Effects of experimental volume-overload hypertrophy on myocardial blood flow and cardiac function

Badke, Frederick R.; White, Fred N.; Winter, M; Covell, JW; Andrés, José De; Bloor, Colin M.

doi:10.1152/ajpheart.1981.241.4.h564

Cited by 13 publications

(6 citation statements)

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“…Adaptation also occurs in large arteries as Villari et al [191] found increased cross-section of the left anterior descending coronary artery in patients with aor tic valve deficiency, which regressed after valve replace ment. As a result of these changes there is no impairment of minimal coronary resistance [192,193] or maximal perfusion [166,185,194], Fewer attempts have been made to improve vascular supply in volume overload than in pressure overload hy pertrophy. Pacing-induced bradycardia started 1 month after aortic valve lesion in rabbits, increased capillary density by 60% within 4 weeks in comparison with unpaced hypertrophic hearts, and by 20% compared to control hearts, although it only marginally diminished the degree of hypertrophy [195], It also normalised coronary reserve ratio which was decreased bv hvpertrophv ( fig.…”

Section: Vesselsmentioning

confidence: 99%

Postnatal Growth of the Heart and Its Blood Vessels

Hudlická

Brown²

1996

J Vasc Res

100

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Although rapid growth of the heart during early postnatal development ceases with maturation of the organism, the potential for cardiomyocyte growth is not lost and may be observed even in senescent hearts. Rapid developmental heart growth is accompanied by a proportional growth of capillaries but not always of larger vessels, and thus coronary vascular resistance gradually increases. Growth of adult hearts can be enhanced by thyroid hormones, catecholamines and the renin-angiotensin system hormones, but these do not always stimulate growth of coronary vessels. Likewise, chronic exposure to hypoxia leads to growth, mainly of the right ventricle and its vessels but without vascular growth elsewhere in the heart. On the other hand, ischaemia is a potent stimulus for the release of various growth factors involved in the development of collateral circulation. Heart hypertrophy develops in response to training, pressure or volume overload. Training usually leads to growth of larger coronary vessels but little growth of capillaries, except in young animals. However, growth of the capillary bed, but not the resistance vasculature capacity, can be induced by either increased coronary blood flow, bradycardia (electrically or pharmacologically induced) or increased inotropism, all of which are involved in the training stimulus. Thus, what actually promotes growth of larger vessels as opposed to capillaries in training is unclear. Pressure overload hypertrophy is mediated by both the renin-angiotensin system and the response of cardiomyocytes to stretch; both lead to activation of early oncogenes (c-fos, c-jun, c-myc) and angiotensin II activates several protein kinases involved in cell growth. In this condition, growth of larger vessels is inadequate, although some capillary growth may occur. Volume overload leads to cardiomyocyte hypertrophy and hyperplasia and some increase in vascular supply. Deficits in capillary supply in pressure or volume overload hypertrophy can be reversed by chronic administration of ACE inhibitors, dipyridamole, the bradycardic drug alinidine or pacing-induced bradycardia respectively, but in neither case is training effective. Mechanical and humoral factors are involved in growth of cardiomyocytes and vessels. For cardiomyocytes, stretch is most important, activating oncogenes, protein kinases and possibly the inositol phosphate pathway, but not ion channels, with regulation by the balance of angiotensin II, TGF-β1 and IGF-1, but not FGFs. For vessels, growth is stimulated by stretch and shear stress, possibly with involvement of VEGF. Increased shear stress disrupts the glycocalyx on the luminal side of vessels and releases plasminogen activator and metalloproteinases which disrupt the basement membrane and enable endothelial cell migration and proliferation. It also causes rearrangement of the endothelial cytoskeleton and transmission of mechanical signals to the abluminal side disturbing extracellular matrix and causing distortion of capillary basement membrane. Stretch acting from the ablum...

