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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Testicular torsion affects prepubertal males and causes testicular infarction and subfertility. Animal models of spermatic cord torsion have been used in an attempt to study the mechanism of testicular injury from torsion. Although standardized animal models of torsion have been proposed, their reliability in producing testicular ischemia has not been documented. Dynamic enhanced magnetic resonance imaging (MRI) of the testis was used in a rat model with surgically induced, unilateral, 720 degrees torsion to quantify the severity of ischemia. Intravenous dysprosium diethylenetriaminepentaacetic acid-bis methylamide (Dy-DTPA-BMA) was injected as a bolus followed by serial dynamic Turbo GRASS images. Region of interest (ROI) measurements were obtained within the testicular parenchyma during contrast enhancement and washout. Perfusion abnormalities ranging from minimal delay in contrast enhancement in the torqued testicle to complete absence of intraparenchymal blood flow were documented with dynamic enhanced MRI. Reperfusion scans 1 hour after surgical reduction of torsion showed normalization of testicular blood flow in all animals. Dynamic enhanced MRI appears to be a useful method of documenting the perfusion deficit arising from torsion of the testis. Standard animal models of torsion produce inconsistent results because they do not reliably reproduce testicular ischemia. The ability of MRI to quantify perfusion abnormalities in the testis may provide additional information in the evaluation of human patients with symptoms of testicular torsion.
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PMID:Variability of ischemia during spermatic cord torsion in the rat. 812 96

The resumption of blood flow to organs following ischemia may cause a further increase in tissue damage through an increase in peroxidation of lipids in cell membranes. An experimental study was conducted to investigate the prevention of reperfusion injury after testicular torsion through changes in the lipid peroxide content of the testis. Adult male albino rats were divided into 11 groups, each containing 10 rats. One group served to determine base values of the lipid peroxide content of the testis and kidney; 3 groups were subjected to unilateral testicular torsion lasting 1, 3 and 5 hours; 3 groups were subjected to detorsion following torsion lasting 1, 3 and 5 hours; 3 groups were treated with allopurinol before detorsion following torsion lasting 1, 3 and 5 hours; and 1 group underwent sham operation as a control. Thiobarbituric acid reactive products of lipid peroxidation (TBAR) were assessed in testicular and renal tissues. Testicular torsion caused a significant increase in TBAR in the testis (p < 0.01), but not in the kidneys. Detorsion caused a further significant increase in testicular TBAR (p < 0.01). Pretreatment with allopurinol prevented this further increase (p < 0.01). It is concluded that, biochemically, reperfusion injury occurs in the testis following detorsion after testicular torsion of 720 degrees lasting as long as 5 hours. Pretreatment with allopurinol before detorsion prevents such reperfusion injury.
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PMID:The effect of allopurinol pretreatment before detorting testicular torsion. 818 3

Testis torsion-induced aspermatogenesis is not necessarily due to permanent loss of blood flow nor to dysfunctional Leydig cells or Sertoli cells. This investigation was undertaken to gain further insight into the mechanism underlying torsion-induced germ cell loss. Male rats were subjected to 1-h or 2-h ischemia-inducing torsion, and testes were examined at either 1, 2, 4, 24, or 48 h after torsion, depending on the study. Testes were examined for evidence of 1) in situ apoptosis by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP)-biotin nick-end labeling (TUNEL) technique, 2) apoptosis by the DNA "laddering" technique, 3) leukocyte margination and diapedesis in testicular vessels by immunocytochemical and histological techniques, and 4) testicular lipid peroxidation by the thiobarbituric acid reactive substances assay. The first TUNEL evidence for torsion-induced apoptosis was at 4 h after repair of 1-h torsion. Induction of apoptosis was confirmed by the electrophoretic laddering of DNA fragments. It was hypothesized that apoptosis was induced by reactive oxygen species arising from reperfusing leukocytes. A significant increase in both leukocyte margination and diapedesis occurred 4 h after torsion repair as did a significant increase in intratesticular lipid peroxidation products. These events were contemporaneous with the first appearance of apoptosis and consistent with the hypothesis that post-torsion, germ cell-specific apoptosis is induced by reactive oxygen species.
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PMID:Acute testicular ischemia results in germ cell-specific apoptosis in the rat. 940 30

Testicular torsion requires emergent release of the twisted spermatic cord. Ischemia/reperfusion (I/R) plays an important role in its pathogenesis, and recent data suggest that germ cells undergo apoptosis during I/R. In a model of torsion/detorsion (i.e., I/R) of the rat testis, involvement of calpain and caspase in necrotic and apoptotic cell death was examined. After 1 h of ischemia followed by 0, 0.5, 1, 6, or 24 h of reperfusion, the germ cells positively stained with in situ TUNEL, and DNA fragmentation, activation of caspase-3, and proteolysis of caspase substrates increased with time of reperfusion, demonstrating apoptosis. In addition, m-calpain activation and proteolysis of alpha-fodrin were increased during reperfusion, and its activation is thought to be involved in the necrosis. A calpain inhibitor, acety-leucyl-leucyl-norleucinal, inhibited the phenomena associated with apoptosis and necrosis induced by I/R, although a caspase inhibitor, Z-Val-Ala-Asp-fluoromethlyketone, only inhibited apoptotic changes. The inhibition of calpain but not caspase ameliorated the injury after 60 days of reperfusion following 1 h of ischemia. The calpain inhibitor injected just before reperfusion effectively suppressed alpha-fodrin proteolysis, suggesting its usefulness in the treatment of testicular torsion.
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PMID:Inhibition of calpain but not caspase protects the testis against injury after experimental testicular torsion of rat. 1105 63

