The Effects of Botulinum Toxin A on the Detrusor Muscle in Rats.
- Author:
Il Oh JUN
1
;
Kyung Do KIM
;
Moo Yeol LEE
Author Information
1. Department of Urology, College of Medicine, Chung-Ang University, Seoul, Korea. kim14141@hananet.net
- Publication Type:Original Article
- Keywords:
Detrusor muscle contractility;
Botulinum toxin A;
Urinary bladder;
Rat
- MeSH:
Acetylcholine;
Animals;
Botulinum Toxins*;
Cholinesterases;
Neurons;
Nitroprusside;
Rats*;
Rats, Sprague-Dawley;
Relaxation;
Transducers;
Urinary Bladder;
Verapamil
- From:Korean Journal of Urology
2002;43(4):322-325
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: There is little data on the effects of botulinum toxin A (BoTx A) on detrusor muscle published in the literature. An experimental study was conducted to investigate the effect of BoTx A on the detrusor muscle in rats. MATERIALS AND MTHODS: Sprague-Dawley rats were used to make the detrusor muscle strip (length: 8mm, width: 2mm). An isometric force transducer in the physiologic salt solution was used to measure the contraction and relaxation of this muscle strip. A contraction was induced by acetylcholine (ACh) and electrical field stimulation (40V, 20Hz, 3sec), and relaxation was induced by verapamil and sodium nitroprusside. The BoTx A concentration was 0.1U/ml. The relaxation and contraction of the detrusor muscle in the BoTx A-treated group were analyzed and compared with those in the control group. RESULTS: The time to the maximum contraction induced by electrical field stimulation was lengthened and the time of recovery to the basal state after terminating electrical field stimulation was also increased by BoTx A (p<0.05). However, the contractile reaction induced by ACh and the relaxing reaction induced by verapamil and sodium nitroprusside after maintaining the maximum contraction induced by ACh 10 4M was not influenced by BoTx A. CONCLUSIONS: The results of this experimental study suggest that the time delay of the maximum contraction induced by electrical field stimulation occurred by blocking ACh release at the neuronal endings and the time delay of the recovery to the basal state after terminating electrical field stimulation occurred by reducing cholinesterase activity.
