Control of myocardial tissue components and cardiocyte organelles in pressure‐overload hypertrophy of the cat right ventricle

Lauva, Ines K.; Brody, Eric A.; Tiger, Eric; Kent, Robert L.; Cooper, George; Marino, Thomas A.

doi:10.1002/aja.1001770109

Cited by 4 publications

(3 citation statements)

References 48 publications

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“…Volume overload of the cat right ventricle resulted in a 33.3% increase in this ratio . Even in cats that had developed hypertrophy as a result of a pressure overload, while a t the same time receiving either a-and P-adrenoceptor blockade, the degree of hypertrophy was similar to that seen in this study (Lauva et al, 1986).…”

Section: Musclesupporting

confidence: 84%

“…An increase in the connective tissue component of the myocardium occurs in a complex manner which may contribute to a n increase in the stiffness of the overloaded myocardium (Weber et al, 1987(Weber et al, , 1989Doering et al, 1988). The disproportionate increase in connective tissue that accompanied the pressure overload hypertrophy could be attenuated by a-or P-adrenoceptor blockade (Lauva et al, 1986). Both a-and P-adrenoceptor blockade failed to prevent and did decrease the amount of cardiac hypertrophy that resulted from pressure overload, and in particular this was true when heart muscle cell cross sectional areas were measured and used as a n index of the degree of hypertrophy 0 1991 WILEY-LISS, INC (Lauva et al, 1985).…”

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confidence: 99%

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Norepinephrine‐induced cardiac hypertrophy of the cat heart

et al. 1991

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Norepinephrine administration causes progressive hypertrophy of the mammalian heart as measured by myocardial mass. The purpose of this study was to determine the growth response of the myocardial tissue components as well as the myocardial cell itself to norepinephrine. Young, adult cats were given low doses of norepinephrine in dextrose or dextrose alone twice daily for 15 days. On day 16, there were no changes in the animals body weight, right ventricular systolic pressure, right ventricular end-diastolic pressure, heart rate, cardiac index, or blood pressure. However, the right ventricle/body weight, the left ventricle/body weight and the total heart weight/body weight were increased significantly in the norepinephrine treated animals. The increase was on the order of 40%. The cardiac muscle cell was also significantly increased in size and both the right and left ventricular cardiac muscle cells exhibited a dramatic increase in size as measured by cross sectional area. Upon stereological examination it was found that the amount of hypertrophy as seen in the cardiac muscle cells was paralleled by the hypertrophy seen in the other tissue components of the myocardium. The volume density of the muscle cells, the interstitial components, as well as the blood vessel compartment were identical in the control and in the norepinephrine-treated groups. In conclusion, this study demonstrates that the response of the myocardium to norepinephrine is similar to that seen in response to a volume overload rather than that seen in response to pressure overload.

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Section: Musclesupporting

confidence: 84%

mentioning

confidence: 99%

Norepinephrine‐induced cardiac hypertrophy of the cat heart

et al. 1991

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“…Multiple models mimicking RV pressure overload are available, including models of PH 7,8,9,10,11,12,13,14,15,16,17 and models of proximal RV pressure load 2,3,10,18,19,20,21,22,23 . The choice of either a model of PH or a model of proximal RV pressure load depends on the research question: the effect of an intervention on the pulmonary vasculature and therefore possibly RV afterload modulation (i.e., PH models), or the direct effect on the RV (i.e., proximal RV pressure load models).…”

Section: Introductionmentioning

confidence: 99%

Quantification of Biventricular Function and Morphology by Cardiac Magnetic Resonance Imaging in Mice with Pulmonary Artery Banding

Koop¹,

Hagdorn²,

Kolk³

et al. 2020

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Right ventricular (RV) function and failure are major determinants of outcome in acquired and congenital heart diseases, including pulmonary hypertension. Assessment of RV function and morphology is complex, partly due to the complex shape of the RV. Currently, cardiac magnetic resonance (CMR) imaging is the golden standard for noninvasive assessment of RV function and morphology. The current protocol describes CMR imaging in a mouse model of RV pressure load induced by pulmonary artery banding (PAB). PAB is performed by placing a 6-0 suture around the pulmonary artery over a 23 G needle. The PAB gradient is determined using echocardiography at 2 and 6 weeks. At 6 weeks, the right and left ventricular morphology and function is assessed by measuring both end-systolic and end-diastolic volumes and mass by ten to eleven cine slices 1 mm thick using a 9.4 T magnetic resonance imaging scanner equipped with a 1,500 mT/m gradient. Representative results show that PAB induces a significant increase in RV pressure load, with significant effects on biventricular morphology and RV function. It is also shown that at 6 weeks of RV pressure load, cardiac output is maintained. Presented here is a reproducible protocol for the quantification of biventricular morphology and function in a mouse model of RV pressure load and may serve as a method for experiments exploring determinants of RV remodeling and dysfunction.

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New perspectives on left ventricular hypertrophy: Anatomy, physiology, and significance

et al. 2009

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The advent of echocardiography has added an important and sensitive tool for assessment of left ventricular hypertrophy (increased left ventricular mass). Recent echocardiographic studies in large population‐based samples suggest an epidemic of left ventricular hypertrophy. Preliminary data suggesting important prognostic importance for such left ventricular hypertrophy (independent of standard risk factors) has fueled interest in the development, determinants, and other features of the hypertrophy. Hemodynamic and neurohumoral factors are the most prominent stimuli to adaptive (physiologic) myocardial hypertrophy, which can progress to maladaptive (pathologic) hypertrophy. The overall blood pressure experience, overweight, the cardiovascular response to recurrent psychosocial stress and physical activity level are four important correlates and potential determinants of left ventricular mass in various urban‐suburban populations. Determination of the relative contributions and interrelations of these and other factors (such as heredity) to various forms of left ventricular hypertrophy found in various demographic groups warrants intensive investigation.

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Control of myocardial tissue components and cardiocyte organelles in pressure‐overload hypertrophy of the cat right ventricle

Cited by 4 publications

References 48 publications

Norepinephrine‐induced cardiac hypertrophy of the cat heart

Norepinephrine‐induced cardiac hypertrophy of the cat heart

Quantification of Biventricular Function and Morphology by Cardiac Magnetic Resonance Imaging in Mice with Pulmonary Artery Banding

New perspectives on left ventricular hypertrophy: Anatomy, physiology, and significance

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