Release kinetics of serum cardiac troponin i in ischemic myocardial injury

Bertinchant, Jean-Pierre; Larue, Catherine; Pernel, Isabelle; Ledermann, Bertrand; Fabbro‐Peray, Pascale; Beck, L; Calzolari, Charles; Trinquier, S; Nigond, J; Pau, Bernard

doi:10.1016/s0009-9120(96)00105-1

Cited by 133 publications

(75 citation statements)

References 30 publications

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“…Serum cTn-I seems more sensitive and more specific than CK, CK-MB, and LDH in minor myocardial injury [2,5,16]. In this study, P2X 7 receptor antagonist oxATP significantly inhibited the elevations in serum CK, CK-MB, LDH, and cTn-I after acute MI injury.…”

Section: Discussionmentioning

confidence: 46%

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Peng

et al. 2013

Purinergic Signalling

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P2X receptors participate in cardiovascular regulation and disease. After myocardial ischemic injury, sensorysympathetic coupling between rat cervical DRG nerves and superior cervical ganglia (SCG) facilitated sympathoexcitatory action via P2X 7 receptor. The results showed that after myocardial ischemic injury, the systolic blood pressure, heart rate, serum cardiac enzymes, IL-6, and TNF-α were increased, while the levels of P2X 7 mRNA and protein in SCG were also upregulated. However, these alterations diminished after treatment of myocardial ischemic (MI) rats with the P2X 7 antagonist oxATP. After siRNA P2X 7 in MI rats, the systolic blood pressure, heart rate, serum cardiac enzymes, the expression levels of the satellite glial cell (SGC) or P2X 7 were significantly lower than those in MI group. The phosphorylation of ERK 1/2 in SCG participated in the molecular mechanism of the sympathoexcitatory action induced by the myocardial ischemic injury. Retrograde tracing test revealed the sprouting of CGRP or SP sensory nerves (the markers of sensory afferent fibers) from DRG to SCG neurons. The upregulated P2X 7 receptor promoted the activation of SGCs in SCG, resulting in the formation of sensory-sympathetic coupling which facilitated the sympathoexcitatory action. P2X 7 antagonist oxATP could inhibit the activation of SGCs and interrupt the formation of sensory-sympathetic coupling in SCG after the myocardial ischemic injury. Our findings may benefit the treatment of coronary heart disease and other cardiovascular diseases.

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Section: Discussionmentioning

confidence: 46%

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Peng

et al. 2013

Purinergic Signalling

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“…ischaemia, cardiotoxic agents, etc. Bertinchant et al (1996) showed the high specificity of cTnI in human medicine and described this protein to be a suitable marker for an early and late diagnosis of acute myocardial infarction. Our experiment was based on the results of a pilot study and focused on obtaining detailed knowledge of the kinetics of cardiac enzymes (cTnI, CKMB).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the specificity of cardiac troponin I and creatine kinase MB in isoproterenol-induced cardiotoxicity model in rats

et al. 2015

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The aim of this study was to implement the determination of cardiac markers in preclinical research at our department. For this purpose, the pathophysiological model of acute cardiotoxicity induced by high doses of isoproterenol was used. Isoproterenol hydrochloride was intraperitoneally administrated to 42 Wistar male rats at a dose of 50 mg/kg body weight. Cardiac injury was determined by assessing the concentrations of the cardiac markers (cTnI -cardiospecific troponin I and CKMB -cardiac isoenzyme creatine kinase) in the blood at predetermined time-intervals (2, 4, 6, 12, 24 and 36 h), and confirmed by ECG. Isoproterenol hydrochloride caused an elevation in the plasma concentrations of both markers. The results showed a significant difference (P < 0.01) in the concentrations of cTnI between the experimental and control groups at 2, 4, 6 and 24 h with a maximum peak between the fourth and sixth hour. However, the difference in the concentrations of CKMB between the experimental and control groups was non-significant. This experiment confirmed that cTnI is more cardiospecific than CKMB. It also revealed the possibility to use this marker in preclinical testing.

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“…The very recent findings of Davies et al (34), for the measurement of troponin I using the antibodies against troponin I from Spectral Co., confirmed that cross-reactivity with skeletal troponin I was absent in concentrations up to 2.0 mg/1. This means that troponin I methods (5,33,34) are very specific for cardiac muscle damage in patients without renal failure, while troponin T is not 100% specific for cardiac damage (24,26,31,32).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Troponin T and Troponin I ELISA Tests, as Measured by Microplate Immunoassay Techniques, in Diagnosing Acute Myocardial Infarction

Penttilä

Penttilä²,

Bonnell³

et al. 1997

CCLM

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Summary:We describe an improved procedure using a standard microplate immunoassay reader to measure the concentration of troponin T in human serum. We also describe an immunoassay for troponin I in serum. Only 160 μΐ of serum are needed for a single analysis of each troponin. For comparison, creatine kinase MB mass analysis in serum was performed with a commercial luminometric method. From 95 apparently healthy people the following values were obtained: creatine kinase MB mass 2.6 ±1.2 μg/l, troponin Τ 0.027 ± 0.025 μg/l and troponin I 0.03 ± 0.031We compared the results of troponin Τ and troponin I methods with each other, as well as with those of creatine kinase MB mass measured in 48 patients with verified acute myocardial infarction and in 60 control patients with non-cardiac chest pain. The correlation between troponin Τ and troponin I values was 0.91 for the total material and 0.94 for 48 patients with acute myocardial infarction. Troponin I showed better earlier sensitivity than troponin Τ (ρ = 0.043). In nine patients in the control group, creatine kinase MB mass exceeded the reference limit of 5.0 μg/l, while in two patients the cut-off limit of 10.0 μ §/1 was also surpassed, pointing to non-specificity.In the group of infarct patients, the highest serum creatinine value was 193 μηιοΐ/ΐ, whereas in the control group it was 406 μιηοΙ/1. The sera of patients with impaired renal function without any cardiac failure showed no increase in troponin Τ and troponin I values.In conclusion, serum creatine kinase MB mass and troponin I seem to confirm an acute myocardial infarction more rapidly than does troponin T; troponin I has the highest cardiac specificity.

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Release kinetics of serum cardiac troponin i in ischemic myocardial injury

Cited by 133 publications

References 30 publications

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Sensory–sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor

Comparison of the specificity of cardiac troponin I and creatine kinase MB in isoproterenol-induced cardiotoxicity model in rats

Comparison of the Troponin T and Troponin I ELISA Tests, as Measured by Microplate Immunoassay Techniques, in Diagnosing Acute Myocardial Infarction

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