A depressão miocárdica pós-isquemia/reperfusão não altera a resposta cardíaca à elevação da freqüência de contrações

Abstract

ObjectiveTo assess the influence of the postischemia/reperfusion stunned myocardium (PIRSM) on the inotropic and lusitropic effects of heart rate (HR). [2][3][4][5][6] showed that postischemia/reperfusion stunned myocardium is generated by 2 factors: 1) the action of reactive oxygen species released during reperfusion, and 2) the increase in intracellular calcium concentration (calcium overload) that occurs during both ischemia and reperfusion. Calpaine, a protease that promotes the lysis of troponin I, plays a relevant role in triggering myocardial depression after ischemia/reperfusion. The consequence is the decrease in the myofilament reactivity to calcium, the typical functional impairment of postischemia/reperfusion stunned myocardium. In this circumstance, the affinity of the ligation between troponin and calcium decreases, the quantity of the ion bound to troponin decreases, and, consequently, myocardial contractility decreases. Latency in the recovery of the inotropism lasts until troponin I integrity is reestablished. Methods Nine preparations of isolated dog hearts in isovolumic conVery convincing indications exist that calcium kinetics is not altered in myocardial depression following ischemia/reperfusion. Therefore, postischemia/reperfusion stunned myocardium has been proven not to reduce the intracellular content of the ion 3,4,7 and to preserve the physiological and pharmacological maneuvers that stimulate inotropism by increasing the intracellular content of calcium ([Ca] i ): beta-adrenergic agonists 8-11 , milrinone 8,12 , calcium administration 5,13 , postpause potentiation 14 , and postextrasystolic potentiation 9,13 . However, the positive inotropic effect depending on heart rate elevation studied in myocardial segments of dogs undergoing regional ischemia has been reported to transform into negative inotropic action after myocardial ischemia/reperfusion 12 . If this inversion of the myocardial response to heart rate elevation is confirmed, the concept of the integrity of calcium kinetics after periods of ischemia/reperfusion should be revised, because, typically, the inotropic action linked to heart rate fluctuations is a physiological maneuver that depends exclusively on calcium kinetics.In most mammals, heart rate elevations trigger the stimulus to myocardial inotropism. This stimulating effect of heart rate on myocardial contractility was given the name the Bowditch effect or treppe phenomenon. Two mechanisms fundamental to the positive inotropic action of the Bowditch effect are 1) an increase in intracellular sodium concentration followed by the reverse action of the sodium/calcium exchanger protein, and consequent elevation in intracellular calcium concentration ([Ca] i ) 15 and 2) an increase

Proteção miocárdica ao coração hipertrofiado: o eterno desafio

“…Fat acids constitute the main energy supply to the myocardium. Nevertheless, glucose plays an important role in this metabolism, once several constituents of their degradation are critical to Krebs cycle adequate functioning [27]. During ischemia, a decline of myocardial metabolism occurs, which eliminates the energy expenditure for contractile activity and focus on maintaining cellular integrity, delaying muscle contraction and relaxation through two mechanisms: initially, an increase on hydrogen ions competing for calcium ions based on troponin activation sites occurs, lentifying the actin-myosin activation and, consequently, the contraction.…”