Fig 1.
Parameters measured in the sarcomere shortening signal.
TMS: time interval to reach the instant of maximal shortening velocity; TPC: time interval to reach the peak of contraction; TMR: time interval to reach the instant of maximal relaxation velocity; THALF: time interval to reach 50% resting sarcomere length.
Fig 2.
Typical echocardiogram obtained from control and diabetic rats.
Bidimensional M-mode echocardiogram from a control (a) and diabetic (b) rats showing the aorta (AO) and left atrium (LA) on top and at the bottom the left ventricular cavity over the cardiac cycle during systole (left ventricle end-systolic dimension, LVESD) and diastole (left ventricle end-diastolic dimension, LVEDD) with corresponding ECG tracings.
Table 1.
M-mode echocardiographic data obtained from control and diabetic groups.
Table 2.
Pulsed-wave doppler and pulsed-wave doppler tissue imaging measured in the control and diabetic groups.
Table 3.
Values of electrocardiography in control and diabetic animals.
Fig 3.
Sarcomere shortening in isolated cardiac myocytes.
(A) Representative examples of sarcomere shortening in cardiac myocytes from control and diabetic rat. In the box-and-whiskers plot, the median (line), inter-quartile range (box) and 5th and 95th percentile (whiskers) of (B) time interval to reach the maximal shortening velocity (TMS), (C) time interval to reach the peak of contraction (TPC), (D) time interval to reach the maximal relaxation velocity (TMR) and (E) time interval to reach the 50% resting sarcomere length (THALF). n = 31 cells from 5 hearts for the control group and n = 33 cells from 8 hearts for the diabetic group. *P < 0.001.
Table 4.
Values of biochemical measurements in control and diabetic animals.
Fig 4.
Determination of interstitial fibrosis.
Interstitial fibrosis was quantified in control and diabetic rats in ventricle (A and B respectively) and atria (C and D, respectively). No changes were observed between groups both for the ventricles (P = 0.17) and atria (P = 0.42). Collagen in atrium was higher than that of ventricles in both control (P = 0.03) and diabetic animals (P = 0.01).
Fig 5.
Determination of ventricular perivascular fibrosis.
Ventricular perivascular fibrosis was analyzed in the myocardium of control (A) and diabetic animals (B). No differences were observed (P = 0.36) between groups.