THE
PROTECTIVE EFFECT OF DEXAMETHASONE ON CARDIAC INJURY IN NEONATAL RAT WITH
ENDOTOXIC SHOCK
Wu YB, Du XH, Li YJ and Han YK.
Pediatric Department of the Second
Clinical College,
China Medical University, Shenyang,
China
Objective:To explore the mechanism of protective effect of dexameth- asone
(Dex) on cardiac injury in neonatal rat with endotoxic shock.
Methods: Health Seven-day-old newborn Wister rat (n=126) were involved
in this study. The agents given by intraparitoneal injection Include: Group
1: 0.9% sodium chloride, Group 2: (LPS group) LPS 5mg/kg, Group 3: (Dex
group)LPS 5mg/kg plus Dex 5mg/kg (n=7, for each group). Plasma TNF Serum
NO. NO. iNOS mRNA of cardiac tissues (CT) measured at the time points of
0,2,4,6,24 hour after injection, respectively. Ultraconstructure of the
myocardial cells was observed at 24th hour.
Results: (1) In LPS group, Plasma TNF concentration increased at 2nd
hour (P<0.01) and decreased at 4h. Serum NO Level elevated signifi-
cantly at 2h (P<0.01) and peaked at 24h (P<0.001). NO concentration
of CT increased markedly at 4h(P<0.001) and peaked at 24h. iNOS mRNA
expression appeared at 4h and disappeared at 24h. The myocardial
congestion, degeneration or necrosis of myocardium were noted markedly. (2)
In Dex group, Plasma TNF Level increase slightly but not significantly.NO
level of serum and CT also significantly elevated at 6th and 4th hour
(P<0.05), respectively, and peaked at 24th hour. However, the Level of
which was significantly lower than that in LPS group (p<0.001). Cardiac
cells iNOSmRNA espression was not found in Dex group. And the cardiac
injury was slight.
Conclusion: the protective effect of Dex on cardiac injury in neonatal rats
with endotoxic shock is conducted by inhibiting TNF secretion enhances iNOS
mRNA expression to reduce the output of NO.