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Introduction: Obstructive bladder dysfunction is directly related to ischemia/reperfusion injury characterized by damage to nerves, synapses and smooth muscle cells within the bladder wall. Antrodia Camphorata (AC) has significant antioxidant, antiinflammatory and cell-cycle inhibition properties. The specific aim of this study was to evaluate whether orally administered AC can protect rabbit bladders from the progressive dysfunctions induced by bilateral ischemia/reperfusion (I/R)., Methods: Twenty-four male NZW rabbits were separated into 4 groups of 6 animals each. Rabbits in groups 1 and 2 were fed Antrodia Camphorata (AC) suspensions; those in groups 3 and 4 received vehicle. Each rabbit in groups 2 and 4 were subjected to in vivo bilateral ischemia for 2 h and then allowed to recover for 1 week. The rabbits in groups 1 and 3 received sham operation and served as control groups. Cystometry, contractile responses to field stimulation, carbachol, ATP and KCl were determined. Biochemical and immuno-histochemical studies were also performed., Results: I/R resulted in decreased compliance, decreased contractile responses, decreased nerve density, and increased apoptosis. AC pretreatment of rabbits subjected to I/R significantly protected the bladder from all contractile, biochemical, and structural dysfunctions resulting in significantly improved bladder.

Objectives: To detect the effect of ischemia/reperfusion (I/R) injury on rabbit bladder, using physiological study and immunoblotting techniques., Methods: Twelve male New Zealand White rabbits were separated into three groups of 4 rabbits each. Group 1 served as control. Group 2 rabbits (ischemia-alone group) underwent in vitro bilateral ischemia surgery for 2 hours. In group 3 (I/R group), bilateral ischemia was similarly induced, and the rabbits were allowed to recover for 2 weeks. The contractile responses to electrical field stimulation, adenosine triphosphate, carbachol, and KCl were recorded. Expression levels of the signaling targets, Rho-kinase (ROK), protein kinase C potentiated inhibitor (CPI-17), caldesmon (CaD), and calponin (CaP) were analyzed by Western blotting., Results: Ischemia alone resulted in significant reductions in the contractile responses, whereas I/R resulted in further decreases after all forms of stimulation. In muscle layer, ROK expression increased immediately after ischemia and recovered to the control level after 2 weeks' recovery. However, in mucosa layer, ROK expression showed no significant change after ischemia but significantly increased after reperfusion. After ischemic damage, CPI-17, the functional protein involved in smooth-muscle Ca(2+) sensitization, was significantly increased and then decreased after 2 weeks of reperfusion. The expression of CaP significantly increased after ischemia and decreased after reperfusion. Levels of high-molecular-weight CaD significantly decreased after ischemia and remained very low after reperfusion., Conclusions: This study provides further understanding of the role of regulatory proteins in detrusor muscle after ischemia and I/R-induced contractile dysfunction.

Aims: Ischemia/reperfusion (I/R) can significantly change the nerve function of the bladder, thus resulting in detrusor weakness and overactivity. CoQ10 is a lipid-soluble cofactor found naturally in the mitochondria and has been reported to have neuroprotective and antiapoptosis effects. The aim of this study is to determine if CoQ10 can protect bladders subjected to I/R injury., Methods: Four groups of male New Zealand White rabbits (N = 4) were treated with CoQ10 (3 mg/kg body weight/day) (groups 1 and 2) or vehicle (groups 3 and 4). In groups 2 and 4 (I/R groups), bilateral vesicular ischemia was induced for 2 hr and the rabbits allowed to recover for 2 weeks. Groups 1 and 3 were controls and given sham surgery. The cholinergic nerve marker, vesicular acetylcholine transporter (VAChT), was examined by western blotting. Nerve density and cell apoptosis were calculated by immunohistochemistry., Results: I/R significantly decrease bladder innervation; CoQ10 has significant neuroprotective effects, which are evidenced by increased VAChT expression and neurofilament immunostaining. Detrusor cells apoptosis increase significantly by I/R. CoQ10 control and I/R groups both show significantly lower apoptosis than vehicle groups., Conclusions: The current study clearly demonstrated that these CoQ10 supplement provides significant bladder protection against I/R injury. This protective effect is in part by protecting damage to cholinergic innervation., ((c) 2008 Wiley-Liss, Inc.)

Objectives: To investigate the effects of inosine on in vitro ischemia-reperfusion injury to urinary bladders in adult rats. Inosine has neuroprotective effects against cerebral and cardiac ischemia-reperfusion injury. Methods: A total of 18 adult male rats were used. Each rat was anesthetized, and the bladder was excised, cut longitudinally into 3 equal strips, and mounted in individual baths. Six strips were run simultaneously. Inosine (37.3 mM) was added to the baths containing strips 2, 4, and 6. All strips were equilibrated for 1 hour in oxygenated Tyrode solution containing glucose and at the end of the hour were stimulated with field stimulation, carbachol, and KCl. Strips 1 and 2 were subjected to repetitive stimulation (RS) by field stimulation (32 Hz) every 5 minutes for 1 hour; strips 3 and 4 were subjected to Tyrode equilibrated solution with nitrogen and no glucose for 1 hour; and strips 5 and 6 were subjected to in vitro hypoxia in the absence of substrate plus RS for 1 hour. All strips were then incubated in oxygenated Tyrode solution for 1 hour and stimulated as before. Results: In normoxia, inosine had no beneficial effects either before or after RS. However, in the ischemic model, the bladder strips incubated with inosine showed significantly better contractile responses to stimulation with carbachol and KCl. After hypoxia without substrate plus RS, the strips incubated with inosine showed increased responses to all 3 forms of stimulation. Conclusions: Inosine protected the contractile responses of the bladder strips after in vitro hypoxia without substrate with or without RS. [Copyright &y& Elsevier]