Objective        To study the protective effect of hypertonic sodium chloride hydroxyethyl sta

rch 40 (HHS) on myocardial injury in rats with uncontrolled hemorrhagic shock (UHS) and the possible mechanisms.       Methods        Rat models of UHS were established using the modified Capone method. Thirty SD rats were randomly divided into a normal control (NC) group

a normal saline (NS) group

and a HHS group (

n

=10). The blood pressure of rats in the NS group and HHS group was decreased to 40 mmHg by artery bloodletting

and then active hemorrhage was induced by 75% tail amputation. The rats were given NS and HHS infusion to maintain the MAP at 50 mmHg. In 1 h after resuscitation

the rats underwent operation for hemostasis followed by blood and sufficient fluid transfusion to maintain the MAP at 90 mmHg. Cardiac function indices including left ventricular systolic pressure (LVSP)

left ventricular end-diastolic pressure (LVEDP) and  dp/dt

max

were monitored continuously during the time of UHS and resuscitation. Arterial blood samples were taken at 0 (T0)

30  (T1)

90  (T2) and 210 min (T3) after UHS for determination of the levels of creatine kinase isoenzyme MB (CK-MB)

lactate dehydrogenase (LDH) and cardiac troponin I (cTnI). Myocardium samples of rats were extracted for observation of ultrastructural changes under an electron microscope. All the rats were sacrificed and the heart was made for tissue homogenate to determine the levels of malondialdehyde (MDA)

superoxide dismutase (SOD)

tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) at T3. Myocardial apoptosis was detected by TUNEL staining.       Results       The cardiac function indices were significantly improved in the HHS group than in the NS group (

P

<

0.05). Compared with the NS group

the levels of CK-MB

LDH and cTnI significantly decreased in the HHS group (

P

<

0.05). There were less ultrastructural changes of myocardium in the HHS group than in the NS group. The levels of MDA

TNF-α and IL-6 in the myocardium of the HHS group were significantly lower than those of the NS group

while the

SOD activity was significantly higher in the HHS group than in the NS group (

P

<

0.05). The myocardial apoptosis significantly decreased in the HHS group compared with the NS group (

P

<

0.05).       Conclusion        HHS can reduce myocardial injury induced by UHS in rats. The myocardial protection of HHS is probably mediated by reducing the release of free radical and consumption of SOD

decreasing the generation of TNF-α and IL-6

and inhibiting myocardial apoptosis.