The histological changes produced in the rat testis by temporary and permanent occlusion of the testicular artery

Oettlé, A. G.; Harrison, R. G.

doi:10.1002/path.1700640204

Cited by 99 publications

(28 citation statements)

References 8 publications

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“…Histopathology showed that appearance of multinucleated giant cells in the seminiferous epithelia and interstitial neutrophil infiltration in the degenerative or necrotic tissues resembled the ischemic changes caused by a temporary ligation of the testicular artery (Oettlé and Harrison, 1950), and the seminiferous epithelial cells adjoining the intratesticular arterioles showed milder changes than those far from the arterioles (Chatani, 1996). The data by van Vliet et al (1988) also suggested the restricted testicular changes induced by hCG treatment were probably caused by focal ischemia.…”

Section: Discussionmentioning

confidence: 95%

POSSIBLE MECHANISM FOR TESTICULAR FOCAL NECROSIS INDUCED BY hCG IN RATS

Chatani

2006

J. Toxicol. Sci.

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-Possible mechanisms for testicular focal necrosis induced by human chorionic gonadotropin (hCG) were examined in Fischer 344 rats. A single s.c. injection of 2000 IU/kg hCG produced focal necrosis 2 days later in testicular tissues such as the seminiferous tubules in the frontal lower part of the testis (FLPT) of 11-week-old F344/Jcl rats. This hCG-induced necrosis was suppressed by an oral treatment (concomitant or delayed by 3 hr) with cyclooxygenase inhibitors (indomethacin, rofecoxib) or prostaglandin (PG) receptor blocker (AA-2414). Focal necrosis was also induced by intratesticular injection of PGF 2α or PGE 2 with this necrosis suppressed by previous oral treatment with AA-2414, and the PGF 2 level in the testis increased 4 hr after hCG treatment. These findings suggested that de novo synthesis of PGs beginning at 3-4 hr was responsible for induction of necrosis. No necrosis was induced by hCG in the Leydig cell-devoid testis produced by ethane dimethanesulfonate treatment. Necrosis of spontaneously-induced Leydig cell tumor mass was also induced by hCG, suggesting that Leydig cells are responsible for induction of necrosis. An injection of dye into the testicular artery and laser Doppler flowmetry revealed a continuous reduction of blood flow at the FLPT at 6-48 hr after hCG treatment; contrary to this, the upper part showed an early recovery from the reduced flow. From these results, the mechanism of the hCG-induced necrosis was concluded to be: 1) hCG stimulates Leydig cells to synthesize PGs de novo; 2) PGs induce the intratesticular arteries to contract in the FLPT; and 3) obstruction of blood flow (ischemia) for more than 12 hr induced focal necrosis in the testis.

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Section: Discussionmentioning

confidence: 95%

POSSIBLE MECHANISM FOR TESTICULAR FOCAL NECROSIS INDUCED BY hCG IN RATS

Chatani

2006

J. Toxicol. Sci.

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“…Numer ous animal experiments proved that an interruption of the testicular blood supply lasting 2-4 h leads to an irre versible destruction of the germinal epithelium [Pels and Bur, 1958;Sonda and Lapides, 1961;Gunn et al, 1965;Steinberger and Tjioe, 1969;Kaya and Harrison, 1975;Dixit, 1977;Stiles et al, 1977;Vrzgulov, 1980], There are, however, few investigations into the effects of short term ischaemia on the testicular parenchyma lasting less than 1 h. Furthermore, the individual authors arrive at contradictory results [Oettle and Harrison, 1952;Szarvas andKovacs, 1969: Ludwig et al, 1979], The present animal experimental investigations in tend to throw light on the question, whether short-term clamping of the spermatic cord, frequently practised in the course of clinical exposure of the testes with subse quent immediate section for microscopic examination, can lead to permanent damage to the testicular parenchy ma.…”

Section: Introductionmentioning

confidence: 99%

Histological Changes in Rat Testicles after Short-Term Ischaemia

Gilbert¹,

Wetterauer²,

Wokalek³

1986

Urol Int

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A temporary pinching off of the spermatic cord was carried out in 100 male Wistar rats in order to evaluate the effect of a limited period of ischaemia on the testicular parenchyma. The animals were divided into four groups of equal number, and a certain period of ischaemia was chosen (15, 30, 45 and 60 min). The histological investigation of the testicle parenchyma was performed 2 months after the operation, the contralateral testicle serving as control. Already an ischaemia of 15 min leads to a statistically significant, irreversible damage of 53.5% of the seminiferous tubulus (p = 0.001). The degree of the damage does not increase up to an ischaemic period of 1 h. Since rat testicles have proven to be a model for the judgement of human fertility, operations on testicles which are combined with a temporary ischaemia of this organ, should be ended within a few minutes.

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“…The testicular artery was occluded for a period of 100 min, according to the method of Oettlé & Harrison (1952), as described previously (Steinberger & Tjioe, 1969). Groups of animals were killed at 2-, 7-, 14-and 28-day intervals after the episode of ischaemia.…”

Section: Methodsmentioning

confidence: 99%

“…The first systematic and extensive study of the effect of ischaemia on the mammalian testes was published by Oettlé & Harrison (1952). Utilizing the recently gained knowledge of the dynamics of spermatogenesis, Steinberger & Tjioe (1969) re-evaluated the effect of ischaemia on rat testes and suggested, on the basis of the histological data, that ischaemia produces damage to specific cell types in the germinal epithelium.…”

Section: Introductionmentioning

confidence: 99%