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Section: Vesselsmentioning

confidence: 99%

Postnatal Growth of the Heart and Its Blood Vessels

Hudlická

Brown²

1996

J Vasc Res

100

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“…Although the structural and biochemical alterations in hypertrophied muscle induced by chronic volume overload may cause ventricular dysfunction, there is no consensus in the literature on the mechanisms of heart failure. Experimental studies have shown either preserved [12–15] or depressed myocardial contractility [16,17] caused by aortocaval fistula in rats. Brower et al [17] showed that systolic ventricular dysfunction was related to chamber dilatation and increased compliance.…”

Section: Introductionmentioning

confidence: 99%

Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy

Stefano

Matsubara

Matsubara³

2006

European J of Heart Fail

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The aim this study was to evaluate systolic and diastolic function in volume overload induced myocardial hypertrophy in rats. Volume overload myocardial hypertrophy was induced in thirteen male Wistar rats by creating infrarenal arteriovenous fistula (AVF). The results were compared with a SHAM operated group (n = 11). Eight weeks after surgery, tail-cuff blood pressure was recorded, then rats were sacrificed for isolated heart studies using Langendorff's preparation.AVF rats presented increased left and right ventricular weights, compared to controls. The increased normalized ventricular volume (V0/ LVW, 0.141 T 0.035 mL/g vs. 0.267 T 0.071 mL/g, P < 0.001) in the AVF group indicated chamber dilation. Myocardial hydroxyproline concentration remained unchanged. There was a significant decrease in + dP/dt (3318 T 352 mm Hg s À 1 vs. 2769 T 399 mm Hg s , P < 0.001) in the AVF group, which presented increased ventricular compliance (DV 25 : SHAM = 0.172 T 0.05 mL vs. AVF = 0.321 T 0.072 mL, P < 0.001) with preserved myocardial passive stiffness (Strain 25 : SHAM = 13.5 T 3.0% vs. AVF = 12.3 T 1.9%, P > 0.05).We conclude that volume-overload induced hypertrophy causes myocardial systolic and diastolic dysfunction with increased ventricular compliance. These haemodynamic features help to explain the long-term compensatory phase of chronic volume overload before transition to overt congestive heart failure.

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“…However, even when using these highly controlled conditions, researchers have reported conflicting results. In fact, myocardial hypertrophy has been described as a condition associated with decreased, unchanged, or even increased contractility when heart failure is absent (2,3,(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). The possible causes for these discrepancies are many and may include the type of hypertrophy, the animal used in the study, the time course of the overload-induced hypertrophy, and the indexes used to measure contractility.…”

Section: Introductionmentioning

confidence: 99%

Myocardial contractility of the isovolumetrically beating isolated rat heart

Stefano

Matsubara

2004

Braz J Med Biol Res

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Several indexes of myocardial contractility have been proposed to assess ventricular function in the isovolumetrically beating isolated heart. However, the conclusions reached on the basis of these indexes may be influenced by ventricular geometry rather than contractility itself. The objective of the present study was to assess the performance of widely used contractility indexes in the isovolumetrically beating isolated heart in two experimental models of hypertrophy, the spontaneously hypertensive rat (SHR) and infrarenal aortocava fistula. Compared to normotensive controls (N = 8), SHRs with concentric hypertrophy (N = 10) presented increased maximum rate of ventricular pressure rise (3875 ± 526 vs 2555 ± 359 mmHg/s, P < 0.05) and peak of isovolumetric pressure (187 ± 11 vs 152 ± 11 mmHg, P < 0.05), and decreased developed stress (123 ± 20 vs 152 ± 26 g/cm 2 , P < 0.05) and slope of stress-strain relationship (4.9 ± 0.42 vs 6.6 ± 0.77 g/cm 2 /%). Compared with controls (N = 11), rats with volume overload-induced eccentric hypertrophy (N = 16) presented increased developed stress (157 ± 38 vs 124 ± 22 g/cm 2 , P < 0.05) and slope of stress-strain relationship (9 ± 2 vs 7 ± 1 g/cm 2 /%, P < 0.05), and decreased maximum rate of ventricular pressure rise (2746 ± 382 vs 3319 ± 352 mmHg, P < 0.05) and peak of isovolumetric pressure (115 ± 14 vs 165 ± 13 mmHg/s, P < 0.05). The results suggested that indexes of myocardial contractility used in experimental studies may present opposite results in the same heart and may be influenced by ventricular geometry. We concluded that several indexes should be taken into account for proper evaluation of contractile state, in the isovolumetrically beating isolated heart.

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Effects of experimental volume-overload hypertrophy on myocardial blood flow and cardiac function

Cited by 13 publications

References 0 publications

Postnatal Growth of the Heart and Its Blood Vessels

Postnatal Growth of the Heart and Its Blood Vessels

Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy

Myocardial contractility of the isovolumetrically beating isolated rat heart

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