesthetic halothane.4 

Isoflurane increased aortic distensibility (concomitant with reductions in aortic pressure) and did not affect characteristic aortic impedance when these parameters were calculated using simultaneous measurements of aortic diameter, pressure, and blood flow.5  These findings reinforced the conclusion that alterations in the aortic mechanical properties are not responsible for the actions of isoflurane on left ventricular afterload. In contrast to the findings with isoflurane in dogs with normal left ventricular function, this volatile anesthetic did not exert beneficial changes in total arterial resistance, characteristic aortic impedance, and total arterial compliance in a canine model of heart failure with reduced ejection fraction induced by chronic rapid ventricular pacing.7  We conducted additional investigations in normal and cardiomyopathic dogs with the anesthetic noble gas xenon,8  and with the intravenous anesthetics propofol,9,10  etomidate,11  and dexmedetomidine12  that revealed unique insights into the actions of these medications on the contributions of altered aortic mechanics to left ventricular afterload in vivo. These studies document that the impact of anesthetics on aortic biomechanics has been examined previously in clinically relevant animal models, contrary to the article’s assertion.1 

The authors declare no competing interests.

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