Development of cardioplegic solution for heart transplant and conventional open-heart surgeries.

• Grant number: 12/09130-1
• Support Opportunities: Regular Research Grants
• Start date: October 01, 2012
• End date: September 30, 2014
• Field of knowledge: Health Sciences - Medicine - Surgery
• Principal Investigator: Orlando Petrucci Jr
• Grantee: Orlando Petrucci Jr
• Host Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

The myocardium protection during conventional open-heart surgeries and heart harvesting for heart transplantation is of crucial important. The heart has to assume its paper as a blood pump at the end of an open-heart surgery or right after a heart implant. The majority of cardioplegic solutions employed during open-heart surgeries or/and in heart transplant are hyperkalemic, and its mechanism of action is by membrane depolarization with induction of cardiac arrest. The potassium channels activation and sodium channel blockage also can produce cardiac arrest with beneficial effects during the reperfusion period. The 2,3 butanedione has a direct action by a competitive effect on actin/myosin bridges. This direct effect can lead to cardiac arrest with some evidences of beneficial effects on ATP levels during the reperfusion period.Using several ways for cardiac arrest induction may minimize the deleterious effects observed in commonly used cardioplegic solutions with high potassium concentration. Of note, some others drugs may improve the ATP levels in the harvested hearts for transplant or during open-heart surgeries with long cross clamp periods.The main objective of this project is the development of a cardioplegic and protective solution for heart transplant, originally national, and with potential employment during conventional heart surgeries. This solution should allow myocardium protection for long periods of ischemia, improving the contractility during the reperfusion period and allowing long distance for organ procurement.We work with the hypothesis that three distinct components for cardiac arrest induction (potassium channels opening, sodium channels closing, and direct effect on actin/myosin complex) in cardioplegic solutions for organ preservation may allow better hemodynamic during the reperfusion period and lower tissue lesion. The use of low concentration of three different components may reduce the risk of any toxicity of one component in high concentration alone.We believe the use of three different components for cardiac arrest induction will have a beneficial effect with lower activation of apoptosis pathway. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

REICHERT, KARLA; PEREIRA DO CARMO, HELISON RAFAEL; LIMA, FANY; TORINA, ANALI GALLUCE; DE SOUZA VILARINHO, KARLOS ALEXANDRE; MARTINS DE OLIVEIRA, PEDRO PAULO; SILVEIRA FILHO, LINDEMBERG MOTA; BARBOSA DE OLIVEIRA SEVERINO, ELAINE SORAYA; PETRUCCI, ORLANDO. Desenvolvimento de solução cardioplégica sem potássio: estudo experimental em ratos. Revista Brasileira de Cirurgia Cardiovascular, v. 28, n. 4, p. 524-530, OCT-DEC 2013. (12/09130-1)

DO CARMO, HELISON PEREIRA; REICHERT, KARLA; DE CARVALHO, DANIELA DIOGENES; SILVEIRA-FILHO, LINDEMBERG DA MOTA; VILARINHO, KARLOS; OLIVEIRA, PEDRO; PETRUCCI, ORLANDO. Lidocaine and Pinacidil Added to Blood versus Crystalloid Cardioplegic Solutions: Study in Isolated Hearts. Revista Brasileira de Cirurgia Cardiovascular, v. 33, n. 3, p. 211-216, 2018. (12/09130-1)

REICHERT, KARLA; PEREIRA DO CARMO, HELISON RAFAEL; TORINA, ANALI GALLUCE; DE CARVALHO, DANIELA DIOGENES; SPOSITO, ANDREI CARVALHO; DE SOUZA VILARINHO, KARLOS ALEXANDRE; SILVEIRA-FILHO, LINDEMBERG DA MOTA; MARTINS DE OLIVEIRA, PEDRO PAULO; PETRUCCI, ORLANDO. Atorvastatin Improves Ventricular Remodeling after Myocardial Infarction by Interfering with Collagen Metabolism. PLoS One, v. 11, n. 11, NOV 23 2016. (11/14550-7, 12/09130-1)