thiourea and Capillary-Leak-Syndrome

The present study was to investigate 6-hydroxydopamine (6-OHDA)-induced inflammatory response and underlying mechanisms in the urinary bladder in anesthetized male rats of Long-Evans strain. The magnitude of inflammation was evaluated by morphometric analysis of the relative number of leaky blood vessels expressed by the area density of India ink-labeled blood vessels in whole mount specimens. Light and scanning electron microscopies were employed to study the changes in histologic structure and endothelial ultrastructure of bladder wall. Local injection of 6-OHDA to lumen of urinary bladder induced a dose-dependent increase in plasma leakage. Following application of vehicle, 5 mg/kg 6-OHDA, and 10 mg/kg 6-OHDA, area densities of India ink-labeled leaky vessels were 5.65+/-3.72% (N=6), 22.63+/-5.12% (N=6), and 35.02+/-11.25% (N=6), respectively. Inflammatory response was completely abolished by pretreatment alone with dimethylthiourea (DMTU), a hydroxyl radical scavenger, and was also attenuated by pretreatment with L-732,138, a NK1 receptor antagonist. 6-OHDA caused edema formation and venular endothelial gap formation in bladder tissue. It is concluded that 6-OHDA induced inflammation in the rat urinary bladder, the response of which was dose-dependently increased and free radicals and tachykinins were involved in the inflammatory process.

Topics: Animals; Capillary Leak Syndrome; Capillary Permeability; Cystitis; Dose-Response Relationship, Drug; Inflammation; Male; Oxidopamine; Rats; Rats, Long-Evans; Thiourea; Urinary Bladder