Related Experiment Videos
[Experimental study of voiding dysfunction induced by cerebral infarction in rats]
1Department of Urology, School of Medicine, Kanazawa University, Japan.
Nihon Hinyokika Gakkai Zasshi. the Japanese Journal of Urology
|November 1, 1996
Summary
This study establishes an animal model for neurogenic voiding dysfunction after cerebral infarction. Calcium channel blockers effectively increased bladder capacity in these rats, suggesting a central nervous system effect.
Area of Science:
- Neuroscience
- Urology
- Pharmacology
Context:
- Clinical reports indicate voiding dysfunction following cerebrovascular disease.
- No established animal models exist to experimentally study this condition.
- Cerebral infarction can lead to neurogenic bladder dysfunction.
Purpose:
- To establish a reliable animal model for evaluating neurogenic voiding dysfunction after cerebral infarction.
- To investigate the effects of specific pharmacological agents on bladder capacity in this model.
Summary:
- A rat model of cerebral infarction was developed using middle cerebral artery occlusion.
- Bladder capacity significantly decreased in infarcted rats, correlating with lesion size.
- Nifedipine (a calcium channel blocker) increased bladder capacity without increasing residual urine, suggesting a central mechanism.
Impact:
- This animal model provides a platform for studying neurogenic voiding dysfunction in cerebrovascular disease.
- Findings suggest that calcium channel blockers may target the central nervous system to improve bladder capacity.
- The study highlights the potential for novel therapeutic strategies for post-stroke urinary dysfunction.