This review will focus the roles of TNF-alpha, IL-1 alpha, and IL-1 beta in the mammalian testis and in two testicular pathologies, testicular torsion and orchitis. TNF alpha in the testis is produced by round spermatids, pachytene spermatocytes, and testicular macrophages. The type 1 TNF receptor has been found on Sertoli and Leydig cells and numerous studies suggest a paracrine mode of action for TNF alpha in the normal testis. IL-1 alpha has been reported to be produced by Sertoli cells, testicular macrophages, and possibly postmeiotic germ cells. IL-1 receptors have been reported on Sertoli cells, Leydig cells, testicular macrophages, and germ cells suggesting both autocrine and paracrine functions. While these proinflammatory cytokines have important roles in normal testicular homeostasis, an elevation of their expression can lead to testicular dysfunctions. Testicular torsion is a clinical pathology with results in testicular ischemia and surgical intervention is often required for reperfusion. A pivotal role for IL-1beta in the pathology of testicular torsion has been recently described whereby an increase in IL-1beta production after reperfusion of the testis is correlated with the activation of the stress-related kinase, c-jun N-terminal kinase, and ultimately resulting in neutrophil recruitment to the testis and germ cell apoptosis. In autoimmune orchitis, on the other hand, TNF alpha produced by T-lymphocytes and macrophages of the testis has been implicated in the development and progression of the disease. Thus, both proinflammatory cytokines, TNF alpha and IL-1, have significant roles in normal testicular functions as well as in certain testicular pathologies.
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PMID:The role of tumor necrosis factor-alpha and interleukin-1 in the mammalian testis and their involvement in testicular torsion and autoimmune orchitis. 1501 31

Testis torsion is a surgical emergency that lead to permanent gonad damage. The damage has been ascribed to mechanisms of ischemia-reperfusion similar to other tissues. The mechanisms involved are different, but the lipid peroxidation of plasma membrane, caused by reactive oxygen species (ROS), generated particularly during reperfusion, is one of the most accredited. In the present study, we aimed to evaluate the effects of raxofelast, a vitamin E-like antioxidant with potent action and no systemic toxicity, on lipid peroxidation and histopathology in both testes after unilateral testicular torsion and detorsion. Adult male Wistar rats were subjected to total occlusion (3 h) of the left testis followed by 4 hours of reperfusion (TI/R). Sham testicular ischemia-reperfusion rats (SHAM TI/R) were used as controls. The animals were then randomized to receive either vehicle (1 ml/kg/i.p. of a dimetylsulphoxide/NaCl 0.9% 1:10 v/v solution, injected either 15 min before detorsion and 15 min after detorsion) or raxofelast (20 mg/kg i.p. 15 min before detorsion and 15 min after detorsion). Conjugated dienes (CD) levels, an index of lipid peroxidation, and testis histopathology were evaluated. Testicular ischemia reperfusion (TI/R) in untreated rats produced high testicular levels of CD (3.6+/-0.3 DeltaABS/g protein on the left side and 2.5+/-0.2 DeltaABS/g protein on the right side). Furthermore, histological examination revealed marked damage to the testis interstitium with severe haemorrhage and edema. The administration of raxofelast lowered CD levels (2.8+/-0.2 DeltaABS/g protein on the left side and 1.9+/-0.1 DeltaABS/g protein in the right side) and significantly reduced histological damage. These data suggest that the hydrophilic vitamin E-like antioxidants are good candidates for designing a novel therapeutic strategy to halt the oxidative stress that follows acute testis torsion.
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PMID:Raxofelast, a hydrophilic vitamin E-like antioxidant, reduces testicular ischemia-reperfusion injury. 1531 98

Testicular torsion is described as the twisting of the spermatic cord resulting in acute pain and ischemia. This has a tendency to occur more frequently during adolescence and its cause is unknown. The most common signs and symptoms include red, swollen scrotum and acutely painful testicle, often in the absence of trauma. Nausea and vomiting are common. The most common conditions in the differential diagnosis include epididymitis, strangulated inguinal hernia, traumatic hematoma, testicular tumor, or testicular fracture. Physical examination techniques such as scrotal elevation can be helpful in differentiating between epididymitis and testicular torsion, but emergent imaging with Doppler ultrasound seems to be the most helpful in confirming the diagnosis. Radionuclide testicular scintigraphy with 99mTc is helpful when past the acute phase (the first 12 hours) and vascular compromise has prolonged. The clinician may attempt to manually reduce the torsion, but many need to be immediately referred to a urologist for a surgical exploration. Long-term prognosis for a functional, nonatrophied testicle is improved the sooner the torsion is diagnosed and treated.
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PMID:Testicular torsion: evaluation and management. 1576 47

