Changes of cTnI in myocardial ischemic and reperfusion injury during correction of cardiac defects in children

Objective The purpose of this study is to investgate changes of cTnI in myocardial ischemic and reperfusion injury during correction of cardiac defects in children. Methods From June, 1999 to May,2000,45 children (30 male, 15 female) undergoing correction of cardiac defects were divided into three groups randomly: group Ⅰ no myocardial ischemia,group Ⅱ myocardial ischemia less than 60 minutes, group Ⅲmyocardial ischemia > 60 minutes. There were no significant differences in the three groups in age, sex ratio, C/T ratio, or left ventricular function. Blood samples for analysis were collected before skin incision and at time intervals up to 6 days postoperatively. Analysis of creatine kinase MB.LDH and cardiac-specific troponin I was used for the detection of myocardial damage. Meantime, the ECG was checked for myocardial infarction. After the reperfusion, myocardial tissue was obtained from the free wall of right ventricle myocardial structure studies. Results The level of cTnI was increased significa     

Neuron-specific enolase in patients with acute ischemic stroke and related dementia.

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in acute ischemic stroke patients as compared with the controls. The altered CSF NSE levels correlated well with the infarct size in CT scan. The CSF NSE levels were higher in 6-multiinfarct dementia (MID) patients who were diagnosed after 6-month follow-up than those in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE in the study of dementia related to ischemic stroke is worth further studies.     

Changes of Tumor Necrosis Factor-α and the Effects of Ulinastatin Injection during Cardiopulmonary Cerebral Resuscitation

The changes of tumor necrosis factor-a (TNF-a) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into.control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate,30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-a were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated, The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-a among different time points (P＞0.05). In resuscitation group, the level of TNF-a was increased obviously after resuscitation (P＜0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-a showed in UTI group. There were no differences in TNF-a among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-a was expressed rapidly and kept increasing. It indicated that TNF-a might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-a and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.     

Changes of dopamine transporter function in striatum during acute morphine addiction and its abstinence in rhesus monkey

Background Although dopamine transporter （DAT） is essential for addiction, the effect of additive drugs on DAT function is still controversial, especially for opiates. We investigated the functional changes of dopamine transporter in striatum of rhesus monkeys during acute morphine injection and its abstinence. Methods Four rhesus monkeys, 6 to 9 years old, two male and two female, were examined for 12 days. Single photon emission computed tomography （SPECT） was performed with ^99Tc^m-TRODAT-1 as the radiopharmaceutical dopamine transporter agent during different stages of acute morphine injection and its abstinence. The ratios of SPECT signal between striatum and cerebellum （ST/CB） were calculated. Results The ST/CB ratio declined significantly on the first day of morphine injection and continued declining with more morphine injections. After abstinence, the ratio increased with time, but was still significantly lower on the 5th day of abstinence than the normal level. Conclusions In rhesus monkey, acute morphine injection has both rapid and lasting effects on DAT by downregnlating its function. The decline was partially reversible following morphine abstinence. The results suggest that striatum is one effective target of morphine and that the DAT function in striatum is one indicator for morphine addiction.     

A clinicopathologic comparison of acute myocardial infarction in the elderly Chinese and American.

A prospective study was done on 110 patients, 55 Chinese and 55 American elderly who had clinically proved acute myocardial infarction with histologic confirmation. The Chinese patients were much more likely to have typical pain than the American (65.4% vs 49.0%). The incidence of painlessness was only 18.1% vs 36.3%. The difference has statistical significance (P less than 0.05). Cardiac failure, shock, pulmonary infection as a major complication had no statistical significance, but the incidence of cardiac rupture group was 29.0% vs 10.9%. Ventricular fibrillation incidence was 18.1% in the Chinese vs 45.4% in the American. The incidence of recent occlusive coronary thrombi, hemorrhage and rupture of plague in coronary arteries had significant statistical difference. The incidence of triple, double and single vessel diseases were 41.8%, 29.0% and 27.2% in the Chinese group vs 36.3%, 27.2% and 25.4% in the American respectively.

     

Beneficial effects of berberine on hemodynamics during acute ischemic left ventricular failure in dogs.

