Pharmacological preconditioning of ATP‐sensitive potassium channel openers on acute urinary retention‐induced bladder dysfunction in the rat

Ohmasa, Fumiya; Saito, Motoaki; Oiwa, Harunori; Tsounapi, Panagiota; Shomori, Kohei; Kitatani, Kazuyuki; Dimitriadis, Fotios; Kinoshita, Yukako; Satoh, Keisuke

doi:10.1111/j.1464-410x.2012.10965.x

Cited by 7 publications

(7 citation statements)

References 33 publications

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“…IPreC is applied before severe ischemic stress, which renders the organ resistant to subsequent I‐R injury . There are numerous reports that IPreC provides strong protection against I‐R injury in various organs, such as the heart, brain, skeletal muscle, lung, liver, intestine, kidney, bladder and endothelial cells . However, the occurrence of testicular torsion cannot be predicted.…”

Section: Iprec and Ipostcmentioning

confidence: 99%

“…75 There are numerous reports that IPreC provides strong protection against I-R injury in various organs, such as the heart, brain, skeletal muscle, lung, liver, intestine, kidney, bladder and endothelial cells. [76][77][78] However, the occurrence of testicular torsion cannot be predicted. The use of IPreC in the case of testicular torsion is limited because of the unpredictable nature of this clinical emergency.…”

Section: Iprec and Ipostcmentioning

confidence: 99%

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Testicular torsion–detorsion and potential therapeutic treatments: A possible role for ischemic postconditioning

et al. 2016

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Testicular torsion is a common urological emergency among adolescent boys and young men. Rotation of the testis and twisting of the spermatic cord rapidly leads to ischemia, resulting in a loss of germ cells. Thus, prompt diagnosis and urgent surgical intervention are required, but the subsequent release of the torsion induces reperfusion injury, which causes further damage to the ischemic testis. Testicular torsion -detorsion (ischemia-reperfusion) injury triggers the generation of reactive oxygen species, pro-inflammatory cytokines, neutrophil recruitment, lipid peroxidation, anoxia and apoptosis, which carry a significant risk of subsequent infertility. Previously, the effects of numerous pharmacological agents and treatments have been evaluated to prevent testicular ischemia-reperfusion injury in animal models. We propose a new treatment, especially postconditioning, to prevent adverse effects of ischemiareperfusion injury after testicular torsion-detorsion.

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Section: Iprec and Ipostcmentioning

confidence: 99%

Section: Iprec and Ipostcmentioning

confidence: 99%

Testicular torsion–detorsion and potential therapeutic treatments: A possible role for ischemic postconditioning

et al. 2016

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“…Therefore, we included an IR group which was treated with 25% DMSO 75 min after the induction of ischaemia (IR+PostDMSO; n = 6). Based on preliminary studies from our laboratory and others (Robin et al ., ; Ohmasa et al ., and Tsounapi et al ., ), we decided to use the 5‐HD at 40 mg/kg, the diazoxide at 10 mg/kg and the cromakalim at 300 μg/kg. The administration of glibenclamide 75 min after the induction of ischaemia was performed at three concentrations: 1, 5 and 10 mg/kg (IR+PostGlibenclamide1, IR+PostGlibenclamide5, IR+PostGlibenclamide10; n = 6, 6, and 5, respectively).…”

Section: Methodsmentioning

confidence: 91%

Blocking of the ATP sensitive potassium channel ameliorates the ischaemia‐reperfusion injury in the rat testis

