To the Editor:—
It is with interest that we read the study by Stowe et al. 1that evaluates the effects of xenon on isolated guinea pig hearts and cation currents in isolated cardiomyocytes. We agree fully with the authors that xenon anesthesia may be beneficial for patients with cardiac disease who cannot tolerate the depressant effects of commonly used gas anesthetics. However, we would like to express our concerns regarding two points of the methods used in this study. First, in the current work, the halothane and sevoflurane concentrations are measured, but, for xenon, the authors’ description informs us that “after vigorous shaking (the gas mixture and the bath solution) for several minutes to facilitate equilibration, oxygen partial pressure was verified to be near 150 mmHg at one atmosphere.”1They seem to conclude that after determination of the oxygen partial pressure, the rest, i.e. , 610 mmHg at one atmosphere, must be xenon. However, if one tries to show that xenon does not alter cardiac functions, it seems prudent to determine the xenon concentration in the chamber and in the erythrocyte–Krebs–Ringer’s solution. Otherwise, it cannot be excluded that, in the current study, an alteration of cardiac functions could not be shown because a full equilibration of xenon gas mixture with the perfusion medium was not reached during the experiment.
A second minor issue is the isolated heart preparation; the Langendorff heart procedure, perfused with crystalloid buffer and gassed with carbogen (i.e. , 95% O2and 5% CO2), is certainly a commonly accepted experimental setting. 2Replacing the carbogen with 20% O2and 80% N2for equilibration of the cristalloid buffer yields an established model for hypoxia in isolated hearts. 3In the blood-perfused Langendorff model, the isolated heart usually is perfused with blood from an anesthetized support animal, i.e. , with blood at physiologic hemoglobin and hematocrit concentrations. 4,5The experimental setting used in the presented work with crystalloid buffer supplemented with erythrocytes at a concentration of 2.8 g hemoglobin/100 ml equilibrated with an oxygen fraction of 0.2 is not widely used, as far as we know. Although we estimate a sufficient oxygen supply from venous oxygen tension and calculation of the oxygen capacity, the systolic left ventricle pressure is lower than expected for a guinea pig Langendorff model. Possible reasons for this observation are a general lack of oxygen or an inhomogenous perfusion of the myocardium. The authors discuss low calcium as a cause for the low left ventricle pressure; nevertheless, hypoxia should have been excluded. Determination of venous lactate or establishment of an additional control group perfused with the erythrocyte–Krebs–Ringer’s solution and equilibrated with carbogen would have been easy to realize and very convincing.
Because of the general interest in this subject, we would appreciate any further information the authors could provide.