In Reply:-We would like to thank Mann et al. 
for their valuable comment on our publication. Indeed, in pigs, lysine vasopressin is known as the natural antidiuretic hormone. Because a radioimmunoassay for lysine vasopressin is now available, further studies in pigs should use this specific test. This is an important progress in pig experiments. However, even with a more-specific radioimmunoassay, vasopressin levels remain difficult to analyze. This is demonstrated by the Mann et al. 
data. The "marked changes" assessed with the lysine vasopressin radioimmunoassay showed a maximum 2.2-fold increase when compared to baseline values, whereas the "quite stable" levels assessed with the arginine vasopressin radioimmunoassay revealed increases up to four times the baseline values. 
At the time when the experiments were performed (1994), there was no test available for lysine vasopressin in our laboratory. Thus, we used an arginine vasopressin radioimmunoassay with a cross-reactivity for lysine vasopressin of 4-10% (Hermann Bierman GmbH, Bad Nauheim, Germany). Knowing all the problems related to this procedure, we stated in our manuscript that only relative changes were analyzed during the course of the study. In our opinion, this is acceptable because the aim of the study was to clarify the vasodilatory properties of intraabdominally insufflated carbon dioxide on splanchnic arteries. Therefore, we compared insufflation of air with carbon dioxide. For this purpose the interaction term gas x intraabdominal pressure (IAP) of a two-way repeated measurements analysis of variance was used for statistical analysis. With respect to all investigated IAP levels from 0 mmHg to 24 mmHg, insufflation of carbon dioxide resulted in a significantly different pattern (P < 0.05) of all measured vasoactive hormones, including vasopressin. At the clinically, mostly recommended IAP of 12 mmHg, however, insufflation of carbon dioxide resulted in no significantly different pattern of vasopressin, but also no significant changes in central venous pressure, systemic vascular resistance, epinephrine, and norepinephrine plasma levels were seen. 
When Mann et al. 
cited their relevant changes in vasopressin levels in their investigations, presentation of the ventricular filling parameters are the most important for a correct interpretation. Le Roith et al. 
demonstrated in dogs that the vasopressin release during elevated IAP is related to decreases in cardiac output caused by volume depletion and can therefore be prevented by previous volume loading.
Reduction of preload results in a decrease of atrial natriuretic peptide levels 
and stimulates vasopressin release. 
Cyclic guanosine monophosphate is second messenger and specific marker of the atrium natriuretic peptide. 
In our study, however, fluid resuscitation was quite effective. Because inferior vena cava blood flow 
and transmural right and left ventricular filling pressures (Table 1
) were unchanged at IAP = 12 mmHg, cyclic guanosine monophosphate also remained constant (Table 1
). A vasopressin release is therefore most unlikely in our investigation, in other investigations, and in clinical practice with an adequate volume therapy.
Manfred Blobner, M.D.
Associate Professor of Anesthesiology
Ralph Bogdanski, M.D.
Resident in Anesthesia
Eberhard Kochs, M.D.
Professor of Anesthesiology; Chairman; Institut fur Anaesthesiologie; Technische Universitat Munchen; Klinikum rechts der Isar; Munich, Germany; email@example.com
(Accepted for publication February 1, 1999.)
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© 1999 American Society of Anesthesiologists, Inc.