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6 resultats
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
Pretreatment with the gap junction uncoupler heptanol does not limit infarct size in rabbit heart.
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Previous findings indicate that heptanol, an agent well-recognized to disrupt chemical signaling between myocytes by uncoupling of gap junctions, significantly limited infarct size when administered at the time of reperfusion. Our aim was to assess on the potential role of cell--cell communication
The gap junction uncoupler heptanol abrogates infarct size reduction with preconditioning in mouse hearts.
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BACKGROUND
Emerging evidence suggests that gap junction-mediated intercellular transmission of ions, metabolites and/or second messengers may serve as important determinants of myocyte viability. Our aim was to determine, using isolated buffer-perfused mouse hearts, whether the cardioprotection
Spatially and temporally distinct expression of fibroblast connexins after sheep ventricular infarction.
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OBJECTIVE
Myocardial infarction leads to extensive changes in the organization of cardiac myocytes and fibroblasts, and changes in gap junction protein expression. In the immediate period following ischemia, reperfusion causes hypercontraction, spreading the necrotic lesion. Further progressive
Hydrogen peroxide increases gap junctional communication and induces astrocyte toxicity: regulation by brain macrophages.
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Cultured astrocytes are highly coupled by gap junction channels mainly constituted by connexin 43. We have previously shown that gap junctional communication (GJC) represents a functional property of astrocytes that is a target for their interaction with other brain cell types, including neurons and
ACUTE RETINAL DAMAGE AFTER USING A TOXIC PERFLUORO-OCTANE FOR VITREO-RETINAL SURGERY.
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OBJECTIVE
To describe a series of retinal acute toxicity cases with severe visual loss after intraocular use of a toxic perfluoro-octane (PFO). The clinical presentation is described, and the likely causes are analyzed. New biological methods for testing safety of intraocular medical devices are
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