In 18 dogs ischemic left ventricular failure characterized by a 30 percent reduction in peak rate of rise of left ventricular pressure (+dp/dt) and elevation of left ventricular end-diastolic pressure (LVEDP) to 15 mmHg or more was produced by ligation of the proximal left anterior descending coronary artery followed by serial occlusions of the distal left circumflex coronary artery. In 10 days, administration of berberine in an intravenous bolus injection (1 mg/kg, within 3 minutes) followed by a constant infusion (0.2 mg/kg/min, 30 minutes) increased the cardiac output (CO) from 1.25 +/- 0.12 to 1.61 +/- 0.17 L/min (P < 0.05), and +dp/dt from 810 +/- 85 to 1021 +/- 130 mmHg/s (P < 0.01), and decreased LVEDP from 16.5 +/- 1.3 to 12.0 +/- 1.0 mmHg (P < 0.05), diastolic blood pressure from 94 +/- 6 to 84 +/- 5 mmHg (P < 0.01), systemic vascular resistance from 7303 +/- 278 to 5442 +/- 231 dynes.x/cm5 (P < 0.01), but did not affect the heart rate. Injection of 5% glucose with the same volume did not improve CO and dp/dt (P > 0.05) but increased the LVEDP from 17.1 +/- 1.4 to 17.8 +/- 1.6 mmHg (P < 0.01) in 8 dogs. The levels of plasma concentration of berberine was determined with high-performance liquid chromatography. The changes in plasma drug level were found parallel to hemodynamic effects of berberine. The results of this study showed that berberine was able to improve the impaired left ventricular function by its positive inotropic effect and mild systemic vasodilatation.

     

Expression of urotensin Ⅱ and its relationship with pro-inflammatory cytokines of TNF-α and IL-1β in early stage of acute liver failure

目的 探讨小鼠急性肝衰竭(ALF)早期尾加压素Ⅱ(UⅡ)表达和分泌的动态变化及其对前炎症细胞因子的影响.方法 选择6周龄雄性BALB/c小鼠60只,随机分为模型组和预处理组,每组30只.两组均建立ALF动物模型,即采用脂多糖(LPS)50 μg/kg联合右旋半乳糖胺(D-GalN )800 mg/kg(LPS/D-GalN)腹腔注射;预处理组在LPS/D-GalN注射前0.5h,以UⅡ受体拮抗剂urantide 0.6 mg/kg尾静脉注射.两组均在LPS/D-GalN注射后0、0.5、1、2和6h处死动物(每一时间点各6只小鼠),其中0h作为对照(仅腹腔内注射0.2 mL无菌生理盐水);采集动物血清和肝组织标本.采用RT-PCR及ELISA方法分别检测U Ⅱ、肿瘤坏死因子α(TNF-α)及白介素1β(IL-1β)mRNA和蛋白质的表达.结果 LPS/D-GalN注射后0.5h,肝组织和血清中UⅡ的表达和分泌即快速上升并达峰值,且峰值水平持续至LPS/D-GalN攻击2h后,至6h时UⅡ的表达与分泌虽有所降低,但仍显著高于正常水平(p＜0.05);面TNF-α水平在LPS/D-GalN攻击后0.5h内无明显升高(P＞0.05),直到1h后才快速上升达峰值(P＜0.05),至6h时开始下降(P＜0.05);IL-1β的表达与分泌则直到6h后才有明显上升(P＜0.05).Urantide的应用不仅显著抑制了LPS/D-GalN攻击诱导的UⅡ高表达,也使上调的TNF-α和IL-1β表达和分泌明显受抑(P＜0.05).结论 UⅡ可刺激TNF-α的表达,有可能作为炎症级联效应的触发者在ALF的发生或启动中发挥关键性影响.     

Effect of 17β-estradiol on the Brain Damage and Metabolic Changes in Rats

The neuroprotective effect of estrogens has beenextensively demonstrated in in vitro studies and its a-bility to reduce cell death primary cortical neuronesafter oxidative stress and excitotoxic insults suggeststhat estrogens enhance survival during several typesof cytotoxic events in vivo[1-2 ] . In rats,it has beenshown that physiological levels of estradiol are suffi-cient to exert profound protective effects in the is-chemic brain,specially in the cortex.Several poten-tial mechanisms may u…     

Changes in intracellular and extracellular calcium concentration of the myocardial cells during heart failure in children.

ＣｈａｎｇｅｓｉｎｉｎｔｒａｃｅｌｕｌａｒａｎｄｅｘｔｒａｃｅｌｕｌａｒｃａｌｃｉｕｍｃｏｎｃｅｎｔｒａｔｉｏｎｏｆｔｈｅｍｙｏｃａｒｄｉａｌｃｅｌｓｄｕｒｉｎｇｈｅａｒｔｆａｉｌｕｒｅｉｎｃｈｉｌｄｒｅｎＬｉＺｉｐｕ李自普，ＬｉｕＹｕｙａｎｇ刘豫阳...     

Changes of distribution of platelet activating factor in the lung of rats with hypoxic pulmonary hypertension.

OBJECTIVE To investigate the role of platelet activating factor (PAF) in the hypoxic pulmonary hypertension.

