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9 resultats
Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts.
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It has been shown that cell-to-cell chemical coupling may persist during severe myocardial hypoxia or ischemia. We aimed to analyze the effects of different, chemically unrelated gap junction uncouplers on the progression of ischemic injury in hypoxic myocardium. First, we analyzed the effects of
Dexmedetomidine protects against apoptosis induced by hypoxia/reoxygenation through the inhibition of gap junctions in NRK-52E cells.
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OBJECTIVE
The α2-adrenoceptor inducer dexmedetomidine (Dex) provides renoprotection against ischemia/reperfusion (I/R) injury, but the mechanism of this effect is largely unknown. The present study investigated the effect of Dex on apoptosis induced by hypoxia/reoxygenation (H/R) and the
Gap junction uncoupler heptanol prevents cell-to-cell progression of hypercontracture and limits necrosis during myocardial reperfusion.
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BACKGROUND
The objective of this study was to test the hypothesis that chemical interaction through gap junctions may result in cell-to-cell progression of hypercontracture and that this phenomenon contributes to the final extent of reperfused infarcts.
RESULTS
Cell-to-cell transmission of
Protection of isolated rat heart against the Ca2+ paradox. Are gap junction channels involved?
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Enzyme release from isolated Langendorff-perfused rat hearts was studied under various protective conditions against the Ca2+ paradox. In addition sarcosolic free cation concentrations and the membrane potential were measured employing ion-selective microelectrode techniques during Ca(2+)-free
Endocochlear potential and endolymphatic K+ changes induced by gap junction blockers.
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OBJECTIVE
To examine the effects of gap junction blockers on the endocochlear potential (EP) and endolymphatic potassium concentration ([K(+)](e)).
METHODS
The EP and [K(+)](e) were monitored using double-barreled ion-selective microelectrodes in the second turn of the guinea pig cochlea during
Involvement of gap junctions between smooth muscle cells in sustained hypoxic pulmonary vasoconstriction development: a potential role for 15-HETE and 20-HETE.
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In response to hypoxia, the pulmonary artery normally constricts to maintain optimal ventilation-perfusion matching in the lung, but chronic hypoxia leads to the development of pulmonary hypertension. The mechanisms of sustained hypoxic pulmonary vasoconstriction (HPV) remain unclear. The aim of
Gap junctions support the sustained phase of hypoxic pulmonary vasoconstriction by facilitating calcium sensitization.
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OBJECTIVE
To determine the role of gap junctions (GJs) in hypoxic pulmonary vasoconstriction (HPV).
RESULTS
Studies were performed in rat isolated intrapulmonary arteries (IPAs) mounted on a myograph and in anaesthetized rats. Hypoxia induced a biphasic HPV response in IPAs preconstricted with
Stem cell-based delivery of Hypoxamir-210 to the infarcted heart: implications on stem cell survival and preservation of infarcted heart function.
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This study seeks to test our hypothesis that transgenic induction of miR-210 in mesenchymal stem cells (MSC) simulates the pro-survival effects of ischemic preconditioning (IPC) and that engraftment of (PC)MSC helps in the functional recovery of ischemic heart by miR-210 transfer to host
Inhibition of gap junction composed of Cx43 prevents against acute kidney injury following liver transplantation.
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Postoperative acute kidney injury (AKI) is a severe complication after liver transplantation (LT). Its deterioration and magnification lead to the increase in mortality. Connexin43 (Cx43) mediates direct transmission of intracellular signals between neighboring cells, always considered to be the
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