Explorando a eficácia da terapia com laser de baixa intensidade em tratamento contínuo no remodelamento cardíaco pós-infarto do miocárdio em ratas: um estudo com variação de energia
Data
2023-10-31
Autores
Antonio, Ednei Luiz 
Orientadores
Tucci, Paulo José Ferreira
Tipo
Tese de doutorado
Título da Revista
ISSN da Revista
Título de Volume
Resumo
A insuficiência cardíaca (IC) pós-infarto do miocárdio continua a representar um
enorme fardo, uma vez que terapias atuais não conseguem anular o mau prognóstico.
A terapia laser de baixa intensidade (LLLT) tem sido apontada como uma abordagem
promissora, que pode atenuar o remodelamento cardíaco pós-infarto. No entanto, não
existe uma energia padrão-ouro conhecida, irradiada no coração infartado, e poucos
estudos avaliaram o impacto da LLLT no desempenho cardíaco. Portanto, este estudo
procurou determinar os efeitos de aplicações repetidas de LLLT com diferentes
parâmetros de irradiação durante o remodelamento cardíaco pós-infarto em ratos.
Ratas com grandes infartos foram tratados por quatro semanas. Ecocardiografia e
medidas hemodinâmicas foram usadas para avaliações funcionais do ventrículo
esquerdo (VE). ELISA, Western blot e ensaios bioquímicos foram utilizados para
avaliar os mediadores inflamatórios, stress oxidativo no miocárdio e proteínas da
cinética do cálcio. Um sistema de laser de diodo de arseneto de gálio e alumínio
semicondutor 830-nm Laser Photon III (DMC, São Carlos, SP, Brasil) foi aplicado
transtoracicamente três vezes por semana durante quatro semanas para cada
subgrupo com base na energia (10 J, 20 J e 40 J; respetivamente). A LLLT de 10J e
20J teve uma ação semelhante na atenuação da congestão pulmonar e da fibrose do
miocárdio. Além disso, 10J e 20J atenuaram a pressão diastólica final do VE e
melhoraram a +dP/dt e -dP/dt do VE. Todos os grupos LLLT apresentaram níveis mais
baixos de mediadores inflamatórios, mas apenas o grupo 10J normalizou os níveis de
lipoperoxidação e carbonilação do miocárdio. Todas as doses de LLLT melhoraram a
atividade da superóxido dismutase; no entanto, apenas o grupo 20J apresentou uma
atividade elevada da enzima anti-oxidante catalase. Havia níveis mais baixos de Ca2+
ATPase 2a do retículo sarcoplasmático/endoplasmático no miocárdio infartado, que
foi normalizado nos grupos 20J e 40J. Foi relatada uma regulação positiva do
fosfolamban no grupo 10J. As três doses (10J, 20J e 40J) de radiação utilizadas neste
trabalho mostraram-se capazes de modificar o curso da fisiopatologia miocárdica pós
infarto do miocárdio, com intensidades de efeitos variáveis. Os resultados do presente
estudo apoiam o papel benéfico da LLLT na remodelação cardíaca pós-infarto em
ratos. Aparentemente, as doses de 10J e 20J foram mais capazes de afetar o curso
das mudanças patológicas.
The post-myocardial infarction heart failure (HF) still carries a huge burden since current therapy is unsuccessful to abrogate poor prognosis. Low-level laser therapy (LLLT) has been targeted as a promising approach that can mitigate post-infarction cardiac remodeling. However, there is no gold standard energy delivered to infarcted heart and few studies have evaluated the impact of LLLT on cardiac performance. Therefore, this study sought to determine the effects of repeated LLLT applications with different irradiation parameters during cardiac post-infarction remodeling in rats. Rats with large infarcts were treated for four weeks. Echocardiography and hemodynamic measurements were used for functional evaluations of left ventricular (LV). ELISA, Western blot and biochemical assays were used to evaluate inflammation, oxidative stress in the myocardium and proteins involved in calcium kinetics. An 830-nm Laser Photon III semiconductor aluminum gallium arsenide diode laser system (DMC, São Carlos, SP, Brazil) was applied transthoracically three times a week for four weeks for each subgroup based on the energy (i.e., 10 J, 20 J, and 40 J; respectively). LLLT on 10J and 20J had a similar action in attenuating pulmonary congestion and myocardial fibrosis. Moreover, 10J and 20J attenuated LV end diastolic pressure and improved +dP/dt and -dP/dt of LV. All LLLT groups had lower levels of inflammatory mediators, but only 10J group had normalized myocardial lipoperoxidation and carbonylation levels. All LLLT doses improved superoxide dismutase activity; however, only 20J group showed a high activity of the anti-oxidant catalase enzyme. There were lower levels of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a in the infarcted myocardium, which was normalized in the 20J and 40J groups. An upregulation of phospholamban has been reported for the 10J group. The results of the present study support the beneficial role of LLLT in post-infarction cardiac remodeling in rats. The three doses (10J, 20J and 40J) of radiation used in this study proved capable of modifying the course of myocardial pathophysiology after myocardial infarction, with varying intensities of effects. Apparently, the 10J and 20J doses were more able to affect the course of pathological changes.
The post-myocardial infarction heart failure (HF) still carries a huge burden since current therapy is unsuccessful to abrogate poor prognosis. Low-level laser therapy (LLLT) has been targeted as a promising approach that can mitigate post-infarction cardiac remodeling. However, there is no gold standard energy delivered to infarcted heart and few studies have evaluated the impact of LLLT on cardiac performance. Therefore, this study sought to determine the effects of repeated LLLT applications with different irradiation parameters during cardiac post-infarction remodeling in rats. Rats with large infarcts were treated for four weeks. Echocardiography and hemodynamic measurements were used for functional evaluations of left ventricular (LV). ELISA, Western blot and biochemical assays were used to evaluate inflammation, oxidative stress in the myocardium and proteins involved in calcium kinetics. An 830-nm Laser Photon III semiconductor aluminum gallium arsenide diode laser system (DMC, São Carlos, SP, Brazil) was applied transthoracically three times a week for four weeks for each subgroup based on the energy (i.e., 10 J, 20 J, and 40 J; respectively). LLLT on 10J and 20J had a similar action in attenuating pulmonary congestion and myocardial fibrosis. Moreover, 10J and 20J attenuated LV end diastolic pressure and improved +dP/dt and -dP/dt of LV. All LLLT groups had lower levels of inflammatory mediators, but only 10J group had normalized myocardial lipoperoxidation and carbonylation levels. All LLLT doses improved superoxide dismutase activity; however, only 20J group showed a high activity of the anti-oxidant catalase enzyme. There were lower levels of sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a in the infarcted myocardium, which was normalized in the 20J and 40J groups. An upregulation of phospholamban has been reported for the 10J group. The results of the present study support the beneficial role of LLLT in post-infarction cardiac remodeling in rats. The three doses (10J, 20J and 40J) of radiation used in this study proved capable of modifying the course of myocardial pathophysiology after myocardial infarction, with varying intensities of effects. Apparently, the 10J and 20J doses were more able to affect the course of pathological changes.