4±0 4 vs 3 1±0 5 cm/s, p<0 001) In terms of diastolic functions

4±0.4 vs. 3.1±0.5 cm/s, p<0.001). In terms of diastolic functions, diastolic parameters, which were acquired

from mitral inflow including E, A velocity, deceleration time and E/A ratio did not significantly SRT1720 order differ between two groups. However, early diastolic mitral annulus velocity (e’) was impaired in diabetes group compared to control (2.9±0.6 vs. 3.8±1.1, p=0.013). Diabetes group showed a significant elevation of E/e’ ratio compared to control (27.1±5.6 vs. 19.7±2.6, p<0.001)(Fig. 2A). Detailed data are presented in Table 2. Fig. 2 A: Major echocardiographic variables. Inhibitors,research,lifescience,medical B: Bar graphs demonstrate major hemodynamic parameters including Ees, PRSW, tau and LV EDP. *p<0.05 for difference from control. FS: fractional shortening, s': mitral annulus peak systolic velocity, e': mitral ... Table 2 Echocardiographic data at 10 weeks after diabetes induction Invasive Hemodynamic Measurement The heart rare was significantly Inhibitors,research,lifescience,medical decreased in diabetes group compared to normal control. (DM: 279±30 vs. Control: 333±57 BPM, p=0.007). Likewise in echocardiography, 10 weeks after diabetes induction, LV volume index of diabetes group were significantly increased compared to normal control (LV ESV index: 419.4±127.5 (DM) vs. 195.3±57.0 µL/g×103 (control), p<0.001 and LV

EDV index: 1718.8±318.9 (DM) vs. 777.5±118.3 Inhibitors,research,lifescience,medical (control) µL/g×103, p<0.001, respectively). Stroke volume (1389.4±307.1 vs. 625.9±125.3 µL/g×103, p<0.001) index and cardiac index (384.9±84.0 vs. 197.2±24.0 µL/min/g, p<0.001) increased significantly in diabetes group compared to normal control (SD). With regard to systolic functions, diabetes group did not show differences in ejection fraction and dP/dtmax compared to normal control. Conversely, Inhibitors,research,lifescience,medical most of loading condition independent parameters of systolic

function were impaired in diabetes group compared with those of normal control: Ees (0.18±0.07 vs. Inhibitors,research,lifescience,medical 0.62±0.18 mmHg/µL, p<0.001), PRSW (51.8±22.0 vs. 90.9±22.5 mmHg, p<0.001) and dP/dt-EDV (8.2±4.3 vs. 17.0±8.7 mmHg/s/µL, p<0.001). As regarding diastolic function parameters, LV end-diastolic pressure (EDP) was significantly elevated (11.2±6.9 vs. 5.1±3.7 mmHg, p=0.015), and time constant of LV pressure decay (τ) was prolonged (20.5±5.2 vs. 14.2±2.3 ms, p=0.002) in diabetes Carnitine dehydrogenase group compared to control. Additionally, the slope of EDPVR was impaired in diabetes group, compared to control (0.07±0.04 vs. 0.01±0.01 mmHg/µL, p<0.001) (Fig. 2B, Table 3). Table 3 Hemodynamic parameters at 10 weeks after diabetes induction Discussion In this study, we tried to re-establish the rat model of type 1 DM induced by streptozocin because the results were conflicting between different authors. Ten weeks after diabetes induction in SD rats, there were no differences in fractional shortening, E/A ratio of mitral inflow and deceleration time.

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