EFFECT OF VASOACTIVE-INTESTINAL-PEPTIDE AND NALOXONE COMBINATION ON URINARY N-ACETYL-BETA-D-GLUCOSAMINIDASE LEVEL AND KIDNEY HISTOLOGY OF RATS EXPOSED TO SEVERE HEMORRHAGE

AKIN M., TUNCEL N., GURER F., KURAL N., USLU S.

PHARMACOLOGY, cilt.47, sa.3, ss.194-199, 1993 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 47 Sayı: 3
  • Basım Tarihi: 1993
  • Dergi Adı: PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.194-199
  • Eskişehir Osmangazi Üniversitesi Adresli: Hayır

Özet

Renal hypoperfusion which occurs in hemorrhagic shock creates an environment in which cellular injury and organ dysfunction can occur during the episode of shock as well as reoxygenation and reperfusion. At the same time, mast cell degranulation which is observed during hemorrhage may have an additinal deleterious effect on the kidney. Twenty-two (Mus norvegicus albinos) rats (200-250 g) of either sex were used. The animals were divided into three groups. Group 1, the control group, was exposed to a 40% hemorrhage. Group 2 was exposed to 40% hemorrhage and then shed blood reperfused. Group 3 was exposed to 40% hemorrhage, and in addition to shed blood reperfusion 2 5 ng kg-1 vasoactive intestinal peptide (VIP) + 5 mg kg-1 naloxone (NLX) were given. At the end of the experiment the kidneys were evaluated either histologically or by measurement of the urinary N-acetyl-beta-D-glucosaminidase (NAG) activity. Shed blood reperfusion caused continuation of ischemic tissue damage and elevation of urinay NAG activity. Addition of VIP and NLX to the blood reperfusion caused a decrease in urinary NAG excretion, and the histology of renal tissue was almost normal.