Selective matrix metalloproteinase inhibition increases breaking strength and reduces anastomotic leakage in experimentally obstructed colon

Selective matrix metalloproteinase inhibition increases breaking strength and reduces anastomotic... Purpose Colonic obstruction causes loss of collagen and im- AZD3342 but decreased by 25% (P = 0.023) in the vehicle pairment of anastomotic integrity by matrix metalloprotein- group. The anastomotic breaking strength of AZD3342- ases (MMPs). Unexpectedly, pharmacological MMP inhibi- treated rats was 44% higher (P = 0.008) than the vehicle- tion increased anastomotic leakage (AL) in obstructed colon treated rats. Furthermore, the AL rate was reduced possibly due to the non-selective nature of these compounds (P = 0.037) with AZD3342 compared with vehicle treatment. and the experimental model applied. We therefore studied the AZD3342 treatment influenced neither the total or insoluble effects of selective MMP inhibition on the healing of anasto- collagen concentrations nor the degree of fragmentation of the moses in colon obstructed by a novel laparoscopic technique. soluble collagen triple helices. Methods Left colonwas obstructedin38maleSprague- Conclusion Selective MMP inhibition increased anastomotic Dawley rats (226–284 g). After 12 h, stenoses were resected breaking strength and reduced AL after resection of colonic and end-to-end anastomoses constructed. Baseline breaking obstruction. strength was determined in 6 animals on day 0. The remaining . . 32 rats were randomized to daily treatment with the selective Keywords Anastomosis Anastomotic leak Breaking . http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Journal of Colorectal Disease Springer Journals

Selective matrix metalloproteinase inhibition increases breaking strength and reduces anastomotic leakage in experimentally obstructed colon

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag GmbH Germany
Subject
Medicine & Public Health; Surgery; Internal Medicine; Gastroenterology; Hepatology; Proctology
ISSN
0179-1958
eISSN
1432-1262
D.O.I.
10.1007/s00384-017-2857-x
Publisher site
See Article on Publisher Site

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