Third prize

Effect of hydrocortisone on porcine ureteral contractility in vitro

Gaurav Bandi, Eric A. Wilkinson, Tawnya L. Cary-Coyle, Travis Jerde, Stephen Y. Nakada

Research output: Contribution to journalArticle

4 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1169-1173
Number of pages5
JournalJournal of Endourology
Volume22
Issue number6
DOIs
StatePublished - Jun 1 2008
Externally publishedYes

Fingerprint

Hydrocortisone
Swine
Adrenal Cortex Hormones
Ureter
Dimethyl Sulfoxide
Indomethacin
Ureteral Calculi
Phospholipases A2
Cyclooxygenase 2
Transducers
Baths
Prostaglandins
Buffers
Anti-Inflammatory Agents
Therapeutics
In Vitro Techniques

ASJC Scopus subject areas

  • Urology

Cite this

Third prize : Effect of hydrocortisone on porcine ureteral contractility in vitro. / Bandi, Gaurav; Wilkinson, Eric A.; Cary-Coyle, Tawnya L.; Jerde, Travis; Nakada, Stephen Y.

In: Journal of Endourology, Vol. 22, No. 6, 01.06.2008, p. 1169-1173.

Research output: Contribution to journalArticle

Bandi, Gaurav ; Wilkinson, Eric A. ; Cary-Coyle, Tawnya L. ; Jerde, Travis ; Nakada, Stephen Y. / Third prize : Effect of hydrocortisone on porcine ureteral contractility in vitro. In: Journal of Endourology. 2008 ; Vol. 22, No. 6. pp. 1169-1173.
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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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AU - Nakada, Stephen Y.

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