Prophylactic effect of magnesium sulfate on reperfusion-airhythmias was studied using a left anterior descending coronary artery occlusion followed by reperfusion in the isolated rat hearts. In the first part of the present work, we observed a bell-shaped relationship between the incidence of reperfusion-induced ventricular fibrillation (VF) and the duration of preceding ischemia. In the second part, the concentration of magnesium sulfate in perfusate was increased to 3.6, 4.8 and 6.0mmol/L, respectively, 1 min before coronary ligation, VF fell in a dose-dependent manner from its control total incidence of 100% to 82%, 73% and 18% (P

Objective To understand the pathogenic mechanism of ?-endorphin(?-EP) on infective brain edema(IBE).Methods Experimental IBE was induced by pertussis bacilli in rabbits.Forteen rabbits were divided randomly into two groups:Normal saline group(NS,n=7),pertussis bacilli group(PB,n=7).Water content(WC) in brain tissue and ?-EP were measured in plasma,cerebrospinal fluid(CSF),cortex and hippocampus in two groups respectively.Results WC was singnificantly higher in the PB group than those in the NS groups(P

Objective:To observe the effect of percutaneous tr ansluminal coronary angioplasty (PTCA) on coronary circulating tumor necrosis fa ctor-α (TNF-α) activity. Methods: Plasma TNF-α levls were measured with radioimmunoassay and bioactive assay respectively. Result s: Plasma TNF-α activity in femoral artery (AO) was significantly incr eased immediately after PTCA ［(15.86±3.75) U/ml vs （41.32±4.36） U/ml， P<0.01］, and plasma TNF-α activity in coronary sinus was remarkably incre ased immediately after PTCA　［(16.72±4.14） U/ml vs （65.61±6.25） U/ml, P<0.01］. There was no change in plasma TNF-α activity in AO 24 h after PT CA ［(18.32±5.12） U/ml vs （15.86±3.75） U/ml, P>0.05］. Conclu sion: The increase in plasma TNF-α activity after PTCA may be associat ed with the injury of coronary artery caused by PTCA, suggesting that TNF-α ma y be involved in the coronary occlusion and the development of coronary restenos is after PTCA.

Objective: To assess the effect of balloon angiopl asty on circulating endothelin (ET) and TNF-α levels and tissue endothelin in experimental atherosclerosis in rabbits. Methods: After 20 New Z ealand rabbits had a high cholesterol diet for at least 8 weeks, successful ball oon angioplasty was performed in rihgt iliac arteries in 18 rabbits. Circulatin g levels of ET and TNF-α were measured before as well as immediately and 24 h after balloon angioplasty. Tissue endothelin immunoreactivity in atherosclerotic iliac artery wall after balloon angioplasty was assessed by immunohistochemica l technique. Results: Plasma levels of ET and TNF-α were signi ficantly increased immediately after ballon angioplasty (76.40±13.58)pg/ml vs (92.67±11.38) pg/ml and (31.35±6.23) U/ml vs (56.26±7.37) U/ml, resp ectively (P<0.05) .There was no change in plasma ET and TNF-α levels 24 h after balloon angioplasty (77.13±12.87) pg/ml vs (76.40±13.58) pg/ml and (33.41±6.79) U/ml vs (31.35±6.23) U/ml， respectively (P>0.05). T issue endothelin immunoreactiuvity was markedly increased in right iliac artery wall after balloon angioplasty than that in opposite iliac artery wall. Conclusion: The increase of plasma ET, TNF-α levels and tissue ET-IR in iliac artery wall after balloon angioplasty may be associated with the injury of l ocal vascular intima, suggesting that ET and TNF-α may take part in the corona ry constriction and the development of coronary restenosis after percutaneous tr ansluminal coronary angioplasty.

