Cardiac troponin I release and cytokine response during experimental human endotoxaemia

被引:25
作者
van Bockel, EAP [1 ]
Tulleken, JE [1 ]
Kobold, ACM [1 ]
Ligtenberg, JJM [1 ]
van der Werf, TS [1 ]
Spanjersberg, R [1 ]
Zijlstra, JG [1 ]
机构
[1] Univ Groningen Hosp, Dept Internal Med, Intens & Resp Care Unit, NL-9700 RB Groningen, Netherlands
关键词
endotoxin; troponin I; myocardial dysfunction; tumour necrosis factor-alpha (TNF-alpha); interleukin-6 (IL-6); interleukin-8 (IL-8); sepsis;
D O I
10.1007/s00134-003-1893-x
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Objective. To study the relationship between cytokine levels and cardiac troponin I (cTnI). Design. Prospective experimental study. Setting. Intensive care unit of a university hospital. Participants. Six healthy male volunteers. Interventions. Endotoxin, 4 ng/kg, was given as a 1-min intravenous infusion. Measurements and results. Circulating cardiac troponin I levels and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8) were analysed at various time points during a 24-h period. TNF-alpha appeared in the circulation 30 min after injection (T=0.5 h), reaching peak levels (5,665+/-1,910 pg/ml) 2 h after infusion. At T=24 h TNF-alpha was still elevated in the circulation compared to T=0. None of the six volunteers had a cTnI value higher than 0.1 mug/l at T=0, 6 h or 24 h. Conclusion. The presence of significant amounts of TNF-alpha, IL-6 and IL-8 in the systemic circulation does not lead to increased levels of cTnI in experimental human endotoxaemia.
引用
收藏
页码:1598 / 1600
页数:3
相关论文
共 14 条
[1]   CARDIAC TROPONIN-I - A MARKER WITH HIGH SPECIFICITY FOR CARDIAC INJURY [J].
ADAMS, JE ;
BODOR, GS ;
DAVILAROMAN, VG ;
DELMEZ, JA ;
APPLE, FS ;
LADENSON, JH ;
JAFFE, AS .
CIRCULATION, 1993, 88 (01) :101-106
[2]   Elevation of troponin I in sepsis and septic shock [J].
Ammann, P ;
Fehr, T ;
Minder, EI ;
Günter, C ;
Bertel, O .
INTENSIVE CARE MEDICINE, 2001, 27 (06) :965-969
[3]   Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study [J].
Arlati, S ;
Brenna, S ;
Prencipe, L ;
Marocchi, A ;
Casella, GP ;
Lanzani, M ;
Gandini, C .
INTENSIVE CARE MEDICINE, 2000, 26 (01) :31-37
[4]   Cardiomyocyte apoptosis contributes to the pathology of the septic shock heart [J].
Beranek, JT .
INTENSIVE CARE MEDICINE, 2002, 28 (02) :218-218
[5]  
BODOR GS, 1995, CLIN CHEM, V41, P1710
[6]   Cardiac troponin: a new serum marker of myocardial injury in sepsis [J].
Fernandes, CJ ;
Akamine, N ;
Knobel, E .
INTENSIVE CARE MEDICINE, 1999, 25 (10) :1165-1168
[7]  
Fijen, 2000, Eur J Intern Med, V11, P89, DOI 10.1016/S0953-6205(00)00068-6
[8]   MYOCARDIAL INJURY IN CRITICALLY ILL PATIENTS - A FREQUENTLY UNRECOGNIZED COMPLICATION [J].
GUEST, TM ;
RAMANATHAN, AV ;
TUTEUR, PG ;
SCHECHTMAN, KB ;
LADENSON, JH ;
JAFFE, AS .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1995, 273 (24) :1945-1949
[9]   Tumor necrosis factor alpha and interleukin 1 beta are responsible for in vitro myocardial cell depression induced by human septic shock serum [J].
Kumar, A ;
Thota, V ;
Dee, L ;
Olson, J ;
Uretz, E ;
Parrillo, JE .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (03) :949-958
[10]   Myocardial cell injury in septic shock [J].
Turner, A ;
Tsamitros, M ;
Bellomo, R .
CRITICAL CARE MEDICINE, 1999, 27 (09) :1775-1780