Journal of cardiovascular pharmacology
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J. Cardiovasc. Pharmacol. · Apr 2009
ReviewEffects of levosimendan on the energy balance: preclinical and clinical evidence.
Levosimendan is a novel inodilator agent, which enhances myocardial performance without substantial changes in oxygen consumption. The combination of positive inotropic and vasodilator effects of levosimendan relates to its Ca-sensitizing and K channel opening effects. Levosimendan is one of the best documented pharmacological agents used in the management of acute heart failure syndromes. ⋯ The ability of levosimendan to improve myocardial function without substantially increasing oxygen consumption may appear paradoxical but is indeed possible via improved efficacy, not only with regard to the effects on the contractile apparatus of the cardiomyocytes but also when its composite hemodynamic effects are considered. The energy balance equation, therefore, should take into account the effect of levosimendan on all energy-consuming and energy-producing paths. Moreover, levosimendan-evoked KATP channel opening may possess favorable effects on mitochondrial adenosine triphosphate synthesis conferring cardioprotection during ischemic insults.
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J. Cardiovasc. Pharmacol. · Mar 2009
Clinical TrialRapid detection of acute kidney injury by plasma and urinary neutrophil gelatinase-associated lipocalin after cardiopulmonary bypass.
Cardiopulmonary bypass (CPB) is associated with a significant risk of postoperative renal dysfunction. We studied the utility of a novel biomarker in predicting acute kidney injury (AKI) in adult patients undergoing cardiac surgery. ⋯ Measurement of this novel biomarker in the urine or plasma of patients in the first hours after CPB is predictive of subsequent renal injury. Although the AUC for plasma NGAL seemed inferior to urine, even an AUC of 0.8 as reported compares very favorably to that for other "outstanding" biomarkers (eg, AUCs in the 0.7 range for troponin).
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J. Cardiovasc. Pharmacol. · Dec 2008
Randomized Controlled TrialProtective effect of ambroxol on pulmonary function after cardiopulmonary bypass.
To evaluate whether ambroxol administered orally during the perioperative period has a protective effect against postoperative pulmonary dysfunction in on-pump coronary artery bypass surgery. ⋯ In on-pump coronary artery bypass grafting, ambroxol improves postoperative PFTs and PaO2 levels without any significant clinical implication, and it exerts these effects possibly in ways other than surfactant modulation.
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J. Cardiovasc. Pharmacol. · Dec 2008
Ivabradine induces an increase in ventricular fibrillation threshold during acute myocardial ischemia: an experimental study.
Tachycardia often facilitates ischemic ventricular fibrillation (VF). ⋯ HR reduction and the decrease in myocardial damage induced by IVA protected against primary ischemic VF without altering myocardial contractility.
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J. Cardiovasc. Pharmacol. · Sep 2008
Acute effect of sidestream cigarette smoke extract on vascular endothelial function.
Acute exposure to passive smoking adversely affects vascular function by promoting oxidative stress and endothelial dysfunction. However, it is not known whether tobacco sidestream (SS) smoke has a greater deleterious effect on the endothelium than non-tobacco SS smoke and whether these effects are related to nicotinic endothelial stimulation. To test these hypotheses, endothelial-dependent relaxation and superoxide anion production were assessed in isolated rat aortas incubated with tobacco SS smoke, non-tobacco SS smoke, or pure nicotine. ⋯ Furthermore, concentration-response curves to Ach and superoxide production remained unaltered with nicotine (0.001, 0.01, or 0.1 mM). In conclusion, despite similar increases in vascular wall superoxide production with tobacco and non-tobacco SS smoke, only the tobacco SS smoke extracts affected endothelium-dependent vasorelaxation. Nicotine alone does not reproduce the effects seen with tobacco SS smoke, suggesting that the acute endothelial toxicity of passive smoking cannot simply be ascribed to a nicotine-dependent mechanism.