METHODS Fifteen of 30 male Wistar rats were exposed to hypoxia for 3 weeks, and another 15 rats served as controls. The pulmonary arterial pressure was examined by catheterization. The sections of rat lung were treated by the avidin-biotin-peroxidase complex method to expose the location of PAF.

RESULTS The rats developed pulmonary hypertension and right ventricular hypertrophy after hypoxic exposure. Under the light microscope, PAF is distributed on the vascular and alveolar walls of normal lung, and the content of PAF in the lung of rats with hypoxic pulmonary hypertension are remarkably higher than those of normoxic controls.

CONCLUSIONS PAF plays not only a physiological role in the rat lung, but also a pathophysiologic role in hypoxic pulmonary hypertension.

     

Common endocrine and metabolic disorders among the Chinese in Hong Kong.

ＣｏｍｍｏｎｅｎｄｏｃｒｉｎｅａｎｄｍｅｔａｂｏｌｉｃｄｉｓｏｒｄｅｒｓａｍｏｎｇｔｈｅＣｈｉｎｅｓｅｉｎＨｏｎｇＫｏｎｇＲ．Ｔ．Ｔ．Ｙｅｕｎｇ杨紫芝ａｎｄＫ．Ｓ．Ｌ．Ｌａｍ林小玲ｎｔｈｉｓｒｅｖｉｅｗ，ｗｅｈａｖｅａｔｅｍｐｔｅｄｔｏｈｉｇｈｌｉｇ...     

Changes in Phosphorylation of Connexin43 in Rats during Acute Myocardial Hypoxia and Effects of Antiarrhythmic Peptide on the Phosphorylation

In order to confirm the hypothesis that during acute hypoxia, the antiarrhythmic peptide (AAP10) could improve conductance by changing the phosphorylation state of connexin43 (Cx43), isolated perfused rat hearts were randomly divided into three groups: control, hypoxia and AAP10 (n=9 in each group). The change in Cx43 phosphorylation was tested by Western-blot; the distribu- tion of Cx43 was observed by confocal immunofluorescence microscopy. Western-blot analysis re- vealed that the expression of total Cx43 protein was significantly decreased during acute hypoxia, while nonphosphorylated Cx43 (NP-Cx43) was unchanged. AAP10 could increase the expression of total Cx43 protein, but had no effects on the NP-Cx43 protein. Immunofluorescence study showed that during acute hypoxia, both total Cx43 and NP-Cx43 proteins were greatly decreased, while AAP10 only increased the expression of total Cx43 protein, but had no effect of the NP-Cx43 protein expression. These findings suggested that the decrease of intercellular communication may be associ- ated with the reduction of phosphorylated Cx43 (p-Cx43) and translocation of NP-Cx43 from the surface of gap junction into intracellular pools during acute hypoxia. AAP10 can improve intercelluar communication by enhancing phosphorylation of Cx43.     

Changes of 5－hydroxytryptamine and dopamine contents in brain microvessels and the influence on cerebral edema at early stage

Ｃｈａｎｇｅｓｏｆ５－ｈｙｄｒｏｘｙｔｒｙｐｔａｍｉｎｅａｎｄｄｏｐａｍｉｎｅｃｏｎｔｅｎｔｓｉｎｂｒａｉｎ　ｍｉｃｒｏｖｅｓｓｅｌｓａｎｄｔｈｅｉｎｆｌｕｅｎｃｅｏｎｃｅｒｅｂｒａｌｅｄｅｍａａｔｅａｒｌｙｓｔａｇｅｏｆｂｒａｉｎｉｎｊｕｒｙＫｅＹ...     

Release of myocardial noradrenaline during acute hibernation in the isolated rat heart

Objective： To explore the release of myocardial noradrenaline during acute hibernation. Methods： The hearts were gained from rats and set up as modified Langendorf preparations beating isometrically. They were perfused with modified Krebs-Henseleit buffer under controlled pressure. Mechanical measurements and coronary effluent were recorded simultaneously at 30min intervals for 150min. Lactate dehydrogenase in coronary effluent was assayed at the beginning, 60min and 120min low-flow ischemia. Noradrenaline in coronary effluent was determined at the beginning of low-flow and 120min of low-flow ischemia and also in control, during hibernation and after 30min reperfusion during stimulation, myocardial noradrenaline response on tyramine was investigated in absence or presence of desipramine after 30min reperfusion. Results： In the control, there was nosignificant chant in noradrenaline overflow during 120min perfusion; In the acute myocardial hibernation group, there was also nosignificant difference in noradrenaline overflow between the beginning and 120min low-flow ischemia. The electrical field stimulation-induced overflow of noradrenaline during hibernation myocardium was significantly less than preischemia or after reperfusion, but there was nosignificant difference between preischemia and reperfusion group. Tyramine induced significant noradrenaline release in absence of desipramine after 30min reperfusion, but this increase in noradrenaline release had nosignificant in the presence of desipramine. These studies indicated that there was not significant spontaneous noadrenaline overflow during acute myocardial hibernation in isolated rat hearts, the stimulation-induced noradrenaline overflow decreased during hibernation and restored to the level of preischemia after reperfusion, myocardial noradrenaline response to tyramine remained after 30min reperfusion. Conclusion： Myocardial noradrenaline overflow may not contribute to the development of acute myocardial hibernation and the function of sympathetic nerve may also maintain in hibernation as myocardium does during acute myocardial hibernation, reperfusion of myocardium may contribute to restoring the function of sympathetic nerve.     

