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Department of Anaesthesiology, Osaka Medical College, Takatsuki, Osaka, Japan
To the Editor:
We have taken a keen interest in the discussion into the validity of the second gas effect since Sun et al. (1) published their findings and the subsequent rebuke by Taheri and Eger II (2) was published. When referring to the original data presented by Epstein et al. (3), unfortunately, no statistical significant difference can be observed over time in the ratio of alveolar (end-tidal) concentration and inspired concentration (FA/FI) between administering 0.5% halothane with 70% N2O and 0.5% halothane with 10% N2O by means of two-way repeated-measures analysis of variance (n = 5, P = 0.5877, Stat View version 5.0; SAS Institute, Cary, NC) at a statistical significance of P < 0.05. Quite to the contrary, the concentration effect is in fact validated by the same method. When comparing the two groups using a paired Student’s t-test, the 70% N2O should first be administered for 1 min before a sample is taken. The 10% N2O can then be administered for 1 min in the same dog, but only after the 70% N2O has been flushed out. For 2-min measurements, different dogs should be used. With Wilcoxon’s signed-ranks test if n 
6, P values of approximately 0.04 at <5% probability were recorded at 2, 3, and 4 min (Table 1).
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References
Respiratory and Critical Care Physiology and Medicine, Department of Anesthesiology, Harbor-University of California Los Angeles Medical Center, Research and Education Institute, Torrance, CA
In Response:
We commend Drs. Uda et al. for their statistical re-analysis of the so-called "second gas effect" data (1) and appreciate the opportunity to comment on the theoretical aspects of this concept.
From a practical viewpoint, we (2) and others (3) have been unable to demonstrate the "second gas effect" that Taheri and Eger (4) found. Their differences in mean arterial pressure (MAP) (86 ± 15 mm Hg versus 76 ± 8 mm Hg) and heart rate (HR) (69 ± 16 bpm versus 76 ± 16 bpm) and broad range of PETCO2 (33–37 mm Hg) suggest that differences in cardiac output and alveolar ventilation ( 
A) (5), may explain their differences in the ratio of alveolar (end-tidal) concentration (FA) to inspired concentration (FI) (FA/FI) (4). Contrariwise, when we maintained a constant A with stable MAP and HR, we found no significant differences in either arterial blood concentration or FA/FI of the second gas with or without 80% N2O (2).
From a theoretical viewpoint, to analyze the "second gas effect," we conclude that a reasonable uptake of 200–400 mL/min in the early period of N2O anesthesia (unpublished data) (2,3,6,7) rather than value as a high as 1400–1500 mL/min (8,9) should be used.
Second, breath-by-breath analysis of "concentrating effect" (8) (with this reasonable N2O uptake and considering changes of O2 and CO2, and assuming the second gas zero uptake) (5,10) shows an increase of only relative 1.7% (absolute 0.01% in FA) in FA and FA/FI of the second gas. In fact, considering the uptake of the second gas minimizes any potential increase in FA and FA/FI.
Third, differences between inspired and expired gases in temperature and water vapor content would diminish the differences between inspired and expired volume (the theoretical basis for the "augmentation effect").
Fourth, "concentration effect" (11) is different from "concentrating effect" and is not an explanation of "second gas effect." Its mechanism is complex and will be discussed separately, but it can not be explained by either "concentrating effect" and/or "augmentation effect."
References
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