Prevention of adhesion formation in a laparoscopic mouse model should combine local treatment with peritoneal cavity conditioning†

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Adhesion formation results from a series of local events at the trauma site. This process can be enhanced by factors derived from the peritoneal cavity such as mesothelial cell hypoxia (pneumoperitoneum with pure CO2), reactive oxygen species (pneumoperitoneum with more than 4% oxygen), desiccation and mesothelial trauma produced through manipulation. Adhesion prevention, therefore, should combine local treatment while minimizing adverse peritoneal factors through conditioning of the pneumoperitoneum.


In a laparoscopic mouse model, adhesion induction comprised a mechanical lesion together with a humidified pneumoperitoneum for 60 min with pure CO2 at 37°C. Adhesion prevention consisted of a combination of treatments known to reduce adhesions, i.e. pneumoperitoneum with CO2 with the addition of 3–4% O2, reduction of body temperature (BT) to 32°C and application of antiadhesion products such as anti-inflammatory drugs (dexamethasone, nimesulide), calcium-channel blockers (diltiem), surfactants (phospholipids), barriers (Hyalobarrier gel), reactive oxygen species scavengers (superoxide dismutase and ascorbic acid) and recombinant plasminogen activator.


The addition of 3% O2 to the pneumoperitoneum or a lower BT decreased adhesions by 32% or 48%, respectively (P < 0.05, Wilcoxon), but were without additional effects when combined. In addition, if dexamethasone or Hyalobarrier® gel were administrated, the total reduction was 76% (P=0.04) or 85% (P < 0.02), respectively.


Combining pneumoperitoneum conditioning together with dexamethasone or a barrier resulted in significant adhesion reduction in a laparoscopic mouse model.

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