Ventricular performance, coronary flow, and MVO 2  in aortic coarctation hypertrophy

Gamble, W. J.; Phornphutkul, Charlie; Kumar, Amit; Gl, Sanders; Fj, Manasek; Rg, Monroe

doi:10.1152/ajplegacy.1973.224.4.877

Cited by 18 publications

(9 citation statements)

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“…Whereas RV hypertrophy is characterized by a marked increase in blood flow per gram of ventricle at rest (1), blood flow to the hypertrophied left ventricle has been shown to be either modestly reduced (16)(17)(18)(19), unchanged (20)(21)(22)(23)(24), or only slightly increased (25). Moreover, in contrast to the results ofthe present study, coronary vascular adjustments to exercise of the hypertrophied left ventricle appear to be largely normal (21,22,(26)(27)(28).…”

Section: Influence Of Perfusion Pressure On Coronary Vascular Responscontrasting

confidence: 93%

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Murray¹,

Vatner²

1981

J. Clin. Invest.

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A B S T R A C T Measurements of right coronary artery blood flow, aortic and right ventricular (RV) pressures and heart rate were radiotelemetered during strenuous, spontaneous exercise in normal dogs and dogs with severe RV hypertrophy induced by chronic (5-6 mo) pulmonary artery stenosis. With fixed pulmonic stenosis, dogs with RV hypertrophy exhibited a decrease (P < 0.01) in arterial pressure during exercise. Under these conditions, exercise increased right coronary artery blood flow and decreased right coronary vascular resistance less (P < 0.05) in dogs with RV hypertrophy compared with normal. This attenuated response of right coronary artery blood flow of dogs with RV hypertrophy was not observed when arterial pressures remained at preexercise values during exercise. However, regardless of changes in arterial pressures during exercise, all dogs with RV hypertrophy demonstrated a striking postexercise coronary hyperemia (P < 0.01), suggesting a perfusion deficit of the hypertrophied right ventricle during exercise. These results imply a fundamental defect in the ability of the coronary circulation of the severely hypertrophied right ventricle to provide sufficient nutrient supply in the face of elevated metabolic demands of exercise.

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Section: Influence Of Perfusion Pressure On Coronary Vascular Responscontrasting

confidence: 93%

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Murray¹,

Vatner²

1981

J. Clin. Invest.

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“…The combination of reduced ENDO citrate synthase activity per gram tissue as shown in the present studies and reduced coronary blood flow described by other investigators (6,7) presents the possibility that myocardial energy requirements may not be adequately supported by aerobic metabolism in the enlarged LV. When the energy demands placed upon the heart exceed aerobic capability, an alternative (anaerobic) source of energy production may be utilized.…”

Section: K 27'" I18 F 4'supporting

confidence: 46%

Transmural Citrate Synthase and Lactate Dehydrogenase Levels in Hypertrophied Rat Left Ventricle

