Myocardial oxygen consumption in experimental hypertrophy and congestive heart failure due to pressure overload

Gunning, J. F.; Cooper, George; Harrison, Carlos E.; Coleman, HN

doi:10.1016/s0002-9149(73)80033-5

Cited by 27 publications

(11 citation statements)

References 25 publications

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“…Mitochondria are a recognized source of ROS in the myocardium. 25 Mechanical stretch increases myocardial oxygen consumption 26,27 and may thus MnTMPyP lowers the basal ANF expression, but ANF expression increased from this lower basal level after either low-or high-amplitude stretch. B, Expression of ANF was normalized to 18S rRNA and expressed as percent change versus control.…”

Section: Stretch-induced Ros Productionmentioning

confidence: 99%

Reactive Oxygen Species Mediate Amplitude-Dependent Hypertrophic and Apoptotic Responses to Mechanical Stretch in Cardiac Myocytes

Pimentel

Amin

Xiao

et al. 2001

Circulation Research

308

196

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Abstract-Oxidative stress stimulates both growth and apoptosis in cardiac myocytes in vitro. We investigated whether oxidative stress mediates hypertrophy and apoptosis in cyclically stretched ventricular myocytes. Neonatal rat ventricular myocytes cultured on laminin-coated silastic membranes were stretched cyclically (1 Hz) at low (nominal 5%) and high (nominal 25%) amplitudes for 24 hours. Stretch caused a graded increase in superoxide anion production as assessed by superoxide dismutase (SOD)-inhibitable cytochrome c reduction or electron paramagnetic resonance spectroscopy. The role of reactive oxygen species (ROS) was assessed using the cell-permeable SOD/catalase mimetics Mn(II/III)tetrakis(1-methyl-4-peridyl) (MnTMPyP) and EUK-8. Stretch-induced increases in protein synthesis ( 3 Hleucine incorporation) and cellular protein content were completely inhibited by MnTMPyP (0.05 mmol/L) at both low and high amplitudes of stretch. In contrast, while MnTMPyP inhibited basal atrial natriuretic factor (ANF) mRNA expression, the stretch-induced increase in ANF mRNA expression was not inhibited by MnTMPyP. In contrast to hypertrophy, only high-amplitude stretch increased myocyte apoptosis, as reflected by increased DNA fragmentation on gel electrophoresis and an Ϸ3-fold increase in the number of TUNEL-positive myocytes. Similarly, only high-amplitude stretch increased the expression of bax mRNA. Myocyte apoptosis and bax expression stimulated by high-amplitude stretch were inhibited by MnTMPyP. Both low-and high-amplitude stretch caused rapid phosphorylation of ERK1/2, while high-, but not low-, amplitude stretch caused phosphorylation of JNKs. Activation of both ERK1/2 and JNKs was ROS-dependent. Thus, cyclic strain causes an amplitude-related increase in ROS, associated with differential activation of kinases and induction of hypertrophic and apoptotic phenotypes.

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Section: Stretch-induced Ros Productionmentioning

confidence: 99%

Reactive Oxygen Species Mediate Amplitude-Dependent Hypertrophic and Apoptotic Responses to Mechanical Stretch in Cardiac Myocytes

Pimentel

Amin

Xiao

et al. 2001

Circulation Research

308

196

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“…In studies using isolated papillary n the muscle preparations, it was concluded that the yper-induction of ventricular hypertrophy led to a depresa, the sion of the contractile state of the myocardium heart (Spann et al, 1967;Bing et al, 1971;Spann et al, ange. 1972;Gunning et al, 1973;Alpert et al, 1974). In a Es for more recent study, however, Williams and Potter mrfor-(1974) showed that, while myocardial depression did :ently occur early (6 weeks) after pulmonary artery bandheart ing, the contractile state of papillary muscles re-1.…”