Objective: To observe the effects of angina pector is on severe ventricular arrhythmia and QTd in patients with first acute myocard ial infarction(AMI). Methods: One hundred and eight-four cases of first AMI were divided into 2 groups: PA group, angina pectoris occurred with in 24 h before AMI onset (n=58), NPA group, no preceeding angina pectori s occurred (n=126). Occurrence of complications and QTd were investigated du ring hospitalization. Results: The basic clinical characteristic s, coronary risk factors, medication before infarction, treatments after admissi on with antiarrhythmic agents, site of infarction, successful rate of thrombolys is and peak CK, CK-MB were not statistically different. Early QTd in PA group and NPA group were (56.22±18.40) ms vs (84.45±21.90) ms, respectively, P <0.05, late QTd in PA group and NPA group were (50.67± 16.34) ms vs (64.1 8(16.41) ms, respectively, P<0.05. Comparison with NPA group, incidence of severe ventricular arrhythmia, heart failure, cardiogenic shock and rate of car diac mortality in-hospital was lower in PA group. Conclusion: P reinfarction angina pectoris can significantly reduce the incidence of severe ve ntricular arrhythmia and QTd in the patients with first AMI, sugges ting that these favorable effects might be associated with protective effects of ischemic preconditioning on myocardium and ventricular pump function and improv ement of repolarizative asynchronism in ventricular myocardium.

Objective To evaluate the therapeutic effect of small bone flap craniotomy decompression of posterior cranial fossa and duraplasty in the treatment of Chiari malformation type Ⅰ.Methods The clinical data of 45 Chiari malformation type Ⅰ patients who were treated with small bone flap craniotomy decompression of posterior cranial fossa and duraplasty were retrospectively analyzed,31 cases among them with syringomyelia.Results According to Tator etc.standard,1 month after surgery,the excellent in 30 cases,good in 15 cases.Follow up from 6 months to 6 years,the excellent in 37 cases,good in 8 cases.Among 31 patients with syringomyelia,26 cases were syringomyelia subsided,5 cases were not obvious change.Conclusion The small bone flap craniotomy decompression of posterior cranial fossa and duraplasty can make the craniocervical decompression,and has obvious effect of treating syringomyelia,is safe and effective in treatment of Chiari malformation type Ⅰ.

AIM: The present study is to investigate the inhibitory effect of the transfer of replication-defective retroviral recombinant plasmid encoding a wild-type P16 ink4a gene on the formation of restenosis after rabbit carotid arterial injury in vivo.METHODS:A replication-defective retroviral recombinant plasmid encoding wild-type gene P16 ink4a was constructed and the packaged high titer virus stock was obtained. It was transferred into the rabbit carotid arterial wall immediately after injury. The P16 ink4a mRNA expression in the arteries was examined by Northern blot and in situ hybridization. The effect of overexpression of the P16 ink4a gene on arterial intima hyperplasia was determined by pathophysiological method. RESULTS: The exogenous P16 ink4a could be effectively transferred into injured arterial wall by retroviral recombinant plasmid and the gene products could inhibit smooth muscle cells proliferation (11.80?3.54 vs 25.20?5.12,P

