Elsevier

Fertility and Sterility

Volume 82, Supplement 3, October 2004, Pages 1149-1153
Fertility and Sterility

Role of vascular endothelial growth factor receptor 1 in basal adhesion formation and in carbon dioxide pneumoperitoneum-enhanced adhesion formation after laparoscopic surgery in mice

Presented partially at the 6th International Symposium on Peritoneum, which was held in Amsterdam, The Netherlands, on April 10–12, 2003, and was awarded with the “Best Paper Prize.”
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Objective

To evaluate the role of vascular endothelial growth factor receptor-1 (VEGFR-1) in adhesion formation after laparoscopic surgery.

Design

Prospective, randomized study.

Setting

Academic research center.

Animal(s)

Forty female Swiss mice.

Intervention(s)

Adhesions were induced by standardized lesions during laparoscopy. The CO2 pneumoperitoneum was maintained for the minimum time needed to perform the lesions (10 minutes) or for a longer period (60 minutes) to evaluate basal adhesions and pneumoperitoneum-enhanced adhesions, respectively. Mice were treated either with IgG or with antibodies against VEGFR-1.

Main outcome measurement(s)

Adhesions were quantitatively and qualitatively scored after 7 days during laparotomy.

Result(s)

In IgG-treated mice, 60 minutes of CO2 pneumoperitoneum increased basal adhesions. In VEGFR-1 antibody-treated mice, basal adhesions were similar to the control group and 60 minutes of CO2 pneumoperitoneum did not increase adhesions. Therefore, in these mice, pneumoperitoneum-enhanced adhesions were lower than in IgG-treated mice.

Conclusion(s)

The data confirm that CO2 pneumoperitoneum is a cofactor in adhesion formation and demonstrate that VEGFR-1 plays a role in pneumoperitoneum-enhanced adhesions, which is consistent with a role of placental growth factor, VEGF-A, and VEGF-B in pneumoperitoneum-enhanced adhesions. These observations give new insight into the pathogenesis of adhesion formation.

Key words

Adhesion formation
laparoscopy
CO2 pneumoperitoneum
VEGF-A
VEGF-B
PlGF
VEGFR-1
mice

Cited by (0)

Partially supported by Karl Storz Endoscopy (Tuttlingen, Germany), the Fonds Wetenschappelijk Onderzoek, Brussels, Belgium, grant no. G.0324.01, and Onderzoeks Toelagen Katholieke Universiteit Leuven, Leuven, Belgium, grant no. TBA/00/27.