Initial Reperfusion with Magnesium after Cardioplegic Arrest Attenuates Myocardial Reperfusion Injury*

Fuchs, Felipe Costa; Meßmer, K.; Kuppe, Herrmann; Habazettl, Helmut

doi:10.1055/s-2002-33091

Cited by 2 publications

(4 citation statements)

References 22 publications

(33 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In vitro studies showed a decrease in lethal cellular injury, but in vivo studies in rabbits showed no myocardial improvement in clinically appropriate dosages (173). Magnesium ion (Mg 2+ ) is an antagonist to Ca 2+ , a cofactor to more than 300 enzymes, and when added to cardioplegia solutions myocardial recovery is enhanced (174). This effect is believed to transpire via the Ca 2+ channel blocking mechanism derived from Mg 2+ (174)(175)(176).…”

Section: Inhibition Of Myocyte Hypercontracturementioning

confidence: 99%

“…Magnesium ion (Mg 2+ ) is an antagonist to Ca 2+ , a cofactor to more than 300 enzymes, and when added to cardioplegia solutions myocardial recovery is enhanced (174). This effect is believed to transpire via the Ca 2+ channel blocking mechanism derived from Mg 2+ (174)(175)(176). Mg 2+ effects on Ca 2+ are believed to also decrease MPT incidence and mitochondria injury (79).…”

Section: Inhibition Of Myocyte Hypercontracturementioning

confidence: 99%

See 1 more Smart Citation

Myocardial Reperfusion Injury: Etiology, Mechanisms, and Therapies

Hoffman

Gilbert

Poston

et al. 2004

J Extra Corpor Technol

117

View full text Add to dashboard Cite

Reperfusion of ischemic myocardium is required for tissue survival; however, reperfusion elicits pathologic consequences. Myocardial reperfusion injury is a multifarious process that is mediated in part by oxygen free radicals, neutrophil–endothelium interactions, apoptosis, and intracellular calcium overload. The oxygen paradox describes the contradictory need to delivery oxygen to ischemic tissue and the resultant reduction of oxygen to form free radicals that are involved in macromolecule oxidation, membrane disfunction, apoptosis, and damaged calcium sequestering ability, which results in hypercontracture. These cell-damaging crises are amplified by the excessive activation of neutrophils, which promote the formation of proinflammatory mediators, oxygen radicals, and the reduction of endothelial nitric oxide formation, leading to increased neutrophil–endothelium interactions and capillary occlusion. Neutrophil action is twofold, however, because it is required for necrotic debris removal after severe ischemia. The oxygen radicals produced by neutrophils, endothelium, and myocytes may also play a role in activating the apoptotic cascade. Although the role of apoptosis in reperfusion injury is controversial, apoptotic cells are found in infarcted tissue. One of the key mediators may be increased inner mitochondrial membrane permeability, resulting in reduced ATP formation, release of cytochrome c, and caspase activation, which is key to promotion of apoptosis. Increased mitochondrial membrane permeability occurs during exposure to supraphysiological calcium concentrations. This occurs because of compensatory Na+/Ca2+ exchange to remove the excess intracellular sodium resulting from decreased Na+/K+ pumping during ischemia and increased Na+/H+ exchange following reperfusion. Supraphysiological calcium elicits hypercontracture and cellular damage. The various therapies being developed to diminish myocardial reperfusion injury involve inhibition of the processes described above as well as others. Although single therapies have shown some promise, the complexity of the response to reperfusion has made dramatic improvement elusive. Effective treatment will most likely require multifaceted antagonism of the numerous pathological cascades initiated by reperfusion.

show abstract

Section: Inhibition Of Myocyte Hypercontracturementioning

confidence: 99%

Section: Inhibition Of Myocyte Hypercontracturementioning

confidence: 99%

Myocardial Reperfusion Injury: Etiology, Mechanisms, and Therapies

Hoffman

Gilbert

Poston

et al. 2004

J Extra Corpor Technol

117

View full text Add to dashboard Cite

show abstract

“…A number of cardiovascular disorders have been associated with low extracellular or intracellular concentrations of Mg, including myocardial infarction, arrhythmias and congestive heart failure 1–4 . Elevated extracellular Mg concentrations are used in cardioplegic solutions, where Mg improves myocardial recovery 5,6 . Given the variety of clinical uses of elevated Mg concentrations and the implication of imbalances in Mg in cardiovascular pathophysiologies, 7–9 the clinical application of Mg therapy remains controversial in acute myocardial infarction 7,10 .…”

Section: Introductionmentioning

confidence: 99%

“…Magnesium is an important cofactor for many enzymatic reactions 16 and could stimulate purine nucleoside formation in the intact myocardium 5,16,17 . Adenosine is known to confer significant protection to the myocardium 18–20 .…”

Section: Introductionmentioning

confidence: 99%

Anti‐infarct effect of magnesium is not mediated by adenosine A₁ receptors in rat globally ischaemic isolated hearts

Ebrahimi

Faghihi

Keshavarz

et al. 2004

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. The aim of present study was to investigate the effects of magnesium (Mg) on cardiac function and infarct size and to compare it effects with those of adenosine. The mechanism of Mg-mediated cardioprotection was explored by combined use of Mg and a selective adenosine A(1) receptor antagonist. 2. Rat isolated hearts were used for Langendorff perfusion. Hearts were either non-preconditioned or preconditioned with Mg (6 mmol/L) or adenosine (1 mmol/L) before 30 min sustained ischaemia followed by 120 min reperfusion. Within each of these protocols, hearts were divided into two groups; one group was exposed to the A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 200 nmol/L). Infarct size was measured by the triphenyltetrazolium chloride method. Left ventricular function was assessed by left ventricular developed pressure (LVDP), the product of heart rate x LVDP and coronary flow (CF). 3. The administration of Mg had an anti-infarct effect independent of its effect on postischaemic functional recovery in rats. Both Mg and adenosine equipotently reduced infarct size, but this effect of Mg was not blocked by the simultaneous administration of DPCPX. Cardiac function was improved by both adenosine and Mg and blockade of adenosine A(1) receptors attenuated these effects for both agents. 4. In conclusion, the results of the present study indicate that stimulation of adenosine A(1) receptors is not responsible for the anti-infarct effect of Mg in ischaemic myocardium in rats, but that the Mg-mediated protection of postischaemic functional recovery in rats is mediated by these receptors.

show abstract

Initial Reperfusion with Magnesium after Cardioplegic Arrest Attenuates Myocardial Reperfusion Injury*

Cited by 2 publications

References 22 publications

Myocardial Reperfusion Injury: Etiology, Mechanisms, and Therapies

Myocardial Reperfusion Injury: Etiology, Mechanisms, and Therapies

Anti‐infarct effect of magnesium is not mediated by adenosine A₁ receptors in rat globally ischaemic isolated hearts

Contact Info

Product

Resources

About

Initial Reperfusion with Magnesium after Cardioplegic Arrest Attenuates Myocardial Reperfusion Injury*

Cited by 2 publications

References 22 publications

Myocardial Reperfusion Injury: Etiology, Mechanisms, and Therapies

Myocardial Reperfusion Injury: Etiology, Mechanisms, and Therapies

Anti‐infarct effect of magnesium is not mediated by adenosine A1 receptors in rat globally ischaemic isolated hearts

Contact Info

Product

Resources

About

Anti‐infarct effect of magnesium is not mediated by adenosine A₁ receptors in rat globally ischaemic isolated hearts