Influence of ischemic preconditioning on blood coagulation, fibrinolytic activity and pancreatic repair in the course of caerulein-induced acute pancreatitis in rats.
Previous studies have shown that ischemic preconditioning protects several organs, including the pancreas, from ischemia/reperfusion-induced injury. The aim of the investigation was to determine whether ischemic preconditioning affects the course edematous pancreatitis.


METHODS
In rats, ischemic preconditioning was performed by short-term clamping the celiac artery. Acute pancreatitis was induced by caerulein. The severity of acute pancreatitis was evaluated between the first and tenth day of inflammation.


RESULTS
Ischemic preconditioning applied alone caused a mild pancreatic damage. Combination of ischemic preconditioning with caerulein attenuated the severity of pancreatitis in histological examination and reduced the pancreatitis-evoked increase in plasma lipase and pro-inflammatory interleukin-1beta. This effect was associated with an increase in plasma level of anti-inflammatory interleukin-10 and partial reversion of the pancreatitis-evoked drop in pancreatic DNA synthesis and pancreatic blood flow. In secretory studies, ischemic preconditioning in combination with induction of acute pancreatitis attenuated the pancreatitis-evoked decrease in secretory reactivity of isolated pancreatic acini to stimulation by caerulein. In the initial period of acute pancreatitis, ischemic preconditioning alone and in combination with caerulein-induced acute pancreatitis prolonged the activated partial thromboplastin time (APTT), increased plasma level of D-dimer and shortened the euglobulin clot lysis time. The protective effect of ischemic preconditioning was observed during entire time of experiment and led to acceleration of pancreatic regeneration.


CONCLUSIONS
Ischemic preconditioning reduces the severity of caerulein-induced pancreatitis and accelerates pancreatic repair; and this effect is related to the activation of fibrinolysis and reduction of inflammatory process.
Warzecha
Z
Z
Department of Physiology, Jagiellonian University Medical College, Krakow, Poland.
Dembiński
A
A
Ceranowicz
P
P
Dembiński
M
M
Cieszkowski
J
J
Kuśnierz-Cabala
B
B
Naskalski
J W
JW
Jaworek
J
J
Konturek
S J
SJ
Pawlik
W W
WW
Tomaszewska
R
R
D000208:Acute Disease; D000681:Amylases / Q000378:metabolism; D000818:Animals; D001777:Blood Coagulation; D002108:Ceruletide / Q000633:toxicity*; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis; D016753:Interleukin-10 / Q000097:blood; D019194:Ischemic Preconditioning; D008297:Male; D010179:Pancreas / Q000473:pathology; D010195:Pancreatitis / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar
D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D016753:Interleukin-10; D002108:Ceruletide; D000681:Amylases