Abstract:Comparative studies of oxidative and glycosylated modification of low density lipoproteins (LDL) were made by biochemical, histochemical and morphometric analysis, in the meantime the effects of prostaglandin E(PGE) on the modified LDL were observed. The results showed that compared with the control's the antioxidizing enzyme activities in oxidized low density lipoprotein(OLDL) group decreased but lipid peroxide(LPO)content increased markedly, while PGE drugs elevated enzyme activities and inhibited LPO production. The results of morphometric studies confirmed that prostaglandin E₂(PGE₂) obviously inhibited foam cells formation. The mechanism of glycosylation was complicated. It was characterized only mildly decreased enzyme activities but markedly increasing of LPO content, suggesting that at the beginning it might be due to non-enzymatic glycosylation and then complicated with the so called glycosyldation of LDL, therefore heavily enhanced tissue injuries and diabetic atherosclerosis, This experiments showed that PGE, especially PGE₂ also possessed the protective effects to LDL glycosylation.

Abstract:To investigate whether smooth muscle cell(SMC)derived fibroblast growth factor(FGF) plays a role in atherogenesis, this growth factor was purified, and some of its biological and biochemical properties were determined.Methods The rabbit aortic SMC were cultured using a substrateattached explant method. The SMC at the 3rd～5th passage which grew well were collected and sonicated. The sonicated was centrifuged at 10 000 r·min~(-1) and the FGF was extracted. The chemotactic activity of the extract for rabbit peripheral blood monocytes(MC) was assayed by using modified Boyden chamber, Subsequently, the extract was loaded on a column of heparin-Sepharose and agradient elution was performed. The effect of the eluate fractions on DNA synthesis of NIH 3T3 fibroblasts was assayed by using ~3H-thymidine( ~3H-TdR ) incorporation into DNA of the cells. To determin the molecular weight and reactivity to anti-bFGF polyclonal antibody, NaDodSO_4-polyacrylamide gel electrophoresis (SDSPAGE), immunoblotting and an image processing system were used.Results The FGF extract was significantly chemotactