The role of poly (ADP ribose) synthetase inhibition in endotoxin-induced diaphragmatic dysfunction Endotoksinin i̇ndüklediǧi diyafragma fonksiyon bozukluǧunda poli (ADP-riboz) sentaz i̇nhibisyonunun rolü


Cinel I., Koçak Z., Tamer L., CİNEL Z. L., Altunkan A., Atici Ş., ...Daha Fazla

Turk Anesteziyoloji ve Reanimasyon, cilt.30, sa.5, ss.198-202, 2002 (Scopus) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 30 Sayı: 5
  • Basım Tarihi: 2002
  • Dergi Adı: Turk Anesteziyoloji ve Reanimasyon
  • Derginin Tarandığı İndeksler: Scopus
  • Sayfa Sayıları: ss.198-202
  • Anahtar Kelimeler: 3-aminobenzamide, Diaphragm, Endotoxemia, Lipid peroxidation
  • Marmara Üniversitesi Adresli: Evet

Özet

In our experimental study, effects of poly (ADP-ribose) synthetase (PARS) inhibition on diaphragm Ca++-ATPase, malondialdehyde (MDA) levels and histopathology in LPS-induced sepsis are investigated. 24 male Wistar rats, weighing 180-200 g were randomly divided into 4 groups. The first group (control; n=6) received saline and II. group (sepsis; n=6) received 10mg/kg LPS intraperitoneally. As a PARS inhibitor; 3-Aminobenzamide (3-AB) was given to the IV. group (S+3-AB, n=6) 20 minutes before giving LPS and to the III. group (C+3-AB, n=6) 20 minutes before giving saline. Six hours later, under Ketamin/Xylasine anaesthesia diapraghmatic specimens were obtained and the rats were decapitated. Tissue MDA levels and Ca++-ATPase activity were measured and diaphragmatic specimens were stained with hematoxylin-eosin for histopathologic assesment. Tissue Ca++-ATPase levels were found to be decreased (548±14 vs 215±22 nmol.Pi/mg.protein/hr) and tissue MDA levels were found to be increased (4.2±0.1 vs 11.7±0.4) in endotoxemic group(p=0.01). In the S+ 3-AB group, 3-AB pretreatment attenuated the increase in MDA formation and Ca++-ATPase levels were similar to those in control group (p=0.01). Except minimal edema, no difference, was seen in diaphragm histopathology among the groups. PARS inhibition with 3-AB prevents not only lipid peroxidation but also biochemical changes concerning Ca++-ATPase in endotoxemia.