Histological and neurotrophic changes triggered by varying models of bladder inflammation

Purpose: We determined whether bladder inflammation causes elevated express ion of nerve growth factor by bladder parenchymal cells, leading to alterat ions in neurons innervating the bladder. To answer this question biochemica l, histological and neuronal size data were obtained in rats following vari ous experimental models of bladder inflammation. Materials and Methods: Chemical (2.5% formalin), immune (lipopolysaccharide 2 x 10(4) cfu/ml.) and mechanical (chromic catgut) inflammation was evalua ted at various times and compared to control bladders. Hematoxylin and eosi n, and Giemsa staining was done to characterize inflammation and quantify m ast cells in the bladder. Nerve growth factor protein and messenger RNA wer e assayed in the bladder and major pelvic ganglion using 2-site enzyme-link ed immunosorbent assay and reverse transcriptase-polymerase chain reaction, respectively. Retrograde axonal tracing was done to size bladder neurons i n the major pelvic and dorsal root ganglia. Results: All forms of inflammation increased bladder weight and produced di ffuse hyperplasia, intramural edema, acute and chronic inflammatory cells, infiltration and mastocytosis. Generally bladder inflammation resulted in a 50% increase in nerve growth factor and 52% to 58% enlargement of peripher al neurons. Conclusions: Inflammation results in altered nerve growth factor content of the bladder, and morphological changes in sensory and motor neurons innerv ating the bladder. Such neuroplasticity may be a possible explanation for t he association of bladder inflammation with long-term symptoms and pain aft er inflammation subsides.