Continuous Monitoring of Serum Tumor Necrosis Factor-α for Patients with TEMIS Treated by Nitrates Postconditioning during PCI

Objective: To investigate the protective effect of nitrates postconditioning on myocardial ischemia-reperfusion injury and whether it plays a regulatory role in TNF-α in patients with STEMI during PCI. Methods: Patients with STEMI who underwent PCI were selected, except for obvious anemia, head trauma, cerebral hemorrhage, hypotension (systolic blood pressure less than 90 mmHg), and patients with autoimmune diseases, all kinds of acute and chronic infections and malignant tumors. They were randomly divided into PCI standardized treatment group and isosorbide dinitrate postconditioning during PCI group. The concentrations of cTnI and TNF-α in serum were detected by ELISA method in each group before PCI and after 2 hours, 1 day, 4 days and 7 days of PCI. Results: 1) There were no statistically significant differences in sex, age, smoking history, diabetes, hypertension and blood lipid abnormality in two groups. 2) Before operation, the concentration of cTnI in two groups was not statistically significant. The concentration of cTnI in the experimental group was lower than that of the control group after 4 days and 7 days of PCI, and P α in two groups before operation. The concentration of TNF-α in the experimental group was lower than that in the control group after 1 day, 4 days and 7 days of PCI, and P α in two groups was both in 1 day after operation, and the peak level of the experimental group and the level of each time after the operation were lower than that of the control group. Conclusion: Nitrates postconditioning during PCI in patients with STEMI has a protective effect on myocardial ischemia-reperfusion injury. Nitrates postconditioning has an effect to reduce the level of TNF-α of patients with STEMI after PCI treatment, and may have the mechanism of alleviating the inflammatory response after myocardial ischemia and reperfusion.

Effect of Minocycline Postconditioning and Ischemic Postconditioning on Myocardial Ischemia-reperfusion Injury in Atherosclerosis Rabbits

This study examined the protective effect of ischemic postconditioning(IPoC) and minocycline postconditioning(MT) on myocardial ischemia-reperfusion(I/R) injury in atherosclerosis(AS) animals and the possible mechanism.Forty male healthy rabbits were injected with bovine serum albumin following feeding on a high fat diet for 6 weeks to establish AS model.AS rabbits were randomly divided into 3 groups:(1) I/R group,the rabbits were subjected to myocardial ischemia for 35 min and then reperfusion for 12 h;(2) IPoC group,the myocardial ischemia lasted for 35 min,and then reperfusion for 20 s and ischemia for 20 s [a total of 3 cycles(R20s/I20s×3)],and then reperfusion was sustained for 12 h;(3) MT group,minocycline was intravenously injected 10 min before reperfusion.The blood lipids,malondialdehyde(MDA),superoxide dismutase(SOD),soluble cell adhesion molecule(sICAM),myeloperoxidase(MPO),and cardiac troponin T(cTnT) were biochemically determined.The myocardial infarction size(IS) and apoptosis index(AI) were measured by pathological examination.The expression of bcl-2 and caspase-3 was detected in the myocardial tissue by using reverse transcription-polymerase chain reaction(RT-PCR).The results showed that the AS models were successfully established.The myocardial IS,the plasma levels of MDA,sICAM,MPO and cTnT,and the enzymatic activity of MPO were significantly decreased,and the plasma SOD activity was significantly increased in IPoC group and MT group as compared with I/R group(P<0.05 for all).The myocardial AI and the caspase-3 mRNA expression were lower and the bcl-2 mRNA expression was higher in IPoC and MT groups than those in I/R group(all P<0.05).It is concluded that the IPoC and MT can effectively reduce the I/R injury in the AS rabbits,and the mechanisms involved anti-oxidation,anti-inflammation,up-regulation of bcl-2 expression and down-regulation of caspase-3 expression.Minocycline can be used as an effective pharmacologic postconditioning drug to protect myocardia from I/R injury.