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      Solução cardioplégica polarizante: estado da arte Translated title: Polarizing cardioplegic solution: state of the art

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          A exegese do termo cardioplegia remete aos significados de "lesão, golpe, ataque ou ferimento", bem diferente, portanto, do sentido em que o termo é empregado na maior parte dos centros de cirurgia cardíaca do Brasil e do mundo, ou seja, como correspondendo à proteção miocárdica. Daí a melhor denominação de solução cardioplégica, para caracterizar as soluções empregadas com finalidade de promover a parada cardíaca controlada do coração. A parada cardíaca induzida por solução cardioplégica pode acontecer por hiperpolarização, despolarização ou com bloqueadores da bomba de cálcio. No presente trabalho, discorreremos sobre os principais agentes que promovem a parada cardíaca por hiperpolarização da membrana miocárdica. Com a solução hiperpolarizante, o coração pára no período diastólico, havendo uma redução ainda maior no seu gasto energético, o que propicia melhores condições ao coração quando este reinicia sua contração ao final do procedimento cirúrgico.

          Translated abstract

          The mean of the term "cardioplegia" is "lesion, attack, wound or blow", very different to how its is most commonly understood in most heart centers, where it relates to cardiac protection. Thus, "cardioplegic solution" is better defined as a solution capable of inducing cardiac arrest. Cardiac arrest induced by cardioplegic solutions can occur by hyperpolarizaton, depolarization or by inhibiting the calcium channels of the myocardial fibers. This paper discusses hyperpolarizing cardioplegic solutions, which arrest the heart in the diastolic phase, thus decreasing the ATP depletion and improving the conditions of the heart to be reanimated at the end of the procedure.

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          Most cited references 53

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          ATP-regulated K+ channels in cardiac muscle.

           A Noma (2015)
          An outward current of unknown nature increases significantly when cardiac cells are treated with cyanide or subjected to hypoxia, and decreases on intracellular injection of ATP. We report here that application of the patch-clamp technique to CN-treated mammalian heart cells reveals specific K+ channels which are depressed by intracellular ATP (ATPi) at levels greater than 1 mM. For these channels, conductance in the outward direction is much larger than the inward rectifier K+ channel which is insensitive to ATP. AMP had no effect on the ATP-sensitive K+ channel, and ADP was less effective than ATP. Thus, the ATP-sensitive K+ channel seems to be important for regulation of cellular energy metabolism in the control of membrane excitability.
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            Basic and clinical pharmacology

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              Protective effects of ATP-sensitive potassium-channel openers in experimental myocardial ischemia.

               G J Grover (1994)
              Adenosine triphosphate (ATP)-sensitive potassium channels (KATP) exist in cardiac tissue and a potential role in the pathogenesis of myocardial ischemia was hypothesized early after their discovery. Studies in in vitro models of myocardial ischemia and reperfusion have indicated that KATP openers, as a class, exert protective effects. This has been assessed by determination of recovery of contractile function, inhibition of contracture, or inhibition of necrosis. This protective effect appears to be exerted directly on the myocardium and is not dependent on peripheral or coronary dilator activities. These protective effects are uniformly abolished by blockers of KATP. The protective effects of KATP openers are accompanied by a conservation of myocardial energy during ischemia, and this occurs despite a relative lack of cardiodepressant effects. In vivo studies have shown more variable results with some investigators showing efficacy and others not showing efficacy. The lack of efficacy for some investigators may be related to the potent vasodilator activity of the KATP openers used. Efficacy for KATP openers has been shown in canine models of infarction and stunned myocardium. KATP blockers also appear to abolish the protective effects of KATP openers in these models. Future work on KATP openers is focused on the determination of the molecular mechanism of action for the cardioprotective effects of these agents, development of tissue selectivity, and the importance of action potential shortening in mediating cardioprotection.

                Author and article information

                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Brazilian Journal of Cardiovascular Surgery
                Braz. J. Cardiovasc. Surg.
                Sociedade Brasileira de Cirurgia Cardiovascular (São José do Rio Preto )
                March 2005
                : 20
                : 1
                : 69-74
                [1 ] Faculdade de Medicina de São José do Rio Preto
                [2 ] Universidade Estadual Paulista Brazil
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