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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
Reentrant circuits and the effects of heptanol in a rabbit model of infarction with a uniform anisotropic epicardial border zone.
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BACKGROUND
The purpose was to study reentry in a rabbit model of infarction.
RESULTS
A model of an infarct epicardial border zone was produced in Langendorff perfused rabbit hearts by freezing the inner two thirds of the left ventricular wall, allowing only a thin epicardial muscle layer to survive.
Heptanol triggers cardioprotection via mitochondrial mechanisms and mitochondrial potassium channel opening in rat hearts.
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OBJECTIVE
To investigate mechanisms behind heptanol (Hp)-induced infarct size reduction and in particular if protection by pre-treatment with Hp is triggered through mitochondrial mechanisms.
METHODS
Langendorff perfused rat hearts, isolated mitochondria and isolated myocytes were used. Infarct
Effect of coronary perfusion of heptanol or potassium on conduction and ventricular arrhythmias.
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Abnormalities in cellular coupling, modulated in part by intracellular gap junctions, have an important role in the genesis of reentrant arrhythmias in the setting of chronic myocardial infarction. The effects of heptanol, which has a relatively selective action on gap junctional resistance at low
Effect of cellular uncoupling by heptanol on conduction in infarcted myocardium.
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Experiments were performed in vitro on six normal thin ventricular epicardial tissue strips and 10 strips removed from the infarcted regions of dogs 21-60 days after experimental myocardial infarction. Conduction was evaluated by mapping activation sequences at 40-45 sites over an area of 1 x 2 cm
The Effects of Heptanol on Electrical Coupling during Ischemia in the Perfused Isolated Rat Heart.
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The aims of the present study were to examine the effect of heptanol on electrical coupling during ischemia, and to assess whether changes in electrical coupling by heptanol is associated with its cardiac protection. Perfused isolated rat hearts were subjected to a 24 min infusion of heptanol (0.05,
The effect of heptanol on the electrical and contractile function of the isolated, perfused rabbit heart.
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Changes in cardiac gap junction expression, such as those following myocardial infarction and produced in connexin knockout mice, are associated with a predisposition to arrhythmias. The present experiments investigated the effects of heptanol, a reversible gap junction inhibitor, on isolated
Delayed uncoupling contributes to the protective effect of heptanol against ischaemia in the rat isolated heart.
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1. It is known that infusion of the gap junction uncoupler heptanol, before ischaemia or during reperfusion, limits myocardial infarct size. However, whether this cardiac effect is linked to the effect of heptanol on communication across gap junctions has not been elucidated. The aims of the present
Protective role of gap junctions in preconditioning against myocardial infarction.
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The aim of the present study was to examine the hypothesis that acceleration of gap junction (GJ) closure during ischemia contributes to anti-infarct tolerance afforded by preconditioning (PC). First, the effects of PC on GJ communication during ischemia were assessed. Isolated buffer-perfused
Pretreatment with D-myo-inositol trisphosphate reduces infarct size in rabbit hearts: role of inositol trisphosphate receptors and gap junctions in triggering protection.
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Pretreatment with D-myo-inositol-1,4,5-trisphosphate hexasodium (D-myo-IP(3)), the sodium salt of the second messenger inositol 1,4,5-trisphosphate (IP(3)), is cardioprotective and triggers a reduction of infarct size comparable in magnitude to that obtained with ischemic preconditioning. However,
Effect of coronary perfusion of heptanol on conduction and ventricular arrhythmias in infarcted canine myocardium.
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BACKGROUND
Abnormal cellular coupling is a major constituent of the slow, dissociated conduction that supports ventricular tachycardia (VT) following myocardial infarction. Agents that modulate cellular coupling may exert either proarrhythmic or antiarrhythmic effects.
RESULTS
The effects of
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
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
Electromechanical coupling between skeletal and cardiac muscle. Implications for infarct repair.
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Skeletal myoblasts form grafts of mature muscle in injured hearts, and these grafts contract when exogenously stimulated. It is not known, however, whether cardiac muscle can form electromechanical junctions with skeletal muscle and induce its synchronous contraction. Here, we report that
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