et al. 2014

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There is increasing evidence that the effects of administered ATP sensitive potassium (KATP ) channel openers or blockers during ischaemia are still controversial in many organs/tissues. Testicular torsion detorsion which causes ischaemia-reperfusion (IR) injury, cannot be predicted, thus an effective drug should be administered during or after the ischaemia. The aim of this study was to examine whether the administration of KATP channel openers or blockers during ischaemia ameliorates IR injury in the testis. Eight-week-old male Sprague-Dawley rats were subjected to 2 h right testicular ischaemia followed by 24 h reperfusion. The selective mitochondrial (mito) KATP channel blocker, 5-hydroxydecanoate (5-HD) (40 mg/kg), the non-selective KATP channel blocker glibenclamide (5 mg/kg), the selective mito KATP channel opener diazoxide (10 mg/kg) and the non-selective KATP channel opener cromakalim (300 μg/kg) were administered intraperitoneally 15 min prior to the ischaemia or 75 min after the induction of ischaemia. Tissue damage was evaluated by malondialdehyde concentration, myeloperoxidase activity, histological evaluation and TdT-mediated dUTP nick end labelling assay in the testis. There was a significant increase in oxidative stress, neutrophil infiltration, histological damage and apoptosis in the testicular IR model. A significant reduction in the testicular IR injury was observed with the administration of glibenclamide, but not 5-HD, diazoxide or cromakalim during ischaemia. The administration of non-selective KATP channel blocker glibenclamide ameliorated the testicular IR injury. On the other hand, the selective mito KATP channel blocker, 5-HD and KATP channel openers did not reduce the testicular IR injury. These data suggest that blocking of the membrane KATP channel may have a protective effect during the testicular ischaemia. Glibenclamide could be an effective drug to manage the post-ischaemic injury caused by the testicular torsion-detorsion.

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“…LPS induced the apoptosis of cardiomyocytes. The sarcK ATP channel prevented the apoptosis of cardiomyocytes induced by oxidative stress ( 21 ) and the apoptosis of the bladder smooth muscle induced by acute urinary retention ( 22 ). The channel also exerts a protective effect against ischemia-reperfusion-induced apoptosis in testicular damage ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

Sarcolemmal ATP-sensitive potassium channel protects cardiac myocytes against lipopolysaccharide-induced apoptosis

Zhang

Yiqun

et al. 2016

International Journal of Molecular Medicine

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The sarcolemmal ATP-sensitive K+ (sarcKATP) channel plays a cardioprotective role during stress. However, the role of the sarcKATP channel in the apoptosis of cardiomyocytes and association with mitochondrial calcium remains unclear. For this purpose, we developed a model of LPS-induced sepsis in neonatal rat cardiomyocytes (NRCs). The TUNEL assay was performed in order to detect the apoptosis of cardiac myocytes and the MTT assay was performed to determine cellular viability. Exposure to LPS significantly decreased the viability of the NRCs as well as the expression of Bcl-2, whereas it enhanced the activity and expression of the apoptosis-related proteins caspase-3 and Bax, respectively. The sarcKATP channel blocker, HMR-1098, increased the apoptosis of NRCs, whereas the specific sarcKATP channel opener, P-1075, reduced the apoptosis of NRCs. The mitochondrial calcium uniporter inhibitor ruthenium red (RR) partially inhibited the pro-apoptotic effect of HMR-1098. In order to confirm the role of the sarcKATP channel, we constructed a recombinant adenovirus vector carrying the sarcKATP channel mutant subunit Kir6.2AAA to inhibit the channel activity. Kir6.2AAA adenovirus infection in NRCs significantly aggravated the apoptosis of myocytes induced by LPS. Elucidating the regulatory mechanisms of the sarcKATP channel in apoptosis may facilitate the development of novel therapeutic targets and strategies for the management of sepsis and cardiac dysfunction.

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Pharmacological preconditioning of ATP‐sensitive potassium channel openers on acute urinary retention‐induced bladder dysfunction in the rat

Cited by 7 publications

References 33 publications

Testicular torsion–detorsion and potential therapeutic treatments: A possible role for ischemic postconditioning

Testicular torsion–detorsion and potential therapeutic treatments: A possible role for ischemic postconditioning

Blocking of the ATP sensitive potassium channel ameliorates the ischaemia‐reperfusion injury in the rat testis

Sarcolemmal ATP-sensitive potassium channel protects cardiac myocytes against lipopolysaccharide-induced apoptosis

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