The basis for the current investigation is a previous clinical study by the same authors in which they observed a rise in plasma catecholamine concentrations after the establishment of pneumoperitoneum at 15 mm Hg.1 The authors are to be commended for their efforts to better characterize this phenomenon using an animal model, but the experimental design ultimately limits the usefulness of the conclusions. The short time spent at each pressure gives little time for equilibration, and the technique of stepping up from 10 mm Hg to 20 mm Hg after a 5-minute interval does not simulate clinical practice. The authors neglect to mention the very fine work of Ho and colleagues,2 also in a porcine model, which demonstrated significant transperitoneal carbon dioxide absorption, with associated increases in systemic and pulmonary vascular resistance, when measured over 1 hour's time at 15 mm Hg. We are left to wonder why Mikami et al did not include measurements at 15 mm Hg, because this is the commonly used upper limit in the clinical setting (and the pressure at which their original clinical observations were made). The experiments resulted in a number of statistically significant differences, but are they clinically relevant? For example, in the subset most similar to the clinical scenario, the supine group undergoing carbon dioxide pneumoperitoneum, there is no significant difference in mean arterial pressure when comparing the baseline group with the group with an intra-abdominal pressure of 20 mm Hg. There is also no significant change in cardiac output or systemic vascular resistance when the baseline group and the group with an intra-abdominal pressure of 20 mm Hg are compared. This study provides an interesting insight into the acute catecholamine response to increases in abdominal compartment pressure. However, it has left some fundamental questions unanswered about the clinical importance of this phenomenon.