Humans ; Myocardium ; chemistry ; Sensitivity and Specificity ; Troponin ; analysis

In an attempt to determine whether myocardial catecholamines vary from season to season, their concentration in rabbits was measured throughout the whole year by the spectrophotofluorometric method. The highest concentration of cardiac catecholamine was observed in summer. Measurement of the atrial response to norepinephrine revealed no significant alteration during the entire period of the experiment.
Animals ; Catecholamines/*analysis ; Heart/*drug effects ; Myocardium/*analysis ; Norepinephrine/*pharmacology ; Rabbits ; *Seasons

BACKGROUND AND OBJECTIVES: The objective of this study was to determine whether long-term exercise training will improve age-related cardiac metabolic derangement using proton magnetic resonance (MR) spectroscopy. MATERIALS AND METHODS: Young and old male Fischer 344 rats were assigned to sedentary controls groups {young control (YC) group-3 months of age: YC, n=10; old control (OC) group-22 months of age: OC, n=10}, and an exercise training group (OT, n=5). After 12-week of treadmill exercise training, MR spectroscopy at 4.7 T was performed to assess myocardial energy metabolism: measurements of myocardial creatine-to-water ratio (Scr/Sw) were performed using the XWIN-NMR software. RESULTS: Exercise capacity was 14.7 minutes greater in OT than that in OC (20.1+/-1.9 minutes in OT, 5.4+/-2.3 minutes in OC; p<0.001). The 12-week exercise training rendered the old rats a maximum exercise capacity matching that of untrained YC rats (17.9+/-1.5 minutes in YC, 20.1+/-1.9 minutes in OT; p>0.05). The creatine-to-water ratios in the interventricular septa of YC did not differ significantly from that of OT (0.00131+/-0.00025 vs. 0.00127+/-0.00031; p=0.37). However, OC showed significant reduction in creatine-to-water ratio compared to OT (0.00096+/-0.00025 vs. 0.00127+/-0.00031; p<0.001). Mean total creatine concentrations in the myocardium were similar between YC and OT (13.3 +/-3.6 vs. 11.5+/-4.1 mmol/kg wet weight; p=0.29). In contrast, the mean total creatine concentration of OC was significantly reduced compared to OT (6.8+/-3.2 vs. 11.5+/-4.1 mmol/kg wet weight; p=0.03). CONCLUSION: Our findings suggest that long-term exercise training in old rats induced prevention of age-related deterioration in myocardial metabolism.
Animals ; Creatine ; Humans ; Magnetic Resonance Spectroscopy ; Magnetics ; Magnets ; Male ; Myocardium ; Protons ; Rats ; Spectrum Analysis

Objective Quantitative analysis and comparison of the expression of ribonucleic acid （RNA） from frozen organs and formaldehyde-fixed and paraffin-embedded （FFPE） tissues. Methods Frozen specimens of human brain, myocardium and liver tissues as well as FFPE samples at different postmortem intervals were collected and mass concentration of RNA was extracted and detected. Reverse transcription-quantitative polymerase chain reaction （RT-qPCR） technology was used to analyze the amplification efficiency and relative expression of each RNA marker. Results The mass concentration and integrity of RNA extracted from FFPE samples were relatively low compared with frozen specimens. The amplification efficiency of RNA markers was related with RNA species and the length of amplification products. Among them, glyceraldehyde-3-phosphate dehydrogenase （GAPDH） and β-actin （ACTB） with relatively long amplification products failed to achieve optimal amplification efficiency, whereas 5S ribosomal RNA （5S rRNA） achieved ideal amplification efficiency and showed quite stable expression across various tissues, therefore it was chosen as internal reference marker. The expression quantity of GAPDH and ACTB in frozen specimens with longer postmortem intervals and in FFPE samples with relatively long amplification products was decreased. The expressions of tissue-specific microRNAs （miRNAs）, GAPDH and ACTB with relatively short amplification products had consistency in the same tissues and FFPE samples. Conclusion Through standardizing the RT-qPCR experiment, selecting the appropriate RNA marker and designing primers of appropriate product length, RNA expression levels of FFPE samples can be accurately quantified.
DNA Primers ; Formaldehyde ; Gene Expression Profiling ; Humans ; MicroRNAs/analysis* ; Myocardium ; Paraffin Embedding ; RNA/analysis* ; Real-Time Polymerase Chain Reaction/standards*

OBJECTIVELeft ventricular remodeling (LVR) following myocardial infarction (MI) is a key pathophysiological process in which MI develops into heart failure. The exact mechanism of LVR remains unclear. We performed differential proteomic analysis on the myocardia of rats with LVR after MI, to explore the mechanism of ventricular remodeling after MI.

