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The aim of this study was to quantitatively define the development of post surgical adhesions (PSAs) in a well characterized experimental model and identify possible windows of pathogenesis where pharmaceutical intervention may be most effective. PSAs were induced, in an established rabbit uterine horn model, using standardized reproducible injury, in 17 experimental groups, each with 8 experimental sites and these PSAs were sampled from 30 seconds to 42 days post surgery. Using design based, unbiased stereology, mean volumes of PSAs and associated tissue damage and reaction per experimental site were calculated for each sample time point. PSA development followed the normal pattern of wound healing with surrounding adjacent tissue having a profound influence and interaction. There was a direct relationship between volume of damage (initial and subsequent) and the volume of injury tissue generated. In vivo weak fibrinous PSAs were present from 10 min following injury, with tenacious fibrinous PSAs present from 1 h and onwards. PSA development can be classified into two distinct stages: (i) PSA modelling - occurring during the first 16 h, in which maximum rate of PSA construction is achieved; and (ii) PSA remodelling - from 16 h onwards. Considering this, PSA prevention should ideally be initiated immediately post injury to prevent PSA modelling or, alternatively, during PSA modelling. |
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