Effects of high intensity military training on cardiovascular system of military personnel / 解放军医学杂志

Objective To explore the changes of cardiovascular system of military personnel during highly intensive training.Methods One hundred and seventy officers and soldiers were as research subjects,including 100 individuals in high-intensity group and 70 in control group.The levels of serum cortisol (COR),high sensitivity C-reactive protein (hs-CRP),cardiacspecific Troponin T (cTnT) and human heart fatty acid binding protein (H-FABP) were measured when military training ended.All subjects were tested with fatigue assessment instrument (FAI).The data of blood pressure and electrocardiogram were collected from 40 individuals randomly selected from high-intensity group and 36 from control group before and after training for analyzing the blood pressure,arrhythmia and heart rate variability (HRV).Results The levels of COR (indicator related to stress) and hs-CRP (indicator related to inflammation) were significantly higher in high intensity group than in control group (P＜0.05).Highly intensive training can lead to the emergence of myocardial micro-injury,the levels of cTnT and H-FABP were obviously higher than those in control group (P＜0.01),and the mean blood pressure and the severity of fatigue status were significantly higher than those in control group (P＜0.05).The incidence of severe ventricular arrhythmia was lower in both groups (P=1.000).The average heart rate,total heart beats,total number of atrial premature beat,total number of ventricular premature beat,the incidence of sinus arrhythmia and intermittent second degree type Ⅰ atrioventricular block were significantly higher in high intensity group than in control group (P＜0.05).The HRV of high intensity group was obviously decreased (P＜0.01).Conclusion Highly intensive training may induce the military personnel into the state of acute stress and inflammation,which may lead to myocardial injury,increase severity of fatigue status,accompanied with the rise of blood pressure,low HRV and increased incidence of various arrhythmias.

The protective role of interleukin-6 monoclonal antibody on experimental autoimmune myocarditis and its mechanism / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the therapeutic effect of IL-6 mAb on experimental autoimmune myocarditis (EAM) in rats, and search the mechanism of the role of IL-6, helper T cells 17 (Th17) and regulative T cells (Treg) in EAM pathogenesis.</p><p><b>METHODS</b>Thirty-four Lewis rats were divided into three groups randomly, i.e. control group (n = 6), EAM group (n = 12), and IL-6 mAb intervention group (n = 16). Rats in EAM group and IL-6 mAb intervention group were injected intracutaneously with myosin to establish EAM model. Rats in IL-6 mAb intervention group were injected intraperitoneally with 1 mg IL-6 mAb on 1st, 7th to 20th day after cardiac myosin immune injection. Myocardial inflammation was examined by HE stain, Masson stain, and TdT assay (TUNEL reaction) on 21st and 84th day after IL-6 mAb therapy in order to assess the therapeutic role. Spleen cells were analyzed by flow cytometry to illustrate Th17 and Treg cells? number and function. The serum concentration of IL-6, IL-10, IL-17, and TGF-beta in each group was measured by ELISA, concentration of STAT3, RORgammat, and Foxp3 mRNA in each group was determined with RT-PCR. Spleen cells derived from EAM were stimulated by IL-6 mAb in vitro, and the concentration of IL-10, IL-17 and TGF-beta was measured by ELISA.</p><p><b>RESULTS</b>Inflammation score, fibrosis score, and apoptosis index in IL-6 mAb intervention group were significantly decreased as compared with those in EAM group (P < 0.01). The number of Th17 and Treg cells in EAM group on the 21st day (experimental acute peak stage) were increased, and those in intervention group on the 21st day were significantly inhibited (P < 0.01). The concentration of serum IL-6, IL-10, IL-17 and TGF-beta in intervention group on the 21st day was decreased dramatically in comparison with that in EAM group on the same day (P < 0.01). The levels of peripheral blood STAT3, RORgammat, Foxp3 mRNA in intervention group on the 21st day was decreased significantly as compared with that in EAM group (P < 0.01). The expression of IL-10, IL-17 and TGF-beta was increased significantly (P < 0.01) by stimulation of IL-6 mAb on spleen cells derived from EAM in vitro.</p><p><b>CONCLUSIONS</b>IL-6 mAb could neutralize IL-6, and ameliorate myocarditis and reduce heart autoimmune responses. IL-6 mAb has significantly protective effects on EAM by suppressing Th17 and Treg cells.</p>

