RESUMO
BACKGROUND AND AIMS: We evaluated the use of body weight (BW) loss soon after acute myocardial infarction (MI) in rats as a marker of acute heart failure (HF). METHODS: Female Wistar rats (200-240 g) were submitted either to sham operation or to coronary artery occlusion. In individual cages, daily BW and food and water intake were measured. Seven days later, cardiac function was evaluated by left ventricular catheterization. HF was defined by a left ventricular end-diastolic pressure greater than the upper limit of the 95% confidence interval. MI group was then divided into those that developed HF (n = 27; MI-HF) and those that did not (n = 47; MI). RESULTS: The MI-HF group experienced increased BW loss (sham: 4.2 ± 0.6% MI: 0.4 ± 0.8%, MI-HF: -4.9 ± 1.2%; p <0.05) and reduced water and food intake compared with other groups. HF animals showed greater lung weight (sham: 1.460 ± 0.076 g, MI: 1.748 ± 0.086 g, MI-HF: 2.033 ± 0.13 g; p <0.05). Infarct area was significantly different between the groups (MI: 35.9 ± 0.9%, MI-HF: 39.7 ± 1.3%; p <0.05). ROC curve showed that BW loss over 7 days has 100% sensitivity and 72.3% specificity for identifying acute HF. Moreover, excluding the effect of infarct area on these results, a sample of animals with the same infarct area displayed similar morphometric and hemodynamic patterns as the entire sample. Multivariate linear regression analysis confirmed that BW loss is a HF marker independent of infarct area. CONCLUSIONS: BW is an easy and reliable noninvasive method to detect HF early after MI in rats.
Assuntos
Peso Corporal , Insuficiência Cardíaca/etiologia , Infarto do Miocárdio/complicações , Infarto do Miocárdio/fisiopatologia , Redução de Peso , Animais , Biomarcadores , Feminino , Insuficiência Cardíaca/fisiopatologia , Hemodinâmica , Humanos , Curva ROC , Ratos , Ratos Wistar , Função Ventricular Esquerda/fisiologiaRESUMO
BACKGROUND: Clinical studies in postmenopausal women suggest that female hormones play an important role in maintaining healthy cardiovascular conditions. The objective of this study was to evaluate the influence of ovarian hormones in the right ventricle contractility in heart failure (HF) rats following myocardial infarction (MI). METHODS: Female Wistar rats were divided into four groups: healthy ovariectomized (OVX), ovariectomized with HF (OVX-HF), HF, and sham operated (SHAM). Ovariectomy was performed in 10-week-old rats, and MI was induced 1 week later. Eight weeks after MI, right ventricular (RV) performance was analyzed using RV strip preparations. RESULTS: Ovariectomy did not change the infarct size (HF: 42 +/- 3.5 vs. OVX-HF: 39 +/- 1.5%). In the presence of isoproterenol (ISO) and calcium, the isometric force was reduced in both HF groups. Ovariectomy did not modify the positive inotropic parameter in the control and in HF rats. Time to peak tension (TPT) was prolonged in both ovariectomized groups compared to SHAM (ISO 10(-7) M OVX: 125 +/- 12( *); SHAM: 81 +/- 4; HF: 87 +/- 4; OVX-HF: 102 +/- 6( *) msec, ( *)p <0.01 vs. SHAM), and relaxation time (RT) was prolonged in OVX (270 +/- 16( *) msec) and OVX-HF (241 +/- 10( *) msec) vs. SHAM (197 +/- 6 msec; ( *)p <0.01 vs. SHAM). CONCLUSIONS: We conclude that the absence of female ovarian hormones during nine weeks does not influence the right ventricle positive inotropic response, but it prolongs the time of contraction and relaxation in normal and in HF rats following MI.
Assuntos
Baixo Débito Cardíaco/fisiopatologia , Estrogênios/fisiologia , Contração Miocárdica , Infarto do Miocárdio/complicações , Disfunção Ventricular Direita/fisiopatologia , Animais , Baixo Débito Cardíaco/etiologia , Cardiotônicos/farmacologia , Feminino , Ventrículos do Coração/efeitos dos fármacos , Isoproterenol/farmacologia , Contração Miocárdica/efeitos dos fármacos , Ovariectomia , Ratos , Ratos WistarRESUMO
Myocardial infarction (MI) was induced in rats by coronary ligation to compare changes in vascular reactivity from animals that developed heart failure (InfHF) with those that did not (Inf). Infarct size was similar in both groups. In vitro preparations of tail vascular bed were used to investigate the vascular responses to acetylcholine, sodium nitroprusside, and phenylephrine. Acetylcholine-induced relaxation was impaired in the Inf group (53 +/- 2%, n = 6) when compared with Sham (80 +/- 2%, n = 6, P < 0.05). The maximal response (E(max)) to phenylephrine increased in the Inf group (423 +/- 10 mm Hg, n = 9, P < 0.01) and decreased in InfHF (279 +/- 10 mm Hg, n = 7, P < 0.05) when compared with Sham (319 +/- 11 mm Hg, n = 8). Regardless of endothelial integrity, E(max) to phenylephrine increased in the Inf, nitro-l-arginine methyl ester, and indomethacin groups. An increased release of a prostanoid vasodilator was detected in the Inf group. Differently, the InfHF group presented a reduction of the E(max) to phenylephrine and an increment of nitric oxide release. This study demonstrates that MI without heart failure impairs endothelium-dependent relaxation and increases the reactivity to phenylephrine. This increase seems to involve a muscular component. The endothelium participates with an increased release of a vasodilator prostanoid, possibly to compensate the increased smooth muscle response. When heart failure follows MI, the reactivity to phenylephrine decreases, possibly due to an increased nitric oxide release.