Objective    To investigate the changes of RAS and its effects to heart function and myocardial damage at early stage of rat scald.     Methods    The rats were grouped as control group (normal group and sham scald group

totally n=12) and scalded group (n=30). The rat model of 30% TBSA of full-thickness burns was made in 30 male Wistar rats. Hemodynamics and myocardiac mechanics index (SBP

DBP

LVSP

LVEDP

+LVdp/dt

max

-LVdp/dt

max

)

cTn-I

AngⅡ

AC

E levels in serum

and AngⅡ

ACE

ACE2 in myocardium were determined 1

3

6

12

24 h after scald.     Results    Compared with control group

LVSP

+LVdp/dt

max

-LVdp/dt

max

were decreased obviously 1 h after scald (P0.01)

whereas LVEDP increased significantly 1 h after scald (P0.01)

and peaked 6 h after scald. The levels of cTn-I

AngⅡ

ACE in serum

and AngⅡ and ACE in myocardium were increased obviously 1 h after scald (P0.01) compared with control group

and peaked 6 h after scald. No obvious changes of myocardiac ACE2 were detected before and after scald.     Conclusion    The changing tendency of ACE-AngⅡ axis similar to that of hemodynamic index and serum level of cTn-I indicted that ACE-AngⅡ axis of RAS plays an important role in myocardial damage at the early stage after scald. No obvious changes of ACE2 before and after scald may be one of the reasons to activate ACE-AngⅡ axis.