Dowell

1978

Experimental Biology and Medicine

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In recent years it has become apparent that inhomogenities exist or can develop between epicardial (EPI) and endocardia1 (ENDO) portions of the left ventricle (LV). Some investigators (1) consider blood flow to the ENDO portion of the LV to be marginally adequate under normal conditions. Biochemical studies (2) revealed a higher level of lactic acid in the normal rat ENDO while the levels of high-energy phosphate compounds (PCr and ATP) were concomitantly lower. Similar transmural gradients have been shown in the dog LV (3, 4). These gradients are accentuated when coronary perfusion pressure and blood flow are reduced (3,4), suggesting that the ENDO is the primary site of metabolic alterations when ischemic conditions are encountered by the myocardium.When a chronic pressure overload is imposed upon the heart, a substantial increase in myocardial tissue occurs. The additional heart tissue as well as hemodynamic factors associated with pressure overload (5) create additional energy and oxygen requirements. Under normal conditions, oxidative metabolism is preferentially utilized in the heart and elevated oxygen demands are met primarily by increasing coronary blood flow. However, recent studies have shown that total coronary blood flow (6) and flow per unit mass of tissue (7) are reduced below normal levels in hypertrophied hearts. The apparent failure to achieve adequate coronary blood flow in the hypertrophied heart presents the possibility that metabolic adaptations may be required. It seemed likely that the ENDO portion of the ventricle would be particularly vulnerable to chronic pressure overload stress. Therefore, the activity of selected enzymes associated with aerobic and anaerobic metabolism ~~ ~ ~ ' This work was supported, in part, by NIH GrantNos. HL16352, HL18839, and the American Heart Association, Texas Affiliate.was measured in EPI and ENDO portions of LV in control animals. These enzyme activity levels were compared with those observed in the LV which had enlarged due to pressure overload. Materials and methods. Animals and surgical procedures. Male, Sprague-Dawley rats initially weighing 250-275 g were used in these experiments. Pressure-induced LV hypertrophy was created by constricting the abdominal aorta above the renal vessels (5). Control animals received sham operations. Aortic constricted and control animals were studied 5 weeks following surgery at which time stable LV hypertrophy would be expected in aortic constricted animals.Tissue preparation. Animals were weighed and then killed by cervical dislocation. The chest cavity was opened, the heart was rapidly excised and placed in crushed ice. Tibialis anterior (TA) muscles were dissected out and placed in ice. Atria, great vessels and the right ventricle were then carefully removed from the excised heart. The remaining LV plus interventricular septum was separated into EPI and ENDO portions by dissecting the ventricle at the mid-wall. These tissue samples were weighed separately and the combined values were taken as LV weight. TA muscles w...

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“…Inadequate perfusion of the hypertrophied ventricle could limit the extent to which the heart can compensate for the pressure overload, and thus may precipitate a decline in ventricular function. Results from recent studies examining the effects of left ventricular hypertrophy on myocardial blood flow appear to be consistent with this hypothesis, in that blood flow per gram of myocardial tissue has been found to be either decreased (1)(2)(3)(4), unchanged (5-9), or only slightly elevated (10). This concept is further supported by the observation of Rembert et al (10), that left ventricular hypertrophy is associated with a relative decline in preferential subendocardial perfusion (i.e., a decrease in the endocardial:epicardial perfusion ratio) at rest.…”

Section: Introductionmentioning

confidence: 53%

Effects of exerimental right ventricular hypertrophy on myocardial blood flow in conscious dogs.

Murray¹,

Baig²,

Fishbein³

et al. 1979

J. Clin. Invest.

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A B S T R A C T The effects of right ventricular hypertrophy on the overall and regional distribution of myocardial blood flow in the absence of an elevated coronary arterial driving pressure were evaluated in 18 conscious dogs subjected to a chronic pressure overload of the right ventricle induced by pulmonary artery constriction. The sustained pressure overload for duration of4-6 wk or 4-5 mo resulted in significant increases in right ventricular mass (45 and 110%, respectively) and right ventricular fiber diameter (22 and 60%, respectively). Moreover, the presence *tmoderate and severe hypertrophy was associated with marked increases in transmural blood flow per gram to the right ventricle proportional to the observed increases in mass, i.e., of 36 and 109%, respectively, from a normal value of 0.67+0.04 ml/min per g, whereas left ventricular blood flow remained unaltered from a normal value of 1.00±0.06 ml/min per g. Despite the large increases in blood flow per gram to moderately and severely hypertrophied right ventricle, no significant changes in the ratio of capillary:muscle fiber number were observed. These data suggest that the development of right ventricular hypertrophy is characterized by a sustained compensatory response of the coronary circulation to the augmented work load and mass, and that it is not associated with a proliferative response of the vasculature supplying the enlarged ventricle.

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Ventricular performance, coronary flow, and MVO 2 in aortic coarctation hypertrophy

Cited by 18 publications

References 0 publications

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Transmural Citrate Synthase and Lactate Dehydrogenase Levels in Hypertrophied Rat Left Ventricle

Effects of exerimental right ventricular hypertrophy on myocardial blood flow in conscious dogs.

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