Myocardial Injury Group Research Articles

Clinical study on myocardial injury diagnosis of the serum CK, CK-MB, cTnI to the infant patients

Objective To explore the diagnostic value of serum CK, CK-MB, cTnI to myocardial injury in the infant patients. Methods Determination was made to serum CK, CK - MB and cTnI for 196 examples and 102patients with electrocardiogram and clinical expression with and without a myocardial impairment performance of no myocardial injury patients and normal children as control. Results Three indexes of the myocardial injury group were CK (236.2 ± 127.2) U/L; CK-MB (32.2 ± 12.7) U/L, cTnI (0.24 ± 0.13) ng/ml respectively, significantly higher than those in the group without myocardial impairment performance and control group(P ＜ 0.01), but the specificity and sensitivity were different, and the sensitivity and accuracy of the Joint inspection attained 93.4% and 80.5%, both data fields had significant improves (P ＜ 0.05). Conclusions The reaction of the serum CK, CK-MB and the cTnI for infant patients myocardial injury showed that CK, CK-MB specificity is not high, at the same time,we should consider the activity increasing of the pure CK, CK-MB may result from physiology, specimens and reagents, without clinical diagnostic value. The cTnI has the highest specificity, but in myocardial mild damage the sensitivity is not high, so the diagnosis to infant patients myocardial injury should combine with these three factors, as well as the electrocardiogram and clinical expression for comprehensive confirmation. Key words: Myocardial injury; Creatine kinase(CK); Creatine kinase isozyme-MB(CK-MB); Troponin Ⅰ(cTnI); Joint survey

P2X 2/3 receptor activity of rat nodose ganglion neurons contributing to myocardial ischemic nociceptive signaling

Myocardial ischemia causes the production of a variety of chemical substances, which act on the cardiac afferent nerve to cause pain. Myocardial damage can affect cardiac vagal afferent activity. Survivors of myocardial infarction are often left with impaired activity of cardiac vagal sensory fibres. The nodose ganglia (NG) are lower ganglia of cardiac vagus nerve, which are chiefly visceral afferent in the sensation of heart. ATP as a possible damage signal may activate nociceptive sensory neurons. Activation of P2X 3, P2X 2/3 receptors by endogenous ATP contributes to the development of hyperalgesia. The present results have shown that the sensitivity of P2X 2/3 receptor in nodose ganglion neurons was increased after myocardial ischemic injury under electrophysiological observation. The inhibitive role of P2X 2/3 antagonist A-317491 on ATP-activated currents in myocardial ischemic rats was significantly increased, compared with that in control group at the same concentration of A-317491. The staining of P2X 2 and P2X 3 receptors in myocardial ischemic injury group appeared to be more intense than those in naive rats and myocardial ischemic rats treated with A-317491 with immunofluorescence double labeling methods. Therefore, the activity of P2X 2/3 receptors in NG neurons was involved in the transmission of myocardial ischemic nociceptive signal.

Myocardial ischemic nociceptive signaling mediated by P2X 3 receptor in rat stellate ganglion neurons

Adenosine 5′-triphosphate (ATP) is implicated in peripheral pain signaling through activation of P2X receptors. P2X 3 receptors have a high level of expression in, and selective location on sensory afferents. P2X receptors, particularly the P2X 3 subtype, are identified as targets for novel analgesics. The stellate ganglion (SG) is peripheral sympathetic ganglia involved in heart function. Surgical interventions of sympathetic afferent pathways abolish or relieve angina pectoris, so it is showed that cardiac pain is mediated by the activation of afferents in sympathetic nerves. The cervicothoracic sympathetic ganglia, including the stellate ganglion, are implicated in sensations associated with myocardial ischemia or cardiac pain. In the present study we have examined P2X 3 involvement in cardiac nociceptive transmission. P2X receptor agonists activated currents ( I ATP) in SG neurons. The I ATP amplitude and P2X 3 mRNA expression in myocardial ischemic injury group were much larger than those obtained in control group. Prostaglandin E 2 (PGE 2) and substance P (SP) increased ATP-activated currents. P2X 3 receptor antagonist A-317491 reduced P2X agonist activated currents and P2X 3 mRNA expression. The results revealed that the myocardial ischemia induced the upregulation of P2X 3 receptor in function and morphous and P2X 3 receptor antagonist A-317491 inhibited P2X agonist activated currents and P2X 3 mRNA expression. The facts indicated that P2X 3 receptor in SG neurons was involved in cardiac nociceptive transmission.

Exploration of P2X 3 in the rat stellate ganglia after myocardial ischemia

ATP is implicated in peripheral pain signaling by actions on P2X receptors, especially P2X(3) receptor. Cardiac primary afferents running in the sympathetic nerves are considered to be essential pathways for transmission of cardiac nociception to the central nervous system. Because little is known about P2X(3) involvement in cardiac nociception, this study observed the difference in P2X(3) localization and expression in stellate ganglia (SG) from naive rats and in a pathological model of myocardial ischemic injury induced by repeated subcutaneous isoprenaline injections. Distribution of P2X(3) and morphometry of neurons in SG were investigated by immunohistochemistry, Western blotting, in situ hybridization (ISH) and by sterological study. Diffuse cytoplasmic P2X(3) immunolabelling was observed by light microsocopy. No nuclear labeling was detected. The intensity of P2X(3) labeling in the experimental myocardial ischemic injury group was increased in relation to that of the control group. Numerical densities of stellate ganglion neurons in the experimental group were higher than those of the control group. By Western blotting and ISH, the signals of P2X(3) protein and its mRNA in the myocardial ischemic group were higher than those of the control group. The P2X(3) labeling intensity and the numerical density in SG of the experimental myocardial ischemic injury group were enhanced, suggesting the involvement of P2X(3) receptor for the transmission of pain after myocardial ischemic injury.

Histologic, ultrastructural, and enzymatic measurements of infarct size following coronary artery stenosis and occlusion

Coronary artery narrowing (CAN), which reduced resting coronary blood flow (BF) by 50%, was induced in 10 conscious dogs and was maintained for 4 hours. Five additional dogs (group 1) with complete coronary artery occlusion were compared to the dogs with CAN. serum isoenzymes of creatine phosphokinase (CK) and latate dehydrogenase (LD) were monitored hourly in all groups. After 36 hours, samples were obtained for regional myocardial BF, quantitative histology, and quantitative ultrastructural (EM) morphology. Six dogs with CAN had small infarcts (MI) of less than 1 gm and persistent myocardial cell injury (group 2). The other four dogs with CAN had only persistent myocardial cell injury by ultrastructural criteria (group 3). Peak serum CK activities in groups 2 and 3 were similar, as were MI sizes calculated from serum CK and myocardial depletion. MB CK was of diagnostic value in group 1 but not in groups 2 and 3. The ratio of LD 1 LD 2 had diagnostic value in all three groups. MI size by enzyme estimates was consistently higher than planimetered MI size at autopsy in both groups 1 and 2. All three groups had significant amounts of ultrastructural damage outside of histologically demonstrated MI. These findings suggest that (1) gross and histologic MI size determination of 36 hours after ischemia underestimate extent of damage, and (2) ultrastructural cell changes cause significant release of CK and LD in coronary disease (CAD).