Echocardiographic and cardiac doppler assessment of mice

Pollick, Charles; Hale, Sharon L.; Kloner, Robert A.

doi:10.1016/s0894-7317(05)80373-6

Cited by 109 publications

(73 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The anterior chest area was shaved and two-dimensional (2D) images and M-mode tracings were recorded from the parasternal short axis view at the level of papillary muscles. From M-mode tracings, anatomical parameters in diastole and systole were obtained (17). Ejection fraction (EF) was derived from LV cross-sectional area in 2D short axis view (17): EF ϭ [(LVDA Ϫ LVSA)͞LVDA] ϫ 100, where LVDA and LVSA correspond to LV areas in diastole and in systole.…”

Section: Methodsmentioning

confidence: 99%

“…From M-mode tracings, anatomical parameters in diastole and systole were obtained (17). Ejection fraction (EF) was derived from LV cross-sectional area in 2D short axis view (17): EF ϭ [(LVDA Ϫ LVSA)͞LVDA] ϫ 100, where LVDA and LVSA correspond to LV areas in diastole and in systole. Mice were anesthetized with chloral hydrate (400 mg͞kg body weight, i.p.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Mobilized bone marrow cells repair the infarcted heart, improving function and survival

Orlic

Kajstura

Chimenti

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

1,893

1,304

View full text Add to dashboard Cite

Attempts to repair myocardial infarcts by transplanting cardiomyocytes or skeletal myoblasts have failed to reconstitute healthy myocardium and coronary vessels integrated structurally and functionally with the remaining viable portion of the ventricular wall. The recently discovered growth and transdifferentiation potential of primitive bone marrow cells (BMC) prompted us, in an earlier study, to inject in the border zone of acute infarcts Lin ؊ c-kit POS BMC from syngeneic animals. These BMC differentiated into myocytes and vascular structures, ameliorating the function of the infarcted heart. Two critical determinants seem to be required for the transdifferentiation of primitive BMC: tissue damage and a high level of pluripotent cells. On this basis, we hypothesized here that BMC, mobilized by stem cell factor and granulocyte-colony stimulating factor, would home to the infarcted region, replicate, differentiate, and ultimately promote myocardial repair. We report that, in the presence of an acute myocardial infarct, cytokine-mediated translocation of BMC resulted in a significant degree of tissue regeneration 27 days later. Cytokineinduced cardiac repair decreased mortality by 68%, infarct size by 40%, cavitary dilation by 26%, and diastolic stress by 70%. Ejection fraction progressively increased and hemodynamics significantly improved as a consequence of the formation of 15 ؋ 10 6 new myocytes with arterioles and capillaries connected with the circulation of the unaffected ventricle. In conclusion, mobilization of primitive BMC by cytokines might offer a noninvasive therapeutic strategy for the regeneration of the myocardium lost as a result of ischemic heart disease and, perhaps, other forms of cardiac pathology.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Mobilized bone marrow cells repair the infarcted heart, improving function and survival

Orlic

Kajstura

Chimenti

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

1,893

1,304

View full text Add to dashboard Cite

show abstract

“…Outflow velocities were obtained by Doppler sampling from apical four-chamber view for measurement of the ejection time (ET). LV ejection fraction (EF) was calculated as follows: EF ϭ (LVEDD 3 -LVESD 3 ͞ LVEDD 3 where LVEDD is the LV end diastolic diameter and LVESD is LV end systolic diameter (16). The mean velocity of circumferential fiber shortening (Vcfc) was corrected for heart rate and calculated as follows: Vcfc ϭ SF͞ETc where SF is shortening fraction obtained as SF ϭ (LVEDD-LVESD)͞ LVEDD, and ETc is the ejection time corrected for heart rate (as ET divided by square root of R-R interval) (17).…”

Section: Methodsmentioning

confidence: 99%

Reversible cardiac fibrosis and heart failure induced by conditional expression of an antisense mRNA of the mineralocorticoid receptor in cardiomyocytes