Study of L-NAME treatment on experimental autoimmune myocarditis / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To observe the therapeutic effect of N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, on experimental autoimmune myocarditis (EAM) in Balb/C mice and discuss the therapeutic mechanism induced by apoptosis.</p><p><b>METHODS</b>Thirty male Balb/C mice were divided into normal control group, model control group and experimental group randomly (n = 10). Model control group and experimental group were created into EAM by injection of porcine cardiac myosin subcutaneously in double groin and axilla and pertussis toxin intraperitoneally on day 0 and 7 respectively. Model control group was intraperitoneally administered 5 mg/(kg x day) of physiological saline after infective myosin and pertussis toxin. Experimental group was intraperitoneally given 5 mg/(kg x day) of L-NAME on day 1-21. The hearts and blood were processed after sacrificed on day 21. Cardiac inflammation score was measured by HE staining. Heart weight / body weight (HW/BW), serum nitric oxide (NO) level, activity of induced nitric oxide synthase (iNOS) and mRNA expression of iNOS in heart were measured in each group. Degree of heart apoptosis were evaluated by cardiac apoptotic index through TUNEL, immunohistochemical examination and real time PCR of Caspase-3, Caspase-8 and Caspase-9.</p><p><b>RESULTS</b>Compared with normal control group, cardiac inflammation score, HW/BW level of NO and activity of iNOS, mRNA expression of iNOS, the levels of mRNA and protein of Caspase-3, Caspase-8 and Caspase-9 and cardiac apoptotic index were significantly higher (P < 0.01) in model control group, and those of model control group were higher than those of experimental group (P < 0.01). HW/BW was only a little elevation in model control group compared with that in the experiment group (P < 0.05).</p><p><b>CONCLUSION</b>The development of EAM is related with the NO catalyzed by iNOS. L-NAME protects cardiac myocyte via suppressing the activity of iNOS and further decreased production of NO in EAM. The mechanism might be that L-NAME alleviated myocardial inflammation through inhibited the apoptosis of cardiac myocyte.</p>

Polymorphisms of angiotensin-converting enzyme 2 gene confer a risk to lone atrial fibrillation in Chinese male patients / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Growing epidemiologic evidence has indicated that genetics can predispose individuals to the occurrence of lone atrial fibrillation (AF). The angiotensin-converting enzyme 2 (ACE2) gene has been established to be associated with hypertension and left ventricular hypertrophy. The objective of our study was to investigate the association of ACE2 gene polymorphisms with lone AF.</p><p><b>METHODS</b>A total of 265 consecutive lone AF patients and 289 healthy controls were successfully investigated. The polymorphisms rs2106809 and rs2285666 were genotyped by polymerase chain reaction (PCR) and direct sequencing. A Logistic regression model was used to determine the odds ratio (OR) and 95% confidence intervals (CI) of variations of ACE2 for lone AF.</p><p><b>RESULTS</b>The T allele of rs2106809 conferred an increased risk for lone AF (OR 1.24, 95% CI 1.01-1.52, P = 0.03) in males after adjustment for conventional risk factors. SNP at rs2285666 in males was not significantly different between AF patients and controls. No association was found between the two polymorphisms in the female population with lone AF. After (36.3 ± 4.5) months of follow-up, the end point data were obtained: death (cardiac and noncardiac), ischemic stroke, and heart failure. In the male subgroup, the associations between rs2106809 T male carriers and combined end points including ischemic stroke, heart failure, and death in our study were of significance (OR 3.6, 95% CI 1.0-13.1, P = 0.04).</p><p><b>CONCLUSIONS</b>The results indicate that polymorphism at ACE2 gene is associated with male lone AF in a Chinese Han population. Lone AF males who carry the rs2106809 T allele are associated with adverse cardiac events.</p>

A prospective study to evaluate the efficacy of an intracardiac electrogram-based atrioventricular and interventricular intervals optimization method in cardiac resynchronization therapy / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Cardiac resynchronization therapy (CRT) with biventricular pacing improves cardiac function, functional capacity and quality of life in selected patients with heart failure. The current study aimed to evaluate the efficacy of the intracardiac electrogram (IEGM)-based optimization method, QuickOpt(TM), in Chinese patients treated with CRT.</p><p><b>METHODS</b>Aortic time velocity integrals (AVTI) achieved at the sensed atrioventricular (AV), paced AV and interventricular (VV) interval settings recommended by both QuickOpt(TM) and standard echocardiographic optimization were measured in 101 patients. Consistency and the strength of the relationship between the two timing cycle optimization methods were assessed by intra-class correlation coefficient (ICC).</p><p><b>RESULTS</b>The ICC showed good agreement and correlation with what the AVTI achieved at the optimal sensed AV (ICC = 0.9683 (0.9535 - 0.9785)), paced AV (ICC = 0.9642 (0.9475 - 0.9757)) and VV (ICC = 0.9730 (0.9602 - 0.9817)) interval settings determined by the two optimization methods. The average time required by echocardiographic optimization and by QuickOpt(TM) were (78.32 ± 32.40) minutes and (1.98 ± 1.64) minutes respectively (P < 0.0001).</p><p><b>CONCLUSION</b>The QuickOpt(TM) algorithm provides a quicker, simpler and reliable alternative to the standard method for timing cycle optimization.</p>

