Preventive effects of propofol and ketamine on renal injury in unilateral ureteral obstruction


DİKMEN B., Yagmurdur H., Akgul T., ASTARCI H. M., Ustun H., Germiyanoglu C.

JOURNAL OF ANESTHESIA, cilt.24, sa.1, ss.73-80, 2010 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 24 Sayı: 1
  • Basım Tarihi: 2010
  • Doi Numarası: 10.1007/s00540-009-0861-1
  • Dergi Adı: JOURNAL OF ANESTHESIA
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.73-80
  • Gazi Üniversitesi Adresli: Hayır

Özet

The aim of the present study was to investigate the preventive effects of propofol and ketamine as anesthetics on renal injury in unilateral ureteral obstruction (UO). Twenty-four male New Zealand white rabbits were randomly assigned to four groups of six rabbits each. Anesthesia was induced and maintained with propofol in groups 1 and 2 and with ketamine in groups 3 and 4. Groups 2 and 4 received complete left ureteral ligation. Groups 1 and 3 (control groups) underwent an identical surgical procedure without ureteral ligation. At 14 days of obstruction, animals were sacrificed and ipsilateral kidneys were removed for determination of tissue nitric oxide (NO) levels and immunohistochemical evaluation of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and apoptosis protease-activating factor 1 (APAF-1). Between groups 1 and 3, there were no differences in tissue NO levels and eNOS, iNOS, and APAF-1 expressions. iNOS and APAF-1 expressions were at the mild to moderate levels in group 2, but these parameters were markedly increased in group 4 at 14 days of obstruction. Also, elevated expression of iNOS was accompanied by a high NO production in group 4 compared with group 2. Although eNOS expressions were increased in both groups 2 and 4, there were no significant differences between these groups. Propofol as an anesthetic agent may attenuate NO-induced renal tubular cell apoptosis by downregulating the expression of iNOS in an animal model of unilateral UO.