Low coronary perfusion pressure is associated with endocardial fibrosis in a rat model of volume overload cardiac hypertrophy

Guido, Maria Carolina; Koike, Marcia Kiyomi; Frimm, Clóvis de Carvalho

doi:10.1590/s0041-87812004000500002

Cited by 7 publications

(11 citation statements)

References 33 publications

(47 reference statements)

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“…Collagen deposition and its removal by matrix metalloproteinases (MMPs) are regulated by focal adhesion kinase (FAK) (19), which is dynamically regulated by mechanical stress and inflammation. We previously demonstrated that silencing FAK in endotoxemic rats protected against the development of cardiac dysfunction and remodeling (11). In addition, myocardial MMP activation induced chamber dilatation and ventricular dysfunction (20).…”

Section: Introductionmentioning

confidence: 97%

“…Septic shock causes a reduction in diastolic arterial pressure (DAP) and, consequently, a reduction in coronary driving pressure (CDP), which is important for maintaining myocardial perfusion (11). The CDP is the difference between DAP and left ventricular end-diastolic pressure (LVEDP).…”

Section: Introductionmentioning

confidence: 99%

“…The CDP is the difference between DAP and left ventricular end-diastolic pressure (LVEDP). This pressure has been shown to be an important factor in several cardiac diseases, and a minimal CDP level is necessary to attain adequate myocardial perfusion (11). However, the roles of CDP and myocardial blood flow in sepsis have not been studied.…”

Section: Introductionmentioning

confidence: 99%

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Endotoxemic Myocardial Dysfunction

Soriano¹,

Guido

Barbeiro

et al. 2014

Shock

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Sepsis impairs the autoregulation of myocardial microcirculatory blood flow, but whether this impairment is correlated with myocardial remodeling is unknown. This study investigated the role of coronary driving pressure (CDP) as a determinant of microcirculatory blood flow and myocardial fibrosis in endotoxemia and sepsis. The study is composed of two parts: a prospective experimental study and an observational clinical study. The experimental study was performed on male Wistar rats weighing 300 to 320 g. Endotoxemia was induced in rats by lipopolysaccharide (LPS) injection (10 mg·kg intraperitoneally). Hemodynamic evaluation was performed 1.5 to 24 h after LPS injection by measuring the mean arterial pressure, CDP, left ventricular end-diastolic pressure, dP/dtmax, and dP/dtmin. Microspheres were also infused into the left ventricle to measure myocardial blood flow, and myocardial tissue was histologically assessed to analyze collagen deposition. The CDP, mean arterial pressure, and myocardial blood flow were reduced by 55%, 30%, and 70%, respectively, in rats 1.5 h after LPS injection compared with phosphate buffer saline injection (P < 0.05). The CDP was significantly correlated with subendocardial blood flow (r = 0.73) and fibrosis (r = 0.8). Left ventricular function was significantly impaired in the LPS-treated rats, as demonstrated by dP/dtmax (6,155 ± 455 vs. 3,746 ± 406 mmHg·s, baseline vs. LPS; P < 0.05) and dP/dtmin (-5,858 ± 236 vs. -3,516 ± 436 mmHg·s, baseline vs. LPS; P < 0.05). The clinical study was performed on 28 patients with septic shock analyzed for CDP. The CDP data and histological slices were collected from septic patients. In addition, the clinical data demonstrated fibrosis and 45% CDP reduction in nonsurvivors compared with survivors. In conclusion, the left ventricular subendocardial blood flow was positively correlated with CDP, and higher CDP was negatively correlated with myocardial collagen deposition. Thus, early reductions in myocardial blood flow and CDP facilitate late myocardial fibrosis in rats and likely in humans.

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Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endotoxemic Myocardial Dysfunction

Soriano¹,

Guido

Barbeiro

et al. 2014

Shock

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“…GUIDO MC et al 1 point out that left ventricular hypertrophy following volume overload is regarded as an example of cardiac remodeling without increased fibrosis accumulation. Infarction is associated with increased fibrosis within the noninfarcted, hypertrophied myocardium, particularly in the subendocardial regions.…”

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confidence: 99%

In the october 2004 issue of Clínicas

Rocha-e-Silva

2004

Rev. Hosp. Clin.

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“…Estudos demonstram que o IAM está associado com uma abundante perda de miocárdio que é substituída por uma cicatriz a base de colágeno (Guido et al, 2004;Frangogiannis, 2014 (Goldman et al, 1995;Francis et al, 2001;Savergnini et al, 2013). …”

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Efeito do tratamento crônico do metotrexato associado à nanoemulsão de LDE no remodelamento cardíaco por infarto do miocárdio em ratos Wistar

Lima¹

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Agradecimentos"Há pessoas que nos falam e nem as escutamos; há pessoas que nos ferem e nem cicatrizes deixam, mas há pessoas que simplesmente aparecem em nossa vida e nos marcam para sempre." Cecília Meireles Ao meu orientador, Prof. Dr. Raul Cavalcante Maranhão, pela oportunidade em realizar os meus sonhos e por acreditar em mim.A todos os funcionários do Laboratório de Metabolismo de Lípides do Incor, principalmente, Dra. Fátima e Dra. Priscila, pelo suporte na realização deste trabalho e pelos momentos de descontração durante o tão apreciado café.À Dra Maria Carolina Guido, pela contribuição durante o trabalho. A todos os companheiros de pós-graduação do Laboratório deMetabolismo de Lípides pelo suporte e amizade.À Neusa Rodrigues Dini e todas as funcionárias da secretaria de pós-graduação, pelo apoio em tornar esse sonho possível. À Profa. Dra. Vera Maria Cury Salemi, pela realização e análise dos ecocardiogramas.Ao Dr. Marcelo Dantas Tavares de Melo, pela análise dos ecocardiogramas. Aos funcionários do Serviço de Apoio à Pesquisa e ExperimentaçãoAnimal do Incor, pela assistência e cuidado com os animais. À CAPES (Coordenação de Aperfeiçoamento de Pessoal de NívelSuperior), pela bolsa de doutorado e de doutorado-sanduíche realizado na Boston University, possibilitando a publicação de um artigo.À minha irmã Ariane, pelo carinho, cuidado e por ser o meu pilar em momentos difíceis. Acute myocardial infarction (AMI) is the main cause of worldwide mortality. Normalização adotadaAMI is accompanied by cardiac remodeling, characterized by genetic, molecular and cellular alterations, with consequent changes in the size, shape and function of the heart, resulting in ventricular dysfunction and heart failure. Experimental and clinical evidence indicate that prevention or treatment of cardiac remodeling benefits the ventricular function. LDE is a lipid nanoparticle with a structure similar to low density lipoprotein (LDL). LDE

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Low coronary perfusion pressure is associated with endocardial fibrosis in a rat model of volume overload cardiac hypertrophy

Abstract: Coronary driving pressure falls and ventricular pressures increase early after aortocaval fistula and are associated with subsequent myocardial fibrosis deposition.

Cited by 7 publications

References 33 publications

Endotoxemic Myocardial Dysfunction

Endotoxemic Myocardial Dysfunction

In the october 2004 issue of Clínicas

Efeito do tratamento crônico do metotrexato associado à nanoemulsão de LDE no remodelamento cardíaco por infarto do miocárdio em ratos Wistar

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