Effect of Vasoactive Intestinal Peptide and Naloxone Combination on Urinary N-Acetyl-β-D-Glucosaminidase Level and Kidney Histology of Rats Exposed to Severe Hemorrhage

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Abstract
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 re-oxygenation 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 25 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-β-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.

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