Oxygen metabolism of the hypertrophic right ventricle in open chest dogs

Saito, Daiji; Tani, Hideki; Kusachi, Shozo; Uchida, Shunya; Ohbayashi, Naotsugu; Marutani, Morio; Maekawa, Kiyoaki; Tsuji, Takao; Haraoka, Shoichi

doi:10.1093/cvr/25.9.731

Cited by 23 publications

(13 citation statements)

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“…In IPAH, the elevated afterload considerably increases the metabolic demand of the right heart. The high median baseline OEF of 0.73 in the present population of patients with IPAH reflects this increased O 2 demand and is consistent with previous open-chest animal studies using chronic RV overload induced by pulmonary artery banding with significantly higher O 2 extraction compared to control (58% vs 51%) 5 22…”

Section: Discussionsupporting

confidence: 90%

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Supine-exercise-induced oxygen supply to the right myocardium is attenuated in patients with severe idiopathic pulmonary arterial hypertension

Wong

Raijmakers

Knaapen³

et al. 2011

Heart

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Section: Discussionsupporting

confidence: 90%

“…Other studies showed that the resting RV MBF or RCA flow in the chronically hypertrophied right myocardium was either unaltered5 22 23 or elevated11 24 25 compared with control values.…”

Section: Discussionmentioning

confidence: 96%

Supine-exercise-induced oxygen supply to the right myocardium is attenuated in patients with severe idiopathic pulmonary arterial hypertension

Wong

Raijmakers

Knaapen³

et al. 2011

Heart

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“…With this comes a greater oxygen requirement. Hypertrophied RV has lower oxygen extraction reserve than normal RV and a higher dependence on coronary flow [16], suggesting an inefficient oxygen utilization despite a greater net oxygen demand. Isolated RV tissue, both in monocrotaline and PAB-induced RVH, shows lower glucose-based O 2 consumption/g of myocardium in RVH [9].…”

Section: Mitochondrial Metabolic Adaptation In Rvhmentioning

confidence: 99%

Mitochondrial metabolic adaptation in right ventricular hypertrophy and failure

2010

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Right ventricular failure (RVF) is the leading cause of death in pulmonary arterial hypertension (PAH). Some patients with pulmonary hypertension are adaptive remodelers and develop RV hypertrophy (RVH) but retain RV function; others are maladaptive remodelers and rapidly develop RVF. The cause of RVF is unclear and understudied and most PAH therapies focus on regressing pulmonary vascular disease. Studies in animal models and human RVH suggest that there is reduced glucose oxidation and increased glycolysis in both adaptive and maladaptive RVH. The metabolic shift from oxidative mitochondrial metabolism to the less energy efficient glycolytic metabolism may reflect myocardial ischemia. We hypothesize that in maladaptive RVH a vicious cycle of RV ischemia and transcription factor activation causes a shift from oxidative to glycolytic metabolism thereby ultimately promoting RVF. Interrupting this cycle, by reducing ischemia or enhancing glucose oxidation, might be therapeutic. Dichloroacetate, a pyruvate dehydrogenase kinase inhibitor, has beneficial effects on RV function and metabolism in experimental RVH, notably improving glucose oxidation and enhancing RV function. This suggests the mitochondrial dysfunction in RVH may be amenable to therapy. In this mini review, we describe the role of impaired mitochondrial metabolism in RVH, using rats with adaptive (pulmonary artery banding) or maladaptive (monocrotaline-induced pulmonary hypertension) RVH as models of human disease. We will discuss the possible mechanisms, relevant transcriptional factors, and the potential of mitochondrial metabolic therapeutics in RVH and RVF.

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“…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).…”

mentioning

confidence: 99%

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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Oxygen metabolism of the hypertrophic right ventricle in open chest dogs

Cited by 23 publications

References 0 publications

Supine-exercise-induced oxygen supply to the right myocardium is attenuated in patients with severe idiopathic pulmonary arterial hypertension

Supine-exercise-induced oxygen supply to the right myocardium is attenuated in patients with severe idiopathic pulmonary arterial hypertension

Mitochondrial metabolic adaptation in right ventricular hypertrophy and failure

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

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