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Página 1 a partir de 142 resultados
Inhibition of the nitric oxide/cyclic guanosine monophosphate pathway limited the cardioprotective effect of post-conditioning in hearts with apical myocardial infarction.
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Reperfusion damage involves opening of the mitochondrial permeability transition pore (mPTP) and loss of ATP synthesis. Several cardioprotective pathways are activated by ischemic or pharmacological post-conditioning (PC). The mechanisms that are activated by PC in no co-morbidity murine models
Rapid decrease in cyclic 3'5'-guanosine monophosphate in the earliest phase of acute myocardial infarction.
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Nitric oxide for inhalation in ST-elevation myocardial infarction (NOMI): a multicentre, double-blind, randomized controlled trial.
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UNASSIGNED
Inhalation of nitric oxide (iNO) during myocardial ischaemia and after reperfusion confers cardioprotection in preclinical studies via enhanced cyclic guanosine monophosphate (cGMP) signalling. We tested whether iNO reduces reperfusion injury in patients with ST-elevation myocardial
Therapeutic effects of continuous infusion of brain natriuretic peptides on postmyocardial infarction ventricular remodelling in rats.
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BACKGROUND
Previous studies have shown protective effects of brain natriuretic peptide (BNP) against the postmyocardial infarction (MI) remodelling process. The transcription factor NF-κB is known to play an important role after MI.
OBJECTIVE
To investigate if NF-κB is involved in the protective
Carperitide induces coronary vasodilation and limits infarct size in canine ischemic hearts: role of NO.
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Carperitide is effective for heart failure (HF) owing to its diuretic and vasodilatory effects. This recombinant peptide may also have direct cardioprotective effects because carperitide reduces the severity of heart failure and limits infarct size. Because coronary vasodilation is an important
Relationship between gene polymorphism of the PAI-1 promoter and myocardial infarction.
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OBJECTIVE
To investigate the association between gene polymorphism of the plasminogen activator inhibitor-1 (PAI-1) and myocardial infarction (MI) in Chinese.
METHODS
PAI-1 genotyping with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and allele specific polymerase
DNA and RNA oxidative damage are associated to mortality in patients with cerebral infarction.
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Infarct limitation by a protein kinase G activator at reperfusion in rabbit hearts is dependent on sensitizing the heart to A2b agonists by protein kinase C.
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PKG activator 8-(4-chlorophenylthio)-guanosine 3',5'-cyclic monophosphate (CPT) at reperfusion protects ischemic hearts, but the mechanism is unknown. We recently proposed that in preconditioned hearts PKC lowers the threshold for adenosine to initiate signaling from low-affinity A2b receptors
B-type natriuretic peptide infusions in acute myocardial infarction.
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BACKGROUND
Natriuretic peptides have actions likely to ameliorate cardiac dysfunction. B-type natriuretic peptide (BNP) is indicated as treatment for decompensated cardiac failure.
OBJECTIVE
To determine the utility of BNP in acute myocardial infarction (MI).
METHODS
Double-blind randomised
Atrial natriuretic peptide administered just prior to reperfusion limits infarction in rabbit hearts.
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We investigated whether atrial natriuretic peptide (ANP) given just prior to reperfusion reduces infarction in rabbit hearts and whether protection is related to activation of protein kinase G (PKG). Isolated rabbit hearts were subjected to a 30-min period of regional ischemia; treated hearts
B-type natriuretic peptide and cardiac remodelling after myocardial infarction: a randomised trial
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Objective: B-type natriuretic peptide (BNP) has favourable effects on left ventricular remodelling, including antifibrotic and antiapoptotic properties. We tested the hypothesis that infusion of BNP after an acute myocardial infarction
Discrepant outcome between myocardial energy-related metabolites and infarct size limitation during retroperfusion of the coronary sinus.
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The basic idea of retroperfusion of the coronary sinus (RCS) is to ameliorate detrimental consequences of myocardial ischaemia. Several experimental models of RCS have been introduced, most with an emphasis on functional myocardial status. Since only few studies have been devoted to energy metabolic
NO-independent stimulation or activation of soluble guanylyl cyclase during early reperfusion limits infarct size.
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OBJECTIVE
Guanylyl cyclase-cyclic guanosine monophosphate signalling plays an important role in endogenous cardioprotective signalling. The aim was to assess the potential of direct pharmacological activation and stimulation of soluble guanylyl cyclase, targeting different redox states of the
Guanosine 3', 5'-cyclic monophosphate level in plasma of patients with cancer and various diseases.
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Guanosine 3'5'-cyclic monophosphate (cGMP) in the plasma of normal persons and patients with lung or breast cancer and other kinds of neoplasma or other diseases was determined using radioimmunoassay. In comparison with normal persons, significant elevation occurred in the cGMP in the plasma of
Role of cyclic guanosine monophosphate in late preconditioning in conscious rabbits.
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BACKGROUND
Although NO has been shown to serve both as the trigger and the mediator of the late phase of ischemic preconditioning (PC), it is unknown whether NO acts via activation of soluble guanylate cyclase (sGC). The objective of this study was to investigate the role of sGC in late PC in
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