Activity of platelet in patients with high level of LDL and the effect of LDL on platelet glycoproteins.

Ｔｈｅｈｉｇｈｌｅｖｅｌｏｆｐｌａｓｍａｃｈｏｌｅｓｔｅｒｏｌｉｓｏｎｅｏｆｔｈｅｉｍｐｏｒｔａｎｔｒｉｓｋｆａｃｔｏｒｓｔｏｃａｕｓｅｃｏｒｏｎａｒｙｈｅａｒｔｄｉｓｅａｓｅａｎｄａｔｈｅｒｏｓｃｌｅｒｏｓｉｓ．Ｔｈｅｍａｊｏｒｃｈｏｌｅｓｔｅｒｏ...     

Does clopidogrel with aspirin after acute minor stroke or transient ischemic attack increase the risk of cerebral hemorrhage？

Wang et al1 recently showed that in patients with transient ischemic attack （TIA） or minor stroke that can be treated within 24 hours after the onset of symptoms, the combination of clopidogrel and aspirin was superior to aspirin alone for reducing the risk of stroke in the first 90 days, without increasing the risk of hemorrhage. We report a patient treated with this combination but suffered recurrent stroke and hemorrhage.     

Changes in monocyte counts and expression of mCD_( 14)and HLA-DR in the peripheral blood of patients with severe acute respiratory syndrome

Severeacuterespiratorysyndrome (SARS)isaninfectiousdiseasethatoriginallyemergedinChinainNovember 2 0 0 2 Itsubsequentlyspreadworldwide Investigatorsinvolvedinaninternationalcollaborationhaveattemptedtodetermineaspecificetiologyinordertoredefinewhatiscurrentlybestdescribedasasyndromeintoaspecificdisease Atpresent,anovelcoronavirusisgenerallyacceptedasthesinglemostprobablecausativeagent InthecaseofHIVinfection ,monocytes/macrophagesareinfectedearlyintheinfectionprocess,andtheactivationofmon…     

Changes of anionic sites on myocardial cell membrane in the early stage after severe burns in rats

Theanionicsitesexistonthesurfaceofmanytypesofcells.Thisstronglyanionicgroupistheprimecontributorofthenetnegativechargecharacteristicofsialoglycoconjugates['j.Furthermore,ithasbeendemonstratedthatacationicprobecouldcharacterizeanionicsite'Sdistributionlzj.Thestaticacidonthesurfaceofmyocardialcellmembraneisakindofglucoproteinandplaysanimportantroleinmaintainingthefunctionofcellularmembrane.Afterburns,markedchangesofthestructureandfunctionofmyocardialcellmembranearefound.However,itisnuclearwheth…     

Changes of Lipid Peroxides and Superoxide Dismutase in Visceral Tissues during Endotoxic Shock in Rats

As compared with the control,the malondialdehyde(MDA)levels in the cardi-ac,pulmonary,and intestinal tissues were elevated(P<0.05),and the superoxide dismu-tase activities in the cardiac,pulmonary,and intestinal tissues increased(P<0.05)at the30th min after endotoxic shock;the former in the cardiac,hepatic,renal,pulmonary,andintestinal tissues were elevated(P<0.05～0.001)and the latter in the cardiac,pulmona-ry,and intestinal tissues decreased in the 2nd h after shock;and the former were marke-dly elevated(P<0.01～0.001)and the latter severely decreased(P<<0.05～0.001)in allthe visceral tissues tested in the 4th h after shock.These data showed that lipid peroxid-ation mediated through oxygen-derived free radicals brought about tissue damage of theviscera listed above,which occurred earlier in the heart,the lungs and the intestines thanin the liver and the kidneys,and superoxide dismutase(SOD)activity was suppressed inthe late stage of endotoxic shock.