Brazilian Journal of Cardiovascular Surgery (Apr 1997)

Proteção cerebral durante parada circulatória total a 28°C

  • Carlos Luiz FILGUEIRAS,
  • Maurício EDE,
  • Lowrence Ryner,
  • Jian YE,
  • Alex ARONOV,
  • Piotr KOZLOWSKI,
  • Jiankang SUN,
  • Loujia YANG,
  • John K. Saunders,
  • Roxane DESLAURIERS,
  • Tomas A SALERNO

DOI
https://doi.org/10.1590/S0102-76381997000200014
Journal volume & issue
Vol. 12, no. 2
pp. 197 – 207

Abstract

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As operações de aneurismas do arco aórtico dependem do tempo de parada circulatória hipotérmica total (PCH). Diversas técnicas têm sido propostas para melhorar a proteção do cérebro e estender o tempo seguro de isquemia (45 minutos em hipotermia profunda). A proteção cerebral durante duas horas de parada circulatória hipotérmica foi estudada em 23 suínos, divididos em quatro grupos. Nos grupos de controle, 8 animais foram submetidos a anestesia (Grupo 1) e a circulação extracorpórea (Grupo 2). Os outros dois grupos foram à PCH associada à perfusão cerebral anterógrada a 28°C (Grupo 3) e a PCH associada a perfusão retrógrada do cérebro a 28°C (Grupo 4). A proteção cerebral foi avaliada pelo estudo histológico e pelo metabolismo celular cerebral estudado pela espectroscopia por ressonância nuclear magnética (RNM). Durante a PCH associada à perfusão cerebral anterógrada a 28°C, o metabolismo cerebral manteve-se normal durante todo o experimento e houve preservação das estruturas cerebrais no estudo histológico. Na PCH com a perfusão cerebral retrógrada a 28°C, o pH intracelular, a fosfocreatina (PCr) e o trifosfato de adenosina (ATP) diminuíram durante o período de parada circulatória e não retornaram aos seus níveis normais durante a reperfusão, permanecendo o cérebro em grave acidose intracelular. Concluímos que, durante duas horas de PCH, a perfusão anterógrada a 28°C proporcionou uma adequada proteção ao cérebro. A PCH associada à perfusão retrógrada em hipotermia moderada a 28°C não proporcionou proteção cerebral, no estudo metabólico e histológico.Aortic surgical treatment of aneurysms is time dependent on the hypothermic circulatory arrest. Many techniques have been proposed to improve brain protection and increase safe time of ischemia (45 minutes in deep hypothermia). Brain protection during two hours of hypothermic circulatory arrest was studied in twenty-three animals that were divided in four groups. In the control groups, eight animals were submitted to anesthesia (group I) and extracorporeal circulation alone (group II). The other two groups underwent circulatory arrest associated with antegrade brain perfusion at 28°C (group III) and hypothermic circulatory arrest with retrograde brain perfusion at 28°C (group IV). Brain protection was evaluated by the histologic study and by the cellular brain metabolism which was studied by 31P Nuclear Magnetic Resonance spectroscopy. During circulatory arrest with antegrade brain perfusion at 28°C, the cellular metabolism remained normal during all the experiments and the brain structures were preserved. In the circulatory arrest with retrograde brain perfusion at 28°C, the intracellular brain pH, phosphocreatine (PCr) and adenosine triphosphate (ATP) decreased during the circulatory arrest period, and did not recover normal levels during reperfusion, the brain remained in severe intracellular acidosis. We conclude that during two hours of hypothermic circulatory arrest, antegrade perfusion at 28°C provides adequate brain protection. The hypothermic circulatory arrest associated with retrograde perfusion at 28°C does not protect the brain, from a metabolic and histologic point of view.

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