Objective: To investigate the changes of myo cardial contractile function during myocardial stunning in calcium overload rats and the protective effects of tetrandrine. Methods: Forty-six rats were randomized into control, myocardial ischemia, myocardial stunning, low and high dose of tetrandrine groups. Another 10 rats were used to identify the calcium overload. vitamin D3 (0.3 million Unit/kg) and nicotinic acid were adm inistered. After 16 d when calcium overload occured, left anterior descending ar tery was ligated. Twenty minutes of myocardial ischemia followed by 60 min of re perfusion was induced. The contractile function parameters were determined dynam ically. At the end of experiment, myocardial cytosolic ［Ca2+］i was deter mined in various groups. In tetrandrine groups, tetrandrine (62.2 or 93.6 μmol/ kg ) was administered by gastrogavage daily.After 16 d, the rats undergone the e xperiments mentioned above. Results: Sixteen days after vitamin D3 , nicotinic acid were given, ［Ca2+］i increased by 2.6 folds (146.8±10.8 ) vs (368.5±22.6) nmol/L, (P<0.01). Whereas, ［Ca2+］i in tetrand rine groups were (210.8±16.4) and (198.6±15.3) nmol/L, which were significantl y lower than that of calcium overload group. Twenty minutes of myocardial ische mia resulted in the decrease of dp/dtmax and Vmax in all groups with the most si gnificant in stunning and calcium overload groups. The contractile function rest ored gradually after reperfusion. At all time points, dp/dtmax and Vmax in both tetrandrine groups were higher than those in both stunning and calcium overload groups. And effect with higher dose of tetrandrine were more significant than in low dose of tetrandrine. After 60 min of reperfusion, dp/dtmax in stunning, cal cium overload, low and high dose of tetrandrine groups were 49.7%, 51.5%, 71.0% and 83.4% of that in control, respectively， and Vmax were 55.0%, 49.8%, 73.9% and 77.5% of that in control, respectively. Conclusion: T he myocardial contractile function in vitamin D3-induced calcium overload gro up is impaired. On basis of myocardiocyte calcium overload, transient ischemia l eads to myocardial stunning. At the stage of ischemia, the impaired degree of my ocardial contractile function is similar to that in stunning group, suggesting a t this stage the effect of ischemia on myocardial function is greater than that of calcium overload. Tetrandrine chronically improves the myocardial function in Vitamin D3-induced calcium overload rats.

Isolated perfused rat hearts were subjected to regional ischemia followed by reperfusion and then tested for responsiveness to acetylcholine (Ach) and nitroglycerin (NTG). The effects of L-Arginine (L-Arg) and NG-monomethyl-L-Arg (L-NMMA) on the endothelium-dependent (ED) and independent (EI) vasodilator were also observed. It was found that both 15 and 30min ischemia followed reperfusion resulted in a decrease in ED vasodilation of Ach. ED vasodilation gradually renewed after 90min reperfusion in the 15min ischemic group, not in the 30min ischemic group. No significant decrease in EI vasodilation of NTG in all groups. L-Arg accelerated the renewing of ED vasodilation of Ach in the 15 min ischemia-reperfusion group, not in the 30min ischemia-reperfusion group. L-NMMA was an inverse action. The results indicate that brief ischemia followed by reperfusion can induce coronary endothelium dysfunction which may be related to the decrease of endothelium derived relaxing factor.

Objective To explore the responses of antigen-specific T cells stimulated by hepatitis B virus(HBV)-specific proteins in chronic hepatitis B patients accepting antiviral therapy. Methods Seventeen patients with chronic hepatitis B (CHB) accepting antiviral therapy were included in this study. The peripheral blood monocular cell ( PBMC) were separated from the whole blood collected at the three different time of before and one and three months after accepting antiviral therapy. ELISPOT assay was used to detect the frequency and strength of secreting IFN-γ cells of PBMC stimulated by HBsAg, HBcAg and HBeAg. HBV virus loading, HBsAg, HBeAg, ALT and AST in serum were detected at the same time. Results After three months therapy, ALT, TBiL were improved in all patients, and HBV DNA level were dropped and undetectable in 11 cases. The rates of T cell response in patients to HBV specific proteins were 64. 7% , 76. 5% and 82. 4% at the time of before and one and three months after accepting antiviral therapy, respectively. The frequency of responses of antigen-specific T cells stimulated by HBcAg was higher than that stimulated by HBsAg or HBeAg, and the frequency was enhanced after antiviral therapy. The average response magnitude was expressed as spot forming cells (SFC) per million input cells. SFC of T cell responses to HBcAg was also higher than to HBsAg or HBeAg. There was no significant difference in SFC of T cell responses to HBsAg or HBeAg at the time of before and after antiviral therapy, but there were significant difference in SFC of T cell responses to HBcAg at the time of before and after antiviral therapy. SFC of T cell responses to HBcAg was negatively associated with HBV DNA, and no associated with level of ALT in serum. Conclusion The responses of antigen-specific T cells were improved in CHB patients accepting antiviral therapy which associated with the decrease of HBV DNA. It suggested to investigate HBV specific T cell responses was important.