Objective: To study the impact of pulmonary fibrosis on erectile function in rats and its mechanism.
Methods: Forty 12-week-old healthy male SD rats were randomly divided into Groups A (4-week pulmonary fibrosis), B (6-week pulmonary fibrosis), C (4-week control, and D (6-week control). The models of pulmonary fibrosis were established by injection of bleomycin at 5 mg/kg in the trachea, while the controls were injected with normal saline only. At 4 and 6 weeks, all the rats were subjected to determination of the serum testosterone (T) level, arterial blood gas analysis, measurement of intracavernous pressure/mean arterial pressure (ICP/MAP), and examination of NOS activity and cGMP content. The mRNA expressions of eNOS, iNOS and nNOS in the corpus cavernosum penis were detected by real-time PCR, and that of eNOS analyzed by Western blot.
Results: The 3 V and 5 V of the ICP/mapx100 in Group C were 16.37 +/- 2.19 and 27.19 +/- 3.18, significantly lower than 30.78 +/- 2.66 and 50.09 +/- 6.97 in Group A (P < 0.05); those in Group D were 10.17 +/- 1.31 and 17.40 +/- 1.74, significantly lower than 31.45 +/- 3.07 and 51.23 +/- 7.23 in Group B (P < 0.05), and so were they in Group D than in C (P < 0.05). PaO2 was significantly lower in Group C than in A ([75.50 +/- 13.87] mmHg vs [103.80 +/- 6.88] mmHg, P < 0.05) , and so was it in Group D than in B ( [83.60 +/- 5.50] mmHg vs [102.70 +/- 5.77] mmHg, P < 0.05). Group C showed a significantly increased serum T level as compared with A ([391.1 +/- 264.7] ng/dl vs [175.9 +/- 53.0] ng/dl, P < 0.05), so did Group D ([745.4 +/- 408.8] ng/dl) versus Group B ([177.8 +/- 52.3] ng/dl) and C (P < 0.05). NOS activity and cGMP content in the corpus cavernosum significantly decreased in Group C ([1.50 +/- 0.14] U/mg prot and [35.69 +/- 3.64] pmol/mg) compared with A ([2.66 +/- 0.39] U/mg prot and [51.10 +/- 7.22] pmol/mg) (P < 0.05), so did they in D ([1.40 +/- 0.20] U/mg prot and [34.55 +/- 4.30] pmol/mg) versus B ([2.75 +/- 0.36] U/mg prot and [52.15 +/- 6.86] pmol/mg) (P < 0.05), but neither showed any significant difference between Groups D and C (P > 0.05). The expression of the eNOS protein was significantly lower in Group C than in A (0.79 +/- 0.01 vs 0.87 +/- 0.01, P < 0.05), so was it in D than in B and C (0.71 +/- 0.02 vs 0.88 +/- 0.01 and 0.79 +/- 0.01, P < 0.05). The expression of eNOS mRNA was significantly higher in Group C than in A (4.46 +/- 0.92 vs 2.61 +/- 0.68, P < 0.05), but did not show any significant difference between D and B (2.79 +/- 0.60 vs 2.69 +/- 0.65, P > 0.05), nor did the expressions of nNOS mRNA and iNOS mRNA between the pulmonary fibrosis groups and the controls (P > 0.05).
Conclusion: Pulmonary fibrosis may induce erectile dysfunction by suppressing the expression of the eNOS protein and reducing NOS activity and cGMP content in the corpus cavernosum penis of rats.