Involved intrinsic apoptotic pathway in the varicocele and varicose veins

Disordered programmed cell death may play a role in the development of venous diseases. Tissue hypoxia caused by blood stagnation and venous hypertension is the similar etiology of varicocele and varicose veins. We studied the vascular histopathology and determined whether there is the same apoptotic pathway in both venous diseases.

The study groups consisted of 1-cm venous segments obtained from 10 patients during vascular stripping surgery for varicose saphenous vein and 1 cm of internal spermatic veins obtained from 12 patients during left varicocele repair. The control samples of 1 cm internal spermatic vein were obtained from 10 male patients who underwent left inguinal herniorrhaphy. The three layers of vascular histology were measured and compared by Masson trichrome stain, and the apoptotic proteins including Bcl-2, Fas, cleaved caspase-9, cleaved caspase-8, and cleaved caspase-3 were detected. Data were analyzed using the one-way analysis of variance with Tukey's comparison test.

The relative thickness of intima and adventitia layer was smaller in both study groups than in the control group. But a significant hypertrophy of media layer was observed in the varicocele and varicose veins than in the control group (p < 0.05). Overexpression of Bcl-2 and decreased expressions of cleaved caspase-9 and cleaved caspase-3 was observed in both study groups. There is no statistical difference in Fas and cleaved caspase-8 expressions in the control and study groups.

Our data showed vascular smooth muscle hypertrophy in the diseased vessels. The same dysregulation of apoptosis through intrinsic pathway was demonstrated in varicocele and varicose veins under tissues hypoxia. This mechanism of reduced apoptosis might contribute to the dilated and thickened walls of both venous diseases.