The effects of ulinastatin on the cells factor and cardiac function after cardiopulmonary resuscitation in rats / 重庆医学

ABSTRACT

Objective To investigate the protective effects of ulinastatin on the hearts of rats with anoxia-induced cardiac arrest-cardiopulmonary resuscitation(CA-CPR) and the mechanism of improving cardiac dysfunction .Methods Twenty male Sprague Dawley(SD) rats were randomly divided into three experimental groupssham operation group (group A ,n= 8 ,only anesthesia , tracheotomy tube and vascular puncture) ,control group(group B ,n= 6 ,normal saline 4 mL · kg -1 injected via vein) ,Ulinastatin treatment group(group C ,n=6 ulinastatin 50 000 U/kg+normal saline 3 mL · kg -1 injected via vein);Factors including mean arte-rial pressure(MAP) ,left ventricular end diastolic pressure(LVEDP) ,the maximum rising and falling rates of left ventricular deep pressure(± LVdp .dt-1max) ,brain natriuretic peptide(BNP) ,cardiac troponin T(cTNT) ,IL-12 and TNF-αwere observed at setting time before and after cardiopulmonary resuscitation in rats .Results Compared with those of the group A and before CA-CPR ,the concentrations of IL-12、cTNT、TNF-α、BNP、and LVEDP increased(P<0 .01)while ± LVdp .dt-1max decreased(P<0 .01) at 6 h after CA-CPR in group B ,C .Compared with those of group B ,the concentrations of IL-12、CTNT、TNF-α、BNP and LVEDP of 6 h after CA-CPR in group C were lower and ± LVdp .dt-1max was higher(P<0 .01) ,The concentrations of MAP of 6 h after CA-CPR in group B was lower Compared with that of group A ,C and before CA-CPR(P<0 .01) .Conclusion Ulinastatin can improve cardiac dysfunction by depressing mediators of inflammation and reducing myocardial injury .