Section: Previous Studies In Patients With Left Ventricular Hypertrophymentioning

confidence: 99%

“…Data derived from in vitro and in vivo experiments as well as available information in human studies suggest that ventricular function is depressed as a result of hypertrophy (Spann et al, 1967(Spann et al, , 1969Bing et al, 1971;Frohlich et al, 1971;Spann et al, 1972;Gunning et al, 1973;Alpert et al, 1974;Mehmel et al, 1975). However, more recent animal experiments suggest that performance is normal in the absence of overt congestive heart failure (Gamble et al, 1973;Malik et al, 1974;Pfeffer et al, 1976;Sasayama et al, 1976).…”

mentioning

confidence: 99%

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

Karlinger¹,

Williams²,

Gorwit³

et al. 1977

Heart

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There is considerable controversy concerning myocardial performance in hypertrophied states. Data derived from in vitro and in vivo experiments as well as available information in human studies suggest that ventricular function is depressed as a result of hypertrophy (Spann et al., 1967(Spann et al., , 1969Bing et al., 1971;Frohlich et al., 1971;Spann et al., 1972;Gunning et al., 1973;Alpert et al., 1974;Mehmel et al., 1975). However, more recent animal experiments suggest that performance is normal in the absence of overt congestive heart failure (Gamble et al., 1973;Malik et al., 1974;Pfeffer et al., 1976;Sasayama et al., 1976 MethodsThe study group consisted of 9 men and 9 women ranging in age from 21 to 72 years (mean=48). Of these patients, 8 were black, 4 Mexican-American, and 6 Caucasian. At the time of study, most patients were receiving treatment for high blood pressure. However, no patient was receiving a digitalis glycoside, reserpine, or guanethidine. Other treatment is detailed in the

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“…In mongrel dogs myocardial oxygen consumption showed a closer correlation to left ventricular function than ATP content [21]. However, there are conflicting reports concerning the oxygen consumption o f hypertrophied left ventricular myocardium [4,8,25]. Pressure overload induces the preferential synthesis of cardiac myosin isozyme (myosin V3), which has reduced ATPase activity.…”

Section: Discussionmentioning

confidence: 99%

Positive correlation between aortic valve pressure gradient and mitochondrial respiratory chain capacity in hypertrophied human left ventricle

Maurer

Zierz²

1992

Clin Investig

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The effect of chronic left ventricular pressure overload on the activities of mitochondrial respiratory chain enzymes was investigated in myocardial biopsies from the left ventricular apex of 13 patients undergoing aortic valve replacement for aortic valve stenosis. Transvalvular pressure gradients measured by left-sided heart catheterization ranged from 52 to 100 mmHg. The specific activity of mitochondrial respiratory chain enzyme complexes I+III (antimycin A sensitive NADH cytochrome c oxidoreductase) and the myocardial concentrations of coenzyme Q10 (CoQ10) increased significantly (P < 0.05) with increasing aortic valve pressure gradient. In contrast, the specific activities of complex IV (cytochrome c oxidase), succinate dehydrogenase, and citrate synthase, a mitochondrial matrix enzyme, showed no significant correlation with the pressure gradient. Since CoQ10 is the rate-limiting compound of the activity of complexes I+III but not of cytochrome c oxidase, succinate dehydrogenase, or citrate synthase, these data suggest that the increase in the activity of complexes I+III is due to the increase in CoQ10 content.

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Myocardial oxygen consumption in experimental hypertrophy and congestive heart failure due to pressure overload

Cited by 27 publications

References 25 publications

Reactive Oxygen Species Mediate Amplitude-Dependent Hypertrophic and Apoptotic Responses to Mechanical Stretch in Cardiac Myocytes

Reactive Oxygen Species Mediate Amplitude-Dependent Hypertrophic and Apoptotic Responses to Mechanical Stretch in Cardiac Myocytes

Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension.

Positive correlation between aortic valve pressure gradient and mitochondrial respiratory chain capacity in hypertrophied human left ventricle

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