Myocardial oxidative stress changes during compensated right heart failure in rats

Pichardo, Julieta; Palace, Vince; Farahmand, Firoozeh; Singal, Pawan K.

doi:10.1007/978-1-4615-5097-6_6

Cited by 24 publications

(30 citation statements)

References 46 publications

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“…Increased dietary levels of UFA can cause these lipids to be incorporated into membrane phospholipids, leading to oxidative stress (24,35,36). Although we observed oxidative stress and other recent investigations have established that free radicals may be important contributors to cardiac dysfunction and myocardial damage (13,(37)(38)(39), in the present study myocardial mechanical function was not altered by the diet. Kako and Vasdev (1) also observed that a high UFA diet did not change the mechanical function of isolated papillary muscle.…”

Section: Discussioncontrasting

confidence: 77%

<a name="home"></a>Effect of unsaturated fatty acids on myocardial performance, metabolism and morphology

Pinotti

Silva

Sugizaki

et al. 2006

Braz J Med Biol Res

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Diets rich in saturated fatty acids are one of the most important causes of atherosclerosis in men, and have been replaced with diets rich in unsaturated fatty acids (UFA) for the prevention of this disorder. However, the effect of UFA on myocardial performance, metabolism and morphology has not been completely characterized. The objective of the present investigation was to evaluate the effects of a UFA-rich diet on cardiac muscle function, oxidative stress, and morphology. Sixty-day-old male Wistar rats were fed a control (N = 8) or a UFArich diet (N = 8) for 60 days. Myocardial performance was studied in isolated papillary muscle by isometric and isotonic contractions under basal conditions after calcium chloride (5.2 mM) and ß-adrenergic stimulation with 1.0 µM isoproterenol. Fragments of the left ventricle free wall were used to study oxidative stress and were analyzed by light microscopy, and the myocardial ultrastructure was examined in left ventricle papillary muscle. After 60 days the UFA-rich diet did not change myocardial function. However, it caused high lipid hydroperoxide (176 ± 5 vs 158 ± 5, P < 0.0005) and low catalase (7 ± 1 vs 9 ± 1, P < 0.005) and superoxide-dismutase (18 ± 2 vs 27 ± 5, P < 0.005) levels, and discrete morphological changes in UFA-rich diet hearts such as lipid deposits and mitochondrial membrane alterations compared to control rats. These data show that a UFA-rich diet caused myocardial oxidative stress and mild structural alterations, but did not change mechanical function.

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Section: Discussioncontrasting

confidence: 77%

<a name="home"></a>Effect of unsaturated fatty acids on myocardial performance, metabolism and morphology

Pinotti

Silva

Sugizaki

et al. 2006

Braz J Med Biol Res

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“…Although prior works have associated oxidative stress and cardiac dysfunction 6,[20][21][22] , this work found no alterations in mechanical function under basal conditions. Results, such as the isolated changes in tension and relaxation with increased extracellular calcium concentration and muscle stiffness constant with isoproterenol in the SF group, allow us to conclude that the diets did not provoke significant myocardial functional changes.…”

Section: Discussioncontrasting

confidence: 66%

Influências de dietas ricas em ácidos graxos saturados e insaturados sobre o miocárdio de ratos

Pinotti¹,

Dal-Pai-Silva²,

Sugizaki³

et al. 2007

Arq. Bras. Cardiol.

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SummaryObjectives: To study the influence of saturated (SFA) and unsaturated fatty acid (UFA) rich diets on mechanical function, morphology and oxidative stress in rat myocardium.Methods: Male, 60-day-old Wistar rats were fed a control (n=8), a SFA (n=8), or a UFA-rich diet (n=8) for sixty days. Mechanical function was studied in isolated left ventricle papillary muscle under isometric and isotonic contractions, in basal conditions (1.25mM calcium chloride) and after 5.2mM calcium chloride and beta-adrenergic stimuli with 1.0µM isoproterenol. Left ventricle fragments were used to study oxidative stress and morphology under light and electron microscopy.Results: SFA and UFA-rich diets did not change myocardium mechanical function. Both diets caused oxidative stress, with high lipid hydroperoxide and low superoxide-dismutase concentrations. UFA rich diet decreased catalase expression and SFA rich diet decreased the amount of myocardial glutathione-peroxidase. Both diets promoted light ultrastructural injuries such as lipid deposits and cell membrane injuries.Conclusion: Results suggest that SFA and UFA rich diets do not alter isolated muscle mechanical function, but promote light myocardial morphological injuries and oxidative stress.

