Objective      To determine the anti-inflammatory effects of heme oxygenase-1 (HO-1) on post-resuscitation myocardial injury in rats.       Methods      The rat model of cardiopulmonary resuscitation (CPR) were established by being asphyxiated f

or 9 min and resuscitated. A total of 60 male Sprague-Dawley rats

weighing 330-380 g

were randomly divided into 4 groups

that is

sham-operation group (placement of related catheter without cardiopulmonary resuscitation)

CPR group

Hemin treatment group (Hemin

30 mg/kg

given in 2 and 18 h before CPR infliction by intraperitoneal injection)

and Hemin+zinc protoporphyrin IX (ZnPP) treatment group (Hemin given as precious description. ZnPP

5 mg/kg

given in 1 and 17 h before CPR infliction by intraperitoneal injection). Resuscitated groups were observed in 6 h and 24 h after cardio-pulmonary resuscitation (with 8 rats for each time point). Sham-operation group (n=12) were observed at the same time points with 6 rats for each time point. HO-1 expression in cardiac tissue was detected by Western blotting. Serum creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH) levels were detected by automatic biochemistry analyzer. Serum concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). Cardiac ultrastructure was observed by transmission electron microscopy.       Results      The expression of HO-1 in resuscitated groups were markedly increased in 6 and 24 h after resuscitation. The level of HO-1 was significantly higher in Hemin group than that in CPR group and Hemin+ZnPP group at the 2 time points after resuscitation (all

P

0.05). Serum levels of CPK-MB and LDH in resuscitated groups were markedly increased at 6 and 24 h after resuscitation. The activity of CPK-MB and LDH in Hemin group were significantly lower than that in CPR group and Hemin+ZnPP group (all

P

0.05）. The level of TNF-α were significantly increased in CPR group and Hemin+ZnPP group at 6 and 24 h after resuscitation（all

P

0.05）; but that in Hemin group was increased only in 6 h after resuscitation and lower than the former 2 groups（all

P

0.05）

  and then returned to baseline in 24 h after resuscitation（

P

0.05）. The level of IL

-6 were significantly increased in CPR group and Hemin+ZnPP group only in 24 h after resuscitation（

P

0.05）

but that in Hemin group had no significant difference after resuscitation（

P

0.05）. The cardiac tissue ultrastructure of rats in Hemin group was more intact than CPR group and Hemin+ZnPP group.       Conclusion      HO-1 attenuates myocardial injury in rats after cardiopulmonary resuscitation

probably through its anti-inflammatory effect.