A Quantitative Study of the Effect of Ischaemia on the Germinal Epithelium of Rat Testes

Tjioe, D.Y.; Steinberger, Emil

doi:10.1530/jrf.0.0210489

Cited by 37 publications

(15 citation statements)

References 3 publications

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“…There is evidence to suggest that the testicular injury caused by acute spermatic cord torsion and detorsion results from classic reperfusion injury with the excessive elaboration of ROS [3,4,191. This mode of injury may be responsible for the observed germ cell degeneration after torsion/detorsion [23]. Our study shows that degenerating germ cells overexpress eNOS and suggest that NO, a ROS, is also involved in reperfusion-induced apoptosis.…”

Section: Discussionmentioning

confidence: 53%

Germ Cell Apoptosis and Endothelial Nitric Oxide Synthase (eNos) Expression Following Ischemia-Reperfusion Injury to Testis

Zini

Abitbol

Girardi

et al. 1998

Archives of Andrology

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Section: Discussionmentioning

confidence: 53%

Germ Cell Apoptosis and Endothelial Nitric Oxide Synthase (eNos) Expression Following Ischemia-Reperfusion Injury to Testis

Zini

Abitbol

Girardi

et al. 1998

Archives of Andrology

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“…These observations suggest that the testis may be particularly sensitive to reductions in its blood flow. In line with this, experimental studies have shown that short‐term total ischaemia and a moderate short‐term decrease in flow results in apoptosis among spermatogonia and early spermatocytes (Steinberger & Tjioe, 1969; Tjioe & Steinberger, 1970; Turner et al. , 1997; Lysiak et al.…”

Section: Introductionmentioning

confidence: 58%

“…These observations suggest that the testis may be particularly sensitive to reductions in its blood flow. In line with this, experimental studies have shown that short-term total ischaemia and a moderate short-term decrease in flow results in apoptosis among spermatogonia and early spermatocytes (Steinberger & Tjioe, 1969;Tjioe & Steinberger, 1970;Turner et al, 1997;Lysiak et al, 2000aLysiak et al, , 2001Bergh et al, 2001) and that a moderate long-term reduction in flow leads to focal damage of the seminiferous tubules (Markey et al, 1994). Sclerotic changes in the testicular vasculature are not uncommon in young and elderly men (Suoranta, 1971;Oshima et al, 1984;Brehmer-Andersson et al, 1985), and the morphological appearance of the seminiferous tubules in old or infertile men is similar to that observed after experimental ischaemia (Regadera et al, 1985;Paniagua et al, 1991;Markey et al, 1994).…”

Section: Introductionmentioning

confidence: 63%

Effects of haemorrhagic hypotension on the subcapsular artery and microvasculature of the rat testis

Lissbrant

Collin

Damber³

et al. 2006

Int J of Andrology

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Summary Developing germ cells may be sensitive to even moderate reductions in blood flow. Surprisingly, however, experimental evidence suggests that the rat testis may be unable to maintain its blood flow during a decrease in systemic blood pressure. This study was therefore performed in order to answer the following questions: Is the testis able to maintain its blood flow during moderate to major reductions in blood pressure and, if so, at which level of the testicular vasculature (main artery or microcirculation) does this compensatory response take place? Moderate (−20%) and major (−40%) reductions in blood pressure were induced in anaesthetized rats by haemorrhage and the effects on testicular microvascular blood flow and subcapsular testicular artery diameter were examined by using laser Doppler flowmetry and in vivo video‐microscopy respectively. Haemorrhagic hypotension led to decreased local testicular blood flow, but the relative reductions in flow were generally only half as large as the reductions in blood pressure. Hypotension also decreased the diameter of the main subcapsular testicular artery. During large reductions in blood pressure the subcapsular testicular artery constricts and testicular blood flow decreases. However, blood flow is reduced proportionally less than the mean arterial pressure, suggesting that local regulatory mechanisms are present in the testicular microvasculature, which may prevent blood flow from falling below a critical level.

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“…Dans l'ischémie expérimentale du testi cule [19,22], les cellules jeunes (spermato gonies) et les cellules en phase S (synthèse d'ADN) sont atteintes en premier lieu. Dans notre expérimentation, le processus est in verse; les cellules germinales matures bor dant la lumière tubulaire sont lésées en pre mier, l'atteinte progressant ensuite de la lu mière vers la périphérie du tube.…”

Section: Discussionunclassified

Etude histologique de l’action du Propranolol sur l’appareil génital du rat mâle

Martínez¹,

Barthe²

1981

Cells Tissues Organs

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Increasing doses of propranolol were injected intraperitoneally to four series of adult male rats in order to study the effect of this β-blocking agent on various organs (testis, epididymis, prostate and seminal vesicle) and endocrine glands (adrenals, pancreas, thyroid, pituitary). Histological damage was observed only in testes: i.e., necrosis and desquamation of germinal cells in the seminiferous tubules associated with light arterial vasoconstriction. Pelviperitoneal fibrosis was observed as well. These lesions seem to be of pharmacological vascular origin and appear to occur in combination with an elective toxic effect of propranolol on the germinal cells.

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A Quantitative Study of the Effect of Ischaemia on the Germinal Epithelium of Rat Testes

Cited by 37 publications

References 3 publications

Germ Cell Apoptosis and Endothelial Nitric Oxide Synthase (eNos) Expression Following Ischemia-Reperfusion Injury to Testis

Germ Cell Apoptosis and Endothelial Nitric Oxide Synthase (eNos) Expression Following Ischemia-Reperfusion Injury to Testis

Effects of haemorrhagic hypotension on the subcapsular artery and microvasculature of the rat testis

Etude histologique de l’action du Propranolol sur l’appareil génital du rat mâle

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