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[Protective effect of ulinastatin on myocardium after cardiopulmonary resuscitation in rats].

Shouquan Chen, Shi-Fang Zhou, Zhang-Ping Li, Jie Zhang, Ping Yan, Weijia Huang, Junyan Cheng, Huiping Li, Wan-Tie Wang

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Abstract

OBJECTIVE: To investigate the changes in serum creatine kinase isoenzyme (CK-MB) and cardiac troponin I (cTnI) levels and the ultrastructure of myocardium, and the effect of ulinastatin after cardiopulmonary resuscitation (CPR) in rats. METHODS: One hundred and twenty Sprague-Dawley (SD) rats were randomly divided into sham operation group, CPR group and ulinastatin group. And each group was divided into five subgroups (n=8) according to time points of 0.5, 3, 6, 12, 24 hours after tracheostomy in sham operation group or after restoration of spontaneous circulation (ROSC) in CPR group and ulinastatin group. Cardiac arrest (CA) and CPR models were reproduced by asphyxia in CPR group and ulinastatin group, with injection of ulinastatin 100 kU/kg via carotid 2 minutes after ROSC in ulinastatin group. Normal saline was given in the same dosage as ulinastatin in CPR group. Serum samples was taken at each time point of subgroups for measuring serum levels of CK-MB and cTnI. The ultrastructure changes in myocardium were observed under the electron microscope. RESULTS: The serum levels of CK-MB and cTnI were increased from 0.5 hours after ROSC in CPR group and ulinastatin group compared with sham operation group ( all P<0.01), and CK-MB peaked at 12 hours, then decreased. The serum CK-MB or cTnI levels started to decreased from 3 hours or 0.5 hours after ROSC in ulinastatin group compared with CPR group (P<0.05 or P<0.01). There were milder pathological changes of ultrastructure of myocardium in ulinastatin group than in CPR group. CONCLUSION: Ulinastatin could decrease serum levels of CK-MB and cTnI, and alleviate myocardial injury after CPR in rats.

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What this paper is about

OBJECTIVE: To investigate the changes in serum creatine kinase isoenzyme (CK-MB) and cardiac troponin I (cTnI) levels and the ultrastructure of myocardium, and the effect of ulinastatin after cardiopulmonary resuscitation (CPR) in rats. METHODS: One hundred and twenty Sprague-Dawley (SD) rats were randomly divided into sham operation group, CPR group and ulinastatin group. And each group was divided into five subgroups (n=8) according to time points of 0.5, 3, 6, 12, 24 hours after tracheostomy in sham operation group or after restoration of spontaneous circulation (ROSC) in CPR group and ulinastatin group. Cardiac arrest (CA) and CPR models were reproduced by asphyxia in CPR group and ulinastatin group, with injection of ulinastatin 100 kU/kg via carotid 2 minutes after ROSC in ulinastatin group. Normal saline was given in the same dosage as ulinastatin in CPR group. Serum samples was taken at each time point of subgroups for measuring serum levels of CK-MB and cTnI. The ultrastructure changes in myocardium were observed under the electron microscope. RESULTS: The serum levels of CK-MB and cTnI were increased from 0.5 hours after ROSC in CPR group and ulinastatin group compared with sham operation group ( all P<0.01), and CK-MB peaked at 12 hours, then decreased. The serum CK-MB or cTnI levels started to decreased from 3 hours or 0.5 hours after ROSC in ulinastatin group compared with CPR group (P<0.05 or P<0.01). There were milder pathological changes of ultrastructure of myocardium in ulinastatin group than in CPR group. CONCLUSION: Ulinastatin could decrease serum levels of CK-MB and cTnI, and alleviate myocardial injury after CPR in rats.

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Available abstract

OBJECTIVE: To investigate the changes in serum creatine kinase isoenzyme (CK-MB) and cardiac troponin I (cTnI) levels and the ultrastructure of myocardium, and the effect of ulinastatin after cardiopulmonary resuscitation (CPR) in rats. METHODS: One hundred and twenty Sprague-Dawley (SD) rats were randomly divided into sham operation group, CPR group and ulinastatin group. And each group was divided into five subgroups (n=8) according to time points of 0.5, 3, 6, 12, 24 hours after tracheostomy in sham operation group or after restoration of spontaneous circulation (ROSC) in CPR group and ulinastatin group. Cardiac arrest (CA) and CPR models were reproduced by asphyxia in CPR group and ulinastatin group, with injection of ulinastatin 100 kU/kg via carotid 2 minutes after ROSC in ulinastatin group. Normal saline was given in the same dosage as ulinastatin in CPR group. Serum samples was taken at each time point of subgroups for measuring serum levels of CK-MB and cTnI. The ultrastructure changes in myocardium were observed under the electron microscope. RESULTS: The serum levels of CK-MB and cTnI were increased from 0.5 hours after ROSC in CPR group and ulinastatin group compared with sham operation group ( all P<0.01), and CK-MB peaked at 12 hours, then decreased. The serum CK-MB or cTnI levels started to decreased from 3 hours or 0.5 hours after ROSC in ulinastatin group compared with CPR group (P<0.05 or P<0.01). There were milder pathological changes of ultrastructure of myocardium in ulinastatin group than in CPR group. CONCLUSION: Ulinastatin could decrease serum levels of CK-MB and cTnI, and alleviate myocardial injury after CPR in rats.

Key concepts: Ulinastatin, Medicine, Cardiopulmonary resuscitation, Troponin I, Anesthesia, Creatine kinase, Saline, Creatine

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[Protective effect of ulinastatin on myocardium after cardiopulmonary resuscitation in rats]. — Research Paper | ScholarLens