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Increased vasoconstrictor reactivity and decreased endothelial function in high grade varicocele; functional and
Oguzhan Yildiz1, Husamettin Gul, Yaşar Ozgok
1Department of Pharmacology, Gülhane Military Medical Academy, Faculty of Medicine, 06018 Etlik, Ankara, Turkey. oyildiz@gata.edu.tr
Urological Research
|October 24, 2003
Summary
Varicocele pathophysiology involves impaired endothelial function and increased vasoconstrictor sensitivity, particularly in higher grades. This suggests endothelial dysfunction contributes to varicocele progression.
Area of Science:
- Urology
- Vascular Biology
- Pathophysiology
Background:
- The exact pathophysiology of human varicocele remains unclear.
- Understanding vascular changes is crucial for varicocele management.
Purpose of the Study:
- To investigate vasoconstrictor reactivity, endothelial function, and morphological changes in different varicocele grades.
- To elucidate the underlying pathophysiology of varicocele.
Main Methods:
- Organ bath technique to assess contractile responses to vasoconstrictors (phenylephrine, norepinephrine, serotonin, histamine) in isolated spermatic veins.
- Endothelial function assessed via acetylcholine-induced relaxation, with nitric oxide synthase (NOS) and cyclooxygenase (COX) inhibition.
- Measurement of cyclic guanosine monophosphate (cGMP) levels and morphological evaluation using light microscopy.
Main Results:
- Higher grades (II and III) showed increased sensitivity and maximal contractions to vasoconstrictors compared to grade I.
- Endothelial dysfunction was indicated by reduced vasorelaxation and lower cGMP levels in higher varicocele grades.
- Morphological changes included increased vessel wall thickness (grade II) and dilatation (grade III).
Conclusions:
- Endothelial dysfunction, characterized by reduced vasorelaxant production, is present in higher-grade varicoceles.
- Enhanced vasoconstrictor effects and morphological changes correlate with varicocele severity, suggesting a role in pathophysiology.