METHODSIn the LVR group (n = 12), after the anterior descending coronary artery was ligated, the rats were fed for four weeks before the LVR models were established. Rats in the sham-operated group (n = 11) underwent thread-drawing without ligation. The hemodynamic parameters, pathological findings, and proteomics were compared between the two groups.

RESULTSIn the LVR group, the left ventricular end-diastolic pressure increased, the maximal left ventricular pressure increase/decrease ratio decreased significantly, and the left ventricular systolic pressure decreased. H-E staining and Masson staining of cardiac muscle tissues of the LVR group showed myocytolysis, disarray, and collagen proliferation. Twenty-one differentially expressed proteins were detected by proteomic analysis. We validated two proteins using western blot analysis. The differentially expressed proteins could be divided into six categories: energy metabolism-related proteins, cytoskeletal proteins, protein synthesis-related proteins, channel proteins, anti-oxidation- related proteins, and immune-related proteins.

CONCLUSIONThese differentially expressed proteins might play key roles in LVR following MI.

Animals ; Male ; Myocardial Infarction ; complications ; pathology ; Myocardium ; metabolism ; pathology ; Proteome ; analysis ; Proteomics ; Rats ; Rats, Wistar ; Ventricular Remodeling

BACKGROUND AND OBJECTIVES: Myocardial injury after percutaneous coronary intervention (PCI) occurs frequently and it is associated with an adverse clinical outcome. Mechanical factors have been implicated in this complication and the role of inflammation has not yet been clearly determined. We evaluated the effect of an inflammatory response during PCI on periprocedural myocardial injury. SUBJECTS AND METHODS: We prospectively studied 231 patients (mean age: 62.8+/-10.6 years, males: 60.6%) who underwent elective coronary stenting. For the exclusion of mechanical injury to the myocardium, we excluded those patients who developed complications during PCI. Blood samples for measuring the high sensitivity C-reactive protein (hsCRP) and troponin T (TnT) were obtained before the procedure and at 6 hours and 24 hours after PCI. The inflammatory response to PCI was calculated as the difference between the peak postprocedural hsCRP level and the preprocedural hsCRP level (delta CRP). We divided the patients according to the median value of delta CRP: Group I <2.2 mg/dL and Group II > or =2.2 mg/dL. RESULTS: Postprocedural TnT elevation was were observed in 72 (31.2%) patients. The baseline clinical and angiographic characteristics were not difference between the two groups. The incidence of any TnT elevations was higher in the Group II than that in Group I (19.8% vs 42.6%, respectively, p<0.001). The incidences of TnT levels over 3 times the upper normal limit and 5 times the upper normal limit were also higher in Group II than in Group I (11.2% vs 21.7%, respectively, p=0.031, for a TnT level 3 times the upper normal limit, and 6.0% vs 13.9%, respectively, for a TnT level 5 times the upper normal limit). Multivariate analysis revealed that postprocedural hsCRP elevation and complex lesion were the significant independent predictors of postprocedural TnT elevation. CONCLUSION: Elevated hsCRP levels were associated with a higher risk of postprocedural troponin elevation in patients undergoing uncomplicated PCI. These results emphasized the role of inflammation in the pathogenesis of periprocedural myocardial injury.
Angioplasty ; C-Reactive Protein ; Humans ; Incidence ; Inflammation ; Multivariate Analysis ; Myocardium ; Percutaneous Coronary Intervention ; Prospective Studies ; Stents ; Trinitrotoluene ; Troponin ; Troponin T

Although there are many methods to estimate the early postmortal interval, more attention has been paid to the research on measuring the amount of DNA in cells. This paper introduce several different measuring ways, law of variation and application situation of DNA in cells. In addition, the result evaluation of measuring methods and application prospect is given.
DNA/analysis* ; Flow Cytometry ; Forensic Medicine ; Humans ; Kidney/chemistry* ; Liver/chemistry* ; Myocardium/chemistry* ; Postmortem Changes ; Time Factors

