EFFECT OF EXPERIMENTAL PERITONITIS AND ISCHEMIA ON PERITONEAL FIBRINOLYTIC-ACTIVITY

Citation
Mn. Vipond et al., EFFECT OF EXPERIMENTAL PERITONITIS AND ISCHEMIA ON PERITONEAL FIBRINOLYTIC-ACTIVITY, The European journal of surgery, 160(9), 1994, pp. 471-477
Citations number
19
Categorie Soggetti
Surgery
ISSN journal
11024151
Volume
160
Issue
9
Year of publication
1994
Pages
471 - 477
Database
ISI
SICI code
1102-4151(1994)160:9<471:EOEPAI>2.0.ZU;2-6
Abstract
Objective: Measurement of the fibrinolytic response of the peritoneum to experimental peritonitis and ischaemia. Design: Controlled study Se tting: Academic surgical unit, UK Material: Male Wistar rats Intervent ions. Peritoneal injuries were caused in four groups of male Wistar ra ts (n = 35 in each group): (1) control group (''open and close'' lapar otomy); (2) bacterial peritonitis (mixed faecal flora); (3) chemical p eritonitis (10 mg/ml tetracycline) and; (4) ischaemic peritoneum (liga ted peritoneal buttons). Peritoneal biopsy specimens were taken from f ive animals in each group at seven time intervals and plasminogen acti vating activity (PAA) measured by fibrin plate assay. Results: Compare d with the control group the three peritoneal injuries produced a unif orm reduction in PAA during the first 6 and 12 hours: at 6 hours the m edian PAA was 0.029 IU/cm(2) for bacterial peritonitis, 0.021 IU/cm(2) for chemical peritonitis, and 0.05 IU/cm(2) for ischaemic peritoneum compared with 0.112 IU/cm(2) for the control group; p < 0.001, ANOVA. At 12 hours the median PAA was 0.024 IU/cm(2) for bacterial peritoniti s, less than or equal to 0.014 IU/cm(2) for chemical peritonitis, and 0.05 IU/cm(2) for ischaemic peritoneum compared with 0.112 IU/cm(2) fo r the control group; p < 0.001, ANOVA. There then followed a rebound p eak in all groups, maximal at 4-7 days, before a return to baseline va lues at two weeks. Conclusion: Peritoneal fibrinolysis was appreciably inhibited after three different standardised peritoneal injuries. The data support the hypothesis that there is a single pathophysiological mechanism of adhesion formation.