title: The role of adenosine A2a receptors in experimental acute pancreatitis.
abstract: OBJECTIVE
  The role of adenosine and its receptors in acute pancreatitis remains unelucidated. The aim was to evaluate the effects of the adenosine A2a receptor agonist and antagonist in the severe, taurocholate-induced experimental acute pancreatitis (EAP).
  
  
  METHODS
  The experiments were performed on 80 male Wistar rats, subdivided into 4 groups: C--the control rats, I--the EAP group, IIA--EAP group treated with the A2a adenosine receptor agonist CGS 21680, IIB--EAP group treated with the A2a adenosine receptor antagonist ZM 241385. The blood for alpha-amylase and lipase and tissues samples for the morphological examinations and immunohistochemistry for A2a receptors were collected in 2, 6, 24 hours of the experiment.
  
  
  RESULTS
  The serum alpha-amylase tended to decrease in the group IIA as compared to EAP untreated after 6 and 24 h. No significant effect of both treatments on serum lipase was noted. The administration of CGS 21680 resulted in favorable decrease of the inflammatory cell infiltration, hemorrhagic changes, necrosis and vacuolization of acinar cells, without an evident effect on the edema of the interstitial tissue. The administration of ZM 241385 did not affect the scores of necro-hemorrhagic changes and inflammatory infiltration, whereas it decreased the scores of vacuolization and edema. In all groups the expression of A2a receptors was similar.
  
  
  CONCLUSIONS
  Our findings suggest, that A2a adenosine receptors are involved in the course of sodium taurocholate EAP. It is probable that the modulation of some subgroups of adenosine receptors could alleviate the course of severe experimental AP.
authors.affiliation: Department of Gastroenterology, Medical University, Lublin ul. Solarza 16, 20-815 Lublin, Poland. celinski@mp.pl
authors.forename: K
authors.initials: K
authors.lastname: Celiński
authors.forename: B
authors.initials: B
authors.lastname: Prozorow-Król
authors.forename: A
authors.initials: A
authors.lastname: Korolczuk
authors.forename: M
authors.initials: M
authors.lastname: Słomka
authors.forename: E
authors.initials: E
authors.lastname: Korobowicz
authors.forename: W
authors.initials: W
authors.lastname: Biskup
authors.forename: A
authors.initials: A
authors.lastname: Madro
authors.forename: H
authors.initials: H
authors.lastname: Cichoz-Lach
authors.forename: G
authors.initials: G
authors.lastname: Czechowska
mesh_terms: D000208:Acute Disease; D000241:Adenosine / Q000031:analogs & derivatives / Q000494:pharmacology; D058908:Adenosine A2 Receptor Agonists; D058917:Adenosine A2 Receptor Antagonists; D000681:Amylases / Q000097:blood / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D008049:Lipase / Q000097:blood / Q000378:metabolism; D008297:Male; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D010627:Phenethylamines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D043705:Receptor, Adenosine A2A / Q000502:physiology; D013656:Taurocholic Acid / Q000633:toxicity; D014227:Triazines / Q000494:pharmacology; D014230:Triazoles / Q000494:pharmacology
chemical_list: D058908:Adenosine A2 Receptor Agonists; D058917:Adenosine A2 Receptor Antagonists; D010627:Phenethylamines; D043705:Receptor, Adenosine A2A; D014227:Triazines; D014230:Triazoles; C097270:ZM 241385; C061282:2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine; D013656:Taurocholic Acid; D008049:Lipase; D000681:Amylases; D000241:Adenosine