OBJECTIVE: To test cathepsin L as a biomarker of myocardial ischemia by examination of cathepsin L expression in plasma after myocardial ischemia and ischemia-reperfusion in rats. METHODS: The rat models were established and divided in acute myocardial ischemia model (myocardial ischemia 30 min, 1 h, 2 h groups), ischemia-reperfusion model (ischemia-reperfusion group), and isoflurane-pretreated ischemia-reperfusion model (isoflurane-pretreated group), respectively. Normal control group and sham-operated group were established as contrast. The contents of cathepsin L in plasma were examined by ELISA and myocardial infarction areas were measured after TTC staining. RESULTS: No statistical significant changes were found among the experimental groups compared with the normal control group and sham-operated group (P>0.05). The cathepsin L from the ischemia-reperfusion group increased to 2.37 times compared with the normal control group (P<0.05). The cathepsin L and myocardium infarction size of isoflurane-pretreated group decreased compared with the ischemia-reperfusion group (P<0.05). CONCLUSION The cathepsin L in plasma is not a promising biomarker of acute myocardial ischemia. Isoflurane preconditioning can reduce the cathepsin L in plasma caused by ischemia-reperfusion injury.
Animals ; Biomarkers/blood* ; Cathepsin L/analysis* ; Isoflurane ; Myocardial Infarction/metabolism* ; Myocardial Ischemia ; Myocardial Reperfusion Injury/metabolism* ; Myocardium ; Rats

In order to explore the specificity of complement C5 in the postmortem diagnosis of myocardial infarction, changes of C5 staining in normal, infarcted and other non-infarcted myocardia with direct or indirect myocardial injuries (myocarditis, mechanical asphyxia, electrocution, hemorrhagic shock, cardiac contusion and organophosphate poisoning) were studied with immunohistochemistry and image analysis. The results showed that positive C5 staining could be observed in groups of myocardial infarction and myocarditis, but not in groups of mechanical asphyxia, electrocution, hemorrhagic shock, cardiac contusion, and organophosphate poisoning. It is indicated that positive reaction of C5 could only be affected by myocarditis, which means that it was more specific for the diagnosis of myocardial infarction.
Adolescent ; Adult ; Complement C5/analysis* ; Female ; Forensic Medicine ; Humans ; Male ; Myocardial Infarction/diagnosis* ; Myocardium/chemistry* ; Sensitivity and Specificity

OBJECTIVETo study the effect of calcium-sensing receptor (CaSR) agonists and antagonists on the expression of CaSR in neonatal mice with persistent pulmonary hypertension (PPHN), and to clarify the role of CaSR in neonatal mice with PPHN.

METHODSForty-nine neonatal mice were randomly divided into four groups: control (n=10), hypoxia (PPHN; n=11), agonist (n=13), and antagonist (n=15). The mice in the PPHN, agonist, and antagonist groups were exposed to an oxygen concentration of 12%, and those in the control group were exposed to the air. The mice in the agonist and antagonist groups were intraperitoneally injected with gadolinium chloride (16 mg/kg) and NPS2390 (1 mg/kg) respectively once daily. Those in the PPHN and the control groups were given normal saline daily. All the mice were treated for 14 consecutive days. Hematoxylin and eosin staining and immunohistochemistry were used to observe the changes in pulmonary vessels. Laser confocal microscopy was used to observe the site of CaSR expression and measure its content in lung tissues. qRT-PCR and Western blot were used to measure the mRNA and protein expression of CaSR in lung tissues.

RESULTSCompared with the control group, the PPHN group had significant increases in the pulmonary small artery wall thickness and the ratio of right to left ventricular wall thickness (P<0.05), which suggested that the model was successfully prepared. Compared with the control group, the PPHN group had a significant increase in the mRNA and protein expression of CaSR (P<0.05), and the agonist group had a significantly greater increase (P<0.05); the antagonist group had a significant reduction in the mRNA and protein expression of CaSR (P<0.05).

CONCLUSIONSCaSR may play an important role in the development of PPHN induced by hypoxia in neonatal mice.

Animals ; Hypoxia ; complications ; Lung ; pathology ; Mice ; Myocardium ; pathology ; Persistent Fetal Circulation Syndrome ; etiology ; pathology ; Pulmonary Artery ; pathology ; RNA, Messenger ; analysis ; Receptors, Calcium-Sensing ; analysis ; genetics ; physiology