BACKGROUND: In vivo assessment of cardiac injury and contractile deficits after thermal injury remain difficult as neurohumoral compensatory mechanisms maintain cardiac output. While measurement of creatine kinase (CK) and the isoenzyme of creatine kinase (CKMB) have been used as clinical indicators of cardiac injury, these biochemical markers are not completely specific for cardiac muscle. Cardiac protein troponin I (cTnI) is unique to the myocardium but can be detected in the systemic circulation within three to four hours after cardiac injury. The purpose of this study was to examine cardiac contractile function at several postburn intervals and to correlate the appearance of cardiac dysfunction with biochemical measures of cardiac injury (serum concentration of CK, CKMB, and cTnI). STUDY DESIGN: New Zealand white rabbits were deeply anesthetized and a scald burn comprising 34 percent of the total body surface area (n = 36) or sham burn (n = 36) was accomplished using a template device. All burn rabbits were given lactated Ringer's solution (4 mL/kg/percent burn, Parkland formula). Blood samples were collected immediately prior to sacrifice in six animals from both burn and control groups, and animals were sacrificed either two, four, six or 24 hours after burn. Cardiac function was assessed in left ventricular preparations (Langendorff) and serum CK, CKMB, and cTnI levels were determined. RESULTS: Cardiac dysfunction occurred at all times after burn as indicated by a lower peak systolic left ventricular pressure and +/- dP/dt maximum compared with time-matched shams and the shift of left ventricular function curves plotted for burn groups downward and to the right of those calculated for shams, p < 0.05. Left ventricular systolic dysfunction after burn correlated with a progressive rise in cTnI and CK but not CKMB. CONCLUSIONS: The cardiospecificity of the cTnI eliminates concerns about tissue source associated with CK and CKMB and provides a biochemical measure of cardiac injury that is consistent with in vitro assessment of cardiac dysfunction.
BACKGROUND: In vivo assessment of cardiac injury and contractile deficits after thermal injury remain difficult as neurohumoral compensatory mechanisms maintain cardiac output. While measurement of creatine kinase (CK) and the isoenzyme of creatine kinase (CKMB) have been used as clinical indicators of cardiac injury, these biochemical markers are not completely specific for cardiac muscle. Cardiac protein troponin I (cTnI) is unique to the myocardium but can be detected in the systemic circulation within three to four hours after cardiac injury. The purpose of this study was to examine cardiac contractile function at several postburn intervals and to correlate the appearance of cardiac dysfunction with biochemical measures of cardiac injury (serum concentration of CK, CKMB, and cTnI). STUDY DESIGN: New Zealand white rabbits were deeply anesthetized and a scald burn comprising 34 percent of the total body surface area (n = 36) or sham burn (n = 36) was accomplished using a template device. All burn rabbits were given lactated Ringer's solution (4 mL/kg/percent burn, Parkland formula). Blood samples were collected immediately prior to sacrifice in six animals from both burn and control groups, and animals were sacrificed either two, four, six or 24 hours after burn. Cardiac function was assessed in left ventricular preparations (Langendorff) and serum CK, CKMB, and cTnI levels were determined. RESULTS:Cardiac dysfunction occurred at all times after burn as indicated by a lower peak systolic left ventricular pressure and +/- dP/dt maximum compared with time-matched shams and the shift of left ventricular function curves plotted for burn groups downward and to the right of those calculated for shams, p < 0.05. Left ventricular systolic dysfunction after burn correlated with a progressive rise in cTnI and CK but not CKMB. CONCLUSIONS: The cardiospecificity of the cTnI eliminates concerns about tissue source associated with CK and CKMB and provides a biochemical measure of cardiac injury that is consistent with in vitro assessment of cardiac dysfunction.
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