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Two-dimensional (2-D) speckle tracking echocardiography (STE) accurately quantifies circumferential strain (Scare) and radial strain ([S.sub.rad]) in humans and in large and small animals. This study was performed to assess sensitivity of [S.sub.circ] and [S.sub.rad] to left ventricular (LV) dysfunction in mouse models. We performed 2-D and M-mode echocardiography 1) in 6 mice during superficial and profound isoflurane anesthesia, 2) serially in 12 mice to monitor the development of heart failure induced by transverse aortic constriction (TAC) and in 8 corresponding control mice, and 3) in 26 mice with varying degrees of TAC-induced heart failure and 12 corresponding control mice immediately before euthanasia. Fractional shortening (FS) and LV mass were measured from standard M-mode tracings, whereas [S.sub.circ] and [S.sub.rad] were derived by STE. Percent fibrosis and myocyte diameters were assessed from whole heart cross-sectional specimens stained by Masson trichrome. Profound isoflurane anesthesia decreased [S.sub.circ] (P = 0.027) but not [S.sub.rad] (P > 0.05). Mice subjected to TAC showed an immediate and sustained decrease in FS (P = 0.035), [S.sub.circ] (P = 0.016), and [S.sub.rad] (P = 0.012). [S.sub.circ] showed better correlation with FS (r = 0.56 and P < 0.0001) and LV mass (r = 0.42 and P = 0.0003) than [S.sub.rad] (r = 0.54 and P < 0.0001 for FS and r = 0.37 and P = 0.014 for LV mass, respectively). Percent fibrosis correlated better with Scare (r = 0.46 and P = 0.004) than with [S.sub.rad] (r = -0.32 and P = 0.05), whereas myocyte diameter showed similar correlation with both strains (r = 0.45 and r = -0.44, respectively, and P = 0.006 for both). STE correctly identifies LV dysfunction and histological changes in mice and can be used for the serial assessment of cardiac remodeling in murine models. transverse aortic constriction; systolic strain; systolic function

The remodeling process of the arterial wall in atherosclerosis involves intimal thickening, which can be related to the barrier functions of the endothelial cell layer (ECL) and internal elastic lamina (IEL) using horseradish peroxidase (HRP) as a tracer. To evaluate the ECL and IEL permeabilities ([P.sub.ECL] and [P.sub.IEL], respectively) and intimal transport parameters, e.g., apparent HRP velocity ([V.sub.I] and diffusivity, we compared simulations with a mathematical model to experimental data. In this study, we injected HRP into the vein of apolipoprotein E-null mice and measured HRP concentration profiles in lesioned areas of aortas. Lesion size was characterized by lower, middle, and upper ranges of the intimal/medial thickness ([[delta].sub.I]/[[delta].sub.M]): 0 < [[delta].sub.I]/[[delta].sub.M] [less than or equal to] 0.5, 0.5 < [[delta].sub.I]/[[delta].sub.M] [less than or equal to] 1.0, and [[delta].sub.I]/[[delta].sub.M] > 1.0. The [P.sub.ECL] (in micrometers per minute) of 5-mo-old mice in the middle range (0.98 [+ or -] 0.14) was significantly greater than that in the lower range (0.21 [+ or -] 0.03) but not significantly different from mice in the upper range (0.99 [+ or -] 0.55). The [P.sub.ECL] of 12-mo-old mice increased significantly with the relative intimal thickness: 0.27 [+ or -] 0.04 in the lower range, 1.12 [+ or -] 0.15 in the middle range, and 1.74 [+ or -] 0.24 in the upper range. In both age groups, [V.sub.I] (in micrometers per minute) increased significantly from lower to upper ranges of intimal thickness. However, [P.sub.IEL] did not change significantly with relative intimal thickness and age. In the upper range of intimal thickness, [P.sub.ECL] and [V.sub.I] were significantly greater in 12-mo-old mice than in 5-mo-old mice. These data indicate an interaction between lesion growth and aging that leads to progressive loss in the integrity of the endothelial barrier function. Furthermore, the IEL is not a significant barrier between the intima and tunica media in the atherosclerotic process. atherosclerosis; arterial wall transport; endothelial cell layer; intima

Speckle-tracking echocardiography (STE) uses a two-dimensional echocardiographic image to estimate two orthogonal strain components. The aim of this study was to assess sensitivity of circumferential ([S.sub.circ]) and radial ([S.sub.rad]) strains to infarct-induced left ventricular (LV) remodeling and scarring of the LV in a rat. To assess the relationship among [S.sub.circ], [S.sub.rad], and scar size, two-dimensional echo-cardiographic LV short-axis images (12 MHz transducer, Vivid 7 echo machine) were collected in 34 Lewis rats 4 to 10 wk after ligation of the left anterior descending artery. Percent segmental fibrosis was assessed from histological LV cross sections stained by Masson trichrome. Ten normal rats served as echocardiographic controls. [S.sub.circ] and [S.sub.rad] were assessed by STE. Histological data showed consistent scarring of anterior and lateral segments with variable extension to posterior and inferior segments. Both [S.sub.circ] and [S.sub.rad] significantly decreased after myocardial infarction (P < 0.0001 for both). As anticipated, [S.sub.circ] and [S.sub.rad] were lowest in the infarcted segments. Multiple linear regression showed that segmental [S.sub.circ] were similarly dependent on segmental fibrosis and end-systolic diameter (P < 0.0001 for both), whereas segmental [S.sub.rad] measurements were more dependent on end-systolic diameter (P < 0.0001) than on percent fibrosis (P < 0.002). STE correctly identifies segmental LV dysfunction induced by scarring that follows myocardial infarction in rats. infarction; collagen; contractility doi:10.1152/ajpheart.01176.2006

In early diastole, pressure is lower in the apex than in the base of the left ventricle (LV). This early intraventricular pressure difference (IVPD) facilitates LV filling. We assessed how LV diastolic IVPD and intraventricular pressure gradient (IVPG), defined as IVPD divided by length, scale to the heart size and other physiological variables. We studied 10 mice, 10 rats, 5 rabbits, 12 dogs, and 21 humans by echocardiography. Color Doppler M-mode data were postprocessed to reconstruct IVPD and IVPG. Normalized LV filling time was calculated by dividing filling time by RR interval. The relationship between IVPD, IVPG, normalized LV filling time, and LV end-diastolic volume (or mass) as fit to the general scaling equation Y = k[M.sup.[beta]], where M is LV heart size parameter, Y is a dependent variable, k is a constant, and [beta] is the power of the scaling exponent. LV mass varied from 0.049 to 194 g, whereas end-diastolic volume varied from 0.011 to 149 ml. The [beta] values relating normalized LV filling time with LV mass and end-diastolic volume were 0.091 (SD 0.011) and 0.083 (SD 0.009), respectively (P < 0.0001 vs. 0 for both). The [beta] values relating IVPD with LV mass and end-diastolic volume were similarly significant at 0.271 (SD 0.039) and 0.243 (SD 0.0361), respectively (P < 0.0001 vs. 0 for both). Finally, [beta] values relating IVPG with LV mass and end-diastolic volume were -0.118 (SD 0.013) and -0.104 (SD 0.011), respectively (P < 0.0001 vs. 0 for both). As a result, there was an inverse relationship between IVPG and normalized LV filling time (r = -0.65, P < 0.001). We conclude that IVPD decrease, while IVPG increase with decreasing animal size. High IVPG in small mammals may be an adaptive mechanism to short filling times. hemodynamics; diastolic function; comparative physiology doi:10.1152/ajpheart.00081.2006