Abstract
Background and Purpose:
Corticosteroids have been commonly used in medical expulsive therapy for obstructing ureteral calculi. The exact mechanism of action responsible for facilitation of stone expulsion is unknown, but it is attributed to the anti-inflammatory properties of corticosteroids. Corticosteroids inhibit the production of phospholipase A2 and cyclooxygenase-2, both of which are involved in prostaglandin synthesis. We sought to determine if hydrocortisone inhibits ureteral contractility directly by assessing its action in an isolated in vitro contractility assay.
Methods:
Porcine ureters were attached to force displacement transducers and suspended in organ tissue baths containing aerated Krebs buffer. Tissues were equilibrated for 1 hour, and a spontaneous contractility rate was established. After equilibration, tissues were incubated with a 10-fold concentration curve of hydrocortisone (1 nM–10 μM) for 90 minutes, and compared with indomethacin (1 μM) and dimethyl sulfoxide (DMSO) 0.1% as positive and negative controls of contraction, respectively. Contractility rates were recorded on a polygraph and analyzed for changes over exposure time during the course of the experiment.
Results:
Hydrocortisone inhibited ureteral contractility in a concentration dependent trend. After 90 minutes of treatment, 100 nM, 1 μM, and 10 μM all produced a statistically significant decrease in ureteral contractility rates relative to DMSO controls. The average percent decrease was 43.7% by 100 nM, 66.9% by 1 μM, and 66% by 10 μM hydrocortisone. This decrease in ureteral contractility continued to be significant at 120 minutes. In addition, 10 μM and 1 μM hydrocortisone treatment caused a similar reduction in contractility to indomethacin at 120 minutes.
Conclusion:
Hydrocortiosone effectively inhibits stretch-induced ureteral contractility of porcine ureter in an isolated in vitro assay.
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