Testicular torsion is a serious problem in male children and, if not treated at the right time, can lead to subfertility and infertility. The main reason for testicular damage is ischemia-reperfusion injury. A number of chemical substances have been used to protect testes against ischemia-reperfusion injury in experimental animals. The possible protective effect of N-acetylcysteine on testicular tissue after testicular detorsion was examined in the current study. Twenty-four rats were divided into four groups: sham operation, torsion, detorsion, and NAC + detorsion groups (n = 6 for each group). Excluding sham operation group, the rats were subjected to unilateral torsion (720-degree rotation in clockwise direction). After torsion (5 h) and detorsion (2 h), unilateral orchidectomy was performed. Malondialdehyde levels and superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities were determined in testicular tissue. Administration of N-acetylcysteine caused a decrease in malondialdehyde levels and an increase in glutathione peroxidase levels compared to detorsion group. The results suggest that N-acetylcysteine may be a potential protective agent for preventing the negative biochemical changes related to oxidative stress in testicular injury caused by testis torsion.
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PMID:The effects of N-acetylcysteine on antioxidant enzyme activities in experimental testicular torsion. 1641 70

Testicular torsion followed by torsion repair induces an ischemia-reperfusion injury to the testis that can render the testis aspermatogenic. Previous results have demonstrated this loss of spermatogenesis to be the result of germ cell apoptosis induced by oxidative stress. The present work reports protein changes occurring in the mouse testis 24 hours after repair of a testicular torsion known to induce germ cell apoptosis and severe seminiferous impairment. Total proteins were extracted from sham-operated testes and testes having had 2-hour 720 degrees torsion 24 hours previously. Testicular proteins were separated by 2-dimensional electrophoresis and the resulting gel images were analyzed with image analysis software. Of the over 1100 proteins detected on the average gel, over 700 were consistently appearing in multiple gels, and those protein spot intensities were averaged within sham and torsion groups and compared between the 2 groups. Twenty-three proteins were consistently increased after torsion repair and 48 were decreased. Six proteins, 3 of which increased and 3 of which decreased after torsion repair, were identified by mass spectrometry. The 3 proteins that increased after torsion repair, beta2-tubulin and 2 isoforms of serum albumin, as well as the 3 proteins that decreased after torsion repair, vimentin, phosphoglycerate kinase, and t-complex protein 1beta, were for the most part associated with various aspects of cell stress responses. The number of proteins phosphorylated on tyrosine residues exceeded the number of proteins phosphorylated on serine/threonine residues, but among 6 stress-related proteins specifically examined for phosphorylation in sham testes and those examined after torsion repair, increases in threonine phosphorylation of c-Jun NH2 terminal kinase and activating transcription factor 2 were the most prominent. Knowing these proteins and the pathways to which they point will aid in the search for new therapies of oxidative stress in the testis.
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PMID:Testicular torsion alters the presence of specific proteins in the mouse testis as well as the phosphorylation status of specific proteins. 1647 26

Testicular torsion causes an enhanced formation of reactive oxygen species which contributes to the pathophysiology of ischemia-reperfusion injury in the testis. We evaluated here the effect of caffeic acid phenethyl ester (CAPE), a new antioxidant and anti-inflammatory agent on histopathological changes in testicular ischemia-reperfusion injury. Adult male Wistar rats were divided into six groups of five each: control group 1 (n=5), sham operation group 2 (n=5), torsion/detorsion (T/D) group 3 (n=5), T/D+saline group 4 (n=5), T/D+CAPE group 5 (n=5) and T/D+CAPE group 6 (n=5). Group 1 served to determine baseline values of histopathological parameters, group 2 animals that underwent sham operation served as a control, while groups 3-6 animals were subjected to left unilateral torsion (2 h) and detorsion (24 h) periods. All the groups were sacrified 24 h later except group 6. CAPE was injected 2 days with the same dose to the group 6 and it was sacrified 48 h later. One testis removed and fixed in Bouin's solution. After routine tissue processing myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) immunohistochemical methods were studied from paraffin embedded tissues. Treating rats with CAPE (applied at 10 micromol/kg, 30 min prior to T/D) attenuated the testicular injury and as well as the tissue levels of MPO. At the same time testis tissue showed a decrease in iNOS activity. Our results suggest that CAPE treatment have a protective role on testicular T/D and this effect may be due to inhibiting the neutrophil mediated cellular injury.
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PMID:The effect of caffeic acid phenethyl ester (CAPE) on histopathological changes in testicular ischemia-reperfusion injury. 1688 63


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