Background: Previous work has demonstrated that cell-mediated immune f
unction is better preserved in rodents after laparoscopic than open su
rgery. The cause of this laparotomy-related immunosuppression is uncle
ar. Some investigators have attributed it to the length of the incisio
n; others, to peritoneal air exposure. It has also been shown that tum
ors in mice are more easily established and grow larger after sham lap
arotomy than after pneumoperitoneum. Lastly, the differences in tumor
growth have been shown to be, at least in part, attributable to the im
munosuppression that occurs after laparotomy. The purpose of this stud
y was to determine if air pneumoperitoneum, presumably via immunosuppr
ession related to peritoneal air exposure, is associated with increase
d tumor growth in the postoperative period. Methods: A total of 150 im
munocompetent syngeneic mice received high-dose intradermal injections
of mouse mammary carcinoma tumor cells. They were then randomized to
undergo one of the following procedures: (a) anesthesia alone, (b) air
insufflation (4-6 mm Hg), (c) CO2 insufflation, or (d) full laparotom
y. No intraabdominal procedure was carried out. All procedures were 20
min long. After 12 days, the animals were killed and the mean tumor m
ass determined for each group. Results: All animals grew tumors. There
was no significant difference in the mean tumor size of the anesthesi
a control, CO2 insufflation, and air insufflation groups (p > 0.85 by
ANOVA). However, the laparotomy group tumors were 1.5 times as large a
s those of the other three groups (p < 0.05 by ANOVA). Conclusions: In
this model, air insufflation did not significantly affect postoperati
ve tumor growth, nor did CO2 pneumoperitoneum. However, full laparotom
y was associated with increased tumor growth.