metabolismo miocárdico após cardioplegia sangüínea hipotérmica retrógrada contínua com indução anterógrada normotérmica myocardial metabolism after hypothermic retrograde continuous blood cardioplegia with anterograde warm cardioplegic induction

Clicks: 315
ID: 130428
2005
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Abstract
OBJETIVO: Determinar as alterações sofridas pelo miocárdio durante a cardioplegia sangüínea hipotérmica retrógrada contínua com a adição da indução cardioplégica anterógrada normotérmica. MÉTODO: Análise metabólica da cardioplegia sangüínea hipotérmica retrógrada contínua com indução anterógrada normotérmica em estudo prospectivo de 15 pacientes consecutivos. Amostras de sangue arterial e do seio coronário foram simultaneamente colhidas para análise do conteúdo de oxigênio e da concentração de lactato. Quatro biópsias miocárdicas foram obtidas para análise dos níveis de ATP, ADP, AMP e lactato no miocárdio. A isoenzima CK-MB foi analisada no sangue venoso. RESULTADOS: Não houve mortalidade no grupo. Nenhum paciente necessitou de suporte inotrópico na saída de CEC e não foi detectado IAM per ou pós-operatório. Ocorreu diminuição da extração artério-venosa do lactato e do oxigênio pelo coração durante a reperfusão, havendo uma recuperação parcial ao final de 60 minutos de reperfusão. Os níveis miocárdicos de ATP e de seus nucleotídeos foram mantidos durante o pinçamento aórtico, porém houve redução destes nos primeiros 30 minutos de reperfusão. O lactato acumulou-se no músculo cardíaco durante o pinçamento aórtico, havendo redução durante a reperfusão. CONCLUSÕES: Concluímos por uma análise metabólica que o método não conseguiu evitar o metabolismo anaeróbico durante o período de pinçamento aórtico e que somente com 60 minutos de reperfusão foi observado um grau de recuperação metabólica satisfatória. Provavelmente essas alterações são devido à injúria isquêmica celular ocorrida durante o pinçamento aórtico e parecem ter efeito transitório. Observamos melhora da proteção miocárdica com o acréscimo da indução cardioplégica anterógrada normotérmica.
OBJECTIVE: To determinate the alterations suffering by myocardium in the hypothermic retrograde continuous blood cardioplegia with antegrade warm cardioplegic induction. METHOD: A metabolic analysis of hypothermic retrograde continuous blood cardioplegia with antegrade warm cardioplegic induction was performed in a prospective study of 15 patients scheduled for elective coronary artery bypass grafting. Arterial and coronary sinus blood samples were simultaneously taken: before establishing cardiopulmonary bypass, after anterograde warm cardioplegic induction, when the aortic clamp was removed and 10, 30 and 60 minutes after reperfusion to analyze the oxygen content and lactate concentration. Four transmural left ventricular biopsy samples were obtained: before aortic clamping, immediately after the initial cardioplegia bolus, immediately before aortic declamping and 30 minutes after reperfusion to analyze the levels of ATP, ADP, AMP and lactate in the myocardium. The CK-MB isoenzyme was analysed in venous blood samples. RESULTS: There were no mortalities in the group. Inotropic support was not necessary in any patients and no peri- or post-operative myocardial infarction was detected. There was a decrease in the arterial-venous extraction of oxygen and lactate in the heart during reperfusion, a partial recovery occurred at 60 minutes of reperfusion. The levels of ATP and the other nucleotides in the myocardium were maintained during aortic clamping, but these levels decreased during the first 30 minutes of reperfusion. The lactate accumulated in the heart muscle during aortic clamping with a decrease occurring during reperfusion. CONCLUSIONS: From a metabolic point of view the method could not avoid an anaerobic metabolism during cross-clamping and only after 60 minutes of reperfusion there was a satisfactory metabolic recovery. These alterations are probably a reflection of cellular ischemic injury that occurs during cross-clamping and they seem to be of transitory effect. A better myocardium protection was observed with the addiction of anterograde warm induction cardioplegia.
Reference Key
sobrosa2005brazilianmetabolismo Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Claudio G. Sobrosa;Eva Jansson;Lennart Kaijser;Vollmer Bomfim
Journal 2017 international conference on information technology systems and innovation, icitsi 2017 - proceedings
Year 2005
DOI
10.1590/S0102-76382005000400010
URL
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382005000400010
Keywords
adenosine triphosphate heart arrest induced

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