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Role of autonomic innervation in rat prostatic structure maintenance: a morphometric analysis
The Journal of Urology
|October 23, 1998
Summary
Major pelvic ganglion excision caused significant rat prostate atrophy, primarily due to epithelial shrinkage and reduced secretory activity. Smooth muscle cells showed increased ribosomal aggregates, suggesting activation after denervation.
Area of Science:
- Urology
- Neuroscience
- Cell Biology
Background:
- The major pelvic ganglion (MPG) plays a crucial role in regulating autonomic functions, including those of the prostate.
- Understanding the impact of denervation on prostate structure is essential for diagnosing and treating related pathologies.
Purpose of the Study:
- To investigate the structural consequences of major pelvic ganglion (MPG) excision on the rat prostate ventral lobe (VL).
- To analyze morphometric and ultrastructural changes in prostatic epithelial and smooth muscle cells following denervation.
Main Methods:
- Studied 80 Sprague-Dawley rats, with 42 undergoing right MPG excision and 38 serving as controls.
- Prostate ventral lobes were evaluated using macroscopic, light microscopy (LM), and transmission electron microscopy (TEM) after 28-30 days.
- Computerized morphometric analysis assessed epithelial and muscle cell characteristics.
Main Results:
- MPG excision resulted in a 36.6% reduction in ventral lobe fresh weight.
- LM showed decreased epithelial proportion (27.9% to 14.8%) and unchanged stromal/glandular proportions.
- TEM revealed reduced epithelial cell height, cytoplasm, Golgi, and endoplasmic reticulum areas, decreased secretory granules, and fewer microvilli. Smooth muscle cells exhibited increased ribosomal aggregates.
Conclusions:
- Denervation via MPG excision leads to significant rat prostatic ventral lobe atrophy, driven by epithelial component shrinkage.
- Ultrastructural changes indicate a decrease in epithelial cell secretory activity post-denervation.
- Increased ribosomal aggregates in stromal smooth muscle suggest potential cellular activation following denervation.