Ultrastructural study of the pulmonary veins in pigs / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the possible relationship between the ultrastructural characteristics of pulmonary veins and the pathogenesis of atrial fibrillation originating from pulmonary veins.</p><p><b>METHODS</b>The pulmonary veins from domestic pigs were serially sectioned (2 mm) transversely along the vessels. The odd number sections were fixed in 10% phosphate buffered formalin solution and the even number sections were fixed in 3% Glutaral for further electron microscopy observations.</p><p><b>RESULTS</b>Two cell types were found in the pulmonary veins of pigs. One cell type was the P-like cells that had an empty-appearing cytoplasm containing only sparse myofibrils and small mitochondria, both of which were randomly distributed. Another cell type was slender transitional cells with plenty of longitudinally displayed myofibrils.</p><p><b>CONCLUSION</b>P-like cells in the pig pulmonary veins were found using electron microscopy in this study and ectopic beats from P-like cells in the myocardial sleeves in the pulmonary veins might be responsible for atrial fibrillation originating from pulmonary veins.</p>

Effects of atrial excitable period on the stability of atrial fibrillation in goats / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of atrial excitable period (EP) on the stability of atrial fibrillation (AF) in goats.</p><p><b>METHODS</b>Ten female goats were instrumented with epicardial electrodes patches on the left atrium (LA) free wall. AF was induced and maintained by a home-made stimulator with frequency of 50 Hz at a 1-second duration and a 2-seconds interval. The stimulator was disconnected regularly. AF-induced duration, average AF cycle length (AFCL), and atrial effective refractory period during AF (ERP(AF)) were measured; EP was calculated by AFCL-ERP(AF).</p><p><b>RESULTS</b>Eight goats were studied. Persistent AF (> 24 h) could be induced in all the 8 goats within 6-16 days. When the induced AF lasted for 3-10 min or 24 h, the AFCL was 98.3 ms +/- 11.0 ms and 84.9 ms +/- 5.2 ms (P < 0.05), respectively, ERP(AF) was 90.5 ms +/- 13.2 ms and 63.0 ms +/- 4.8 ms (P < 0.05), respectively, and EP was 7.8 ms +/- 2.4 ms and 21.9 ms +/- 3.5 ms (P < 0.05), respectively.</p><p><b>CONCLUSION</b>The decrease in ERP(AF) is more significant than the shortening in AFCL, resulting in the gradually widening of EP which may contribute to the perpetuation of AF.</p>

Comparasion of the actions of human and porcine erythrocyte-derived depressing factor / 中国医学科学院学报

<p><b>OBJECTIVE</b>To compare the action mechanisms of human and porcine derived erythrocyte-derived depressing factor (h-EDDF and p-EDDF) as well as the effects on blood pressure.</p><p><b>METHODS</b>The experiments were carried out in spontaneously hypertensive rats (SHR, n = 5) and two kidney-one click renal hypertensive rats (2K-1C, n = 7). The acute and chronic effects of h-EDDF and p-EDDF on blood pressure were observed, blood pressure test using tail plethysmography under unanaesthetic state. Both EDDF were administrated via jugular vein and/or oral respectively. The isolated thoracic aorta ring perfusion assay was used to examine the effect of EDDF on the asodilation. Primary cultured VSMCs were prepared from the thoracic aorta media of 2K-1C and normal Wistar rats. The effect of EDDF on proliferation of VSMCs were determined by MTT assay. The cell cycle of VSMCs was evaluated by flow cytometric.</p><p><b>RESULTS</b>Both h-EDDF and p-EDDF could significantly decrease blood pressure of Wistar rats through intravenous administration and/or orally (P < 0.01 and P < 0.05 respectively). The contractile response of aorta in 2K-1C rats to PE was significantly enhanced compared with that of the control (P < 0.01) and both EDDF (10(-3) g/ml) remarkably induced a vasodilation with endothelium-dependent manner in SHR and 2K-1C rats (P < 0.05). h-EDDF and p-EDDF could significantly inhibit the proliferation of VSMCs from 2K-1C and control rats. After 24 hours of exposure to EDDFs the cell number of G0/G1 phase obviously increased and cell number in S phase was decreased (P < 0.01, respectively).</p><p><b>CONCLUSIONS</b>It seems that the effects of h-EDDF and p-EDDF on blood pressure and vasodilation as well as inhibition of VSMCs proliferation and regulation of cell cycle have no significant difference.</p>