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“…De Jong et al (1) reported enhanced expression and activity of xanthine oxidase in the RV in PH rats, and any of these sources could increase superoxide production in PH-RV. An increase in SOD activity in the RV has been reported in PH rats (29). Although the upregulation of SOD might act to regulate increased superoxide production of the RV in PH, it might not be sufficient to entirely suppress the augmented superoxide levels.…”

Section: Discussionmentioning

confidence: 94%

“…Therefore, using direct in vivo visualization is desirable when evaluating RV coronary microvascular vasoreactivity in PH. An increase in the oxidative stress in the RV myocardium has been suggested to be a key factor in RV dysfunction in PH (1,2,29).We hypothesized that the vasodilation of RV coronary arterial microvessels of different sizes, induced by NO and EDHF in PH, might be differently affected under conditions of increased superoxide. To test this hypothesis, we observed arterial microvessels (diameter ϭ 30 -200 m) in the RV in vivo in control and monocrotaline (MCT)-treated PH rats using intravital videomicroscopy and evaluated the endotheliumdependent vascular responses to ACh in the absence of prostacyclin under following conditions: ACh alone, in the presence of an NO or an EDHF inhibitor, in the presence of both NO and EDHF inhibitors, and in the presence of superoxide dismutase (SOD).…”

mentioning

confidence: 96%

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Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

Kajiya¹,

Hirota²,

Inai³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats. Am J Physiol Heart Circ Physiol 292: H2737-H2744, 2007. First published January 12, 2007; doi:10.1152/ajpheart.00548.2006.-Pulmonary hypertension (PH) causes right ventricular (RV) hypertrophy and, according to the extent of pressure overload, eventual heart failure. We tested the hypothesis that the mechanical stress in PH-RV impairs the vasoreactivity of the RV coronary microvessels of different sizes with increased superoxide levels. Five-week-old male Sprague-Dawley rats were injected with monocrotaline (n ϭ 126) to induce PH or with saline as controls (n ϭ 114). After 3 wk, coronary arterioles (diameter ϭ 30 -100 m) and small arteries (diameter ϭ 100 -200 m) in the RV were visualized using intravital videomicroscopy. We evaluated ACh-induced vasodilation alone, in the presence of N -nitro-Larginine methyl ester (L-NAME), in the presence of tetraethylammonium (TEA) or catalase with or without L-NAME, and in the presence of SOD. The degree of suppression in vasodilation by L-NAME and TEA was used as indexes of the contributions of endothelial nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), respectively. In PH rats, ACh-induced vasodilation was significantly attenuated in both arterioles and small aretries, especially in arterioles. This decreased vasodilation was largely attributable to reduced NOmediated vasoreactivity, whereas the EDHF-mediated vasodilation was relatively robust. The suppressive effect on arteriolar vasodilation by catalase was similar to TEA in both groups. Superoxide, as measured by lucigenin chemiluminescence, was significantly elevated in the RV tissues in PH. SOD significantly ameliorated the impairment of ACh-induced vasodilation in PH. Robust EDHF function will play a protective role in preserving coronary microvascular homeostasis in the event of NO dysfunction with increased superoxide levels. acetylcholine; N -nitro-L-arginine methyl ester; tetraethylanmonium; catalase; superoxide dimutase; endothelium-derived hyperpolarizing factor PULMONARY HYPERTENSION (PH) causes pressure overload and hypertrophy, finally leading to failure, in the right ventricle (RV) of the heart. Although the right coronary perfusion pressure remains relatively unchanged, the high pressure and hypertrophy of the RV affect the coronary hemodynamics (8, 13), and patients with PH and RV hypertrophy might have symptoms indistinguishable from those of angina pectoris (4, 30). In chronic PH, coronary flow regulation is the only mechanism that maintains the oxygen supply to the RV, since no further increase in the absorption of oxygen is possible (31). The endothelium-dependent vasodilation of coronary small arteries (SAs, diameter ϭ 100 -200 m) isolated from the RV has been shown to be lower in rats with chronic PH (33), whereas in acute PH, endogenous nitric oxide (NO) regulates right coronary blood flow (37). However, the contri...

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Myocardial oxidative stress changes during compensated right heart failure in rats

Cited by 24 publications

References 46 publications

<a name="home"></a>Effect of unsaturated fatty acids on myocardial performance, metabolism and morphology

<a name="home"></a>Effect of unsaturated fatty acids on myocardial performance, metabolism and morphology

Influências de dietas ricas em ácidos graxos saturados e insaturados sobre o miocárdio de ratos

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

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