Beggah

Escoubet

Puttini

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Cardiac failure is a common feature in the evolution of cardiac disease. Among the determinants of cardiac failure, the reninangiotensin-aldosterone system has a central role, and antagonism of the mineralocorticoid receptor (MR) has been proposed as a therapeutic strategy. In this study, we questioned the role of the MR, not of aldosterone, on heart function, using an inducible and cardiac-specific transgenic mouse model. We have generated a conditional knock-down model by expressing solely in the heart an antisense mRNA directed against the murine MR, a transcription factor with unknown targets in cardiomyocytes. Within 2-3 mo, mice developed severe heart failure and cardiac fibrosis in the absence of hypertension or chronic hyperaldosteronism. Moreover, cardiac failure and fibrosis were fully reversible when MR antisense mRNA expression was subsequently suppressed.C ardiac failure is a major health problem with increasing incidence with aging of the population. Cardiac fibrosis is a marker of cardiac failure and a crucial determinant of myocardial heterogeneity, increasing diastolic stiffness, systolic dysfunction, and the propensity for reentry arrhythmias (1). Animal models are necessary to investigate the mechanisms of appearance and regression of cardiac remodeling and to improve therapeutic strategies. In this paper, we report on a conditional mouse transgenic model in which cardiac fibrosis can be induced and reversed. This was achieved by regulating the expression of the mineralocorticoid receptor (MR) in cardiomyocytes.Studies in both experimental animals and humans have suggested that aldosterone excess may have deleterious effects on cardiac function (2). Recently, the Randomized Aldactone Evaluation Study (RALES) showed that treatment of patients experiencing severe heart failure with spironolactone, an antagonist of the aldosterone receptor (mineralocorticoid receptor) used in the treatment of hypertension, improved both morbidity and mortality (3). These findings have resulted in the recommendation of spironolactone use in the treatment of severe heart failure (4). In RALES, the mechanisms and cellular targets involved in the beneficial effect of spironolactone action are largely unknown. Because MR is expressed in both cardiomyocytes (5) and the kidney (6), it has been difficult to separate the direct effects of signaling through the cardiac MR and indirect effects resulting from actions of the drug on renal MR. MR is a ligand-dependent transcription factor of the steroid receptor superfamily (7). In the kidney, aldosterone binding to MR increases sodium reabsorption and potassium excretion (6). Inactivating mutations of MR result in chronic renal salt wasting, and activating mutation of MR causes hypertension, underscoring the essential role of this pathway in sodium balance and the control of blood pressure (8, 9). In the heart, however, the role of MR in physiologic and pathologic situations has not been defined. A MR knockout mouse model is available (10), but these animals die in the first ...

show abstract

“…Transthoracic echocardiography was performed for measurements of LV internal diameter at end diastole and end systole, interventricular septal wall thickness, posterior wall thickness, and LV mass as previously reported. 14 Pulsed Doppler tracings of the estimated mitral inflow velocity were obtained in a modified parasternal long-axis view. 15 The peaks of the E and A waves of the mitral inflow velocity tracing were recorded as the average of 3 beats.…”

Section: Physiological Studiesmentioning

confidence: 99%

Angiotensin II Type 2 Receptor Is Essential for Left Ventricular Hypertrophy and Cardiac Fibrosis in Chronic Angiotensin II–Induced Hypertension

et al. 2001

View full text Add to dashboard Cite

show abstract

Echocardiographic and cardiac doppler assessment of mice

Cited by 109 publications

References 4 publications

Mobilized bone marrow cells repair the infarcted heart, improving function and survival

Mobilized bone marrow cells repair the infarcted heart, improving function and survival

Reversible cardiac fibrosis and heart failure induced by conditional expression of an antisense mRNA of the mineralocorticoid receptor in cardiomyocytes

Angiotensin II Type 2 Receptor Is Essential for Left Ventricular Hypertrophy and Cardiac Fibrosis in Chronic Angiotensin II–Induced Hypertension

Contact Info

Product

Resources

About