高血圧自然発症ラット(SHR)を用いた精巣内血管障害の精子発生能障害に及ぼす影響に関する研究
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In male infertility and in elderly males, it is thought that intratesticular vascular changes contribute to hypospermatogenesis. We employed spontaneously hypertensive rats (SHR) for investigations of the process of hypospermatogenesis induced by vascular changes. We also examined the changes of spermatogenesis by preventive administration of a Ca channel blocker, nifedipine. Sprague-Dawley rats (SDR), used as the control, showed blood pressure of about 130 mmHg, whereas SHR showed elevation of blood pressure even at 8 weeks of age and showed about 190 mmHg from 16 weeks of age. Hypertensive vascular changes developed in intratesticular arteries, especially in arterioles. Although the mature spermatid count/Sertoli cell count of the SDR group was 6.89 at 24 weeks of age, 6.71 at 36 weeks of age, that of the SHR non-treated group was 4.28 at 24 weeks of age, 4.05 at 36 weeks of age, both significantly lower than that of the SDR group. The proliferating cell nuclear antigen (PCNA) positive cell count/Sertoli cell count, employed as the index of DNA synthesis of germ cells, did not differ among the groups. There were no differences of transferrin concentration in testicular cytosol, which was secreted by Sertoli cells in the testis. In contrast, insulin-like growth factor-1 (IGF-1), which was also secreted by Sertoli cells, in the SHR non-treated group, was significantly decreased at 36 weeks of age, suggesting Sertoli cell dysfunction. The degree of hypertensive vascular changes in the nifedipine-treated SHR group was significantly lower than that of the SHR non-treated group at 24 and 36 weeks of age. Spermatogenesis and the IGF-1 concentration in the SHR nifedipine-treated group remained at the same level as the SDR group throughout the experimental period. In conclusion, it could be clarified that spermatogenic damage caused by hypertensive vascular changes was mediated by Sertoli cell dysfunction. Nifedipine has the possibility would prevent the development of hypertensive vascular changes and, as a result, protect spermatogenesis.
- 札幌医科大学の論文
- 1994-12-01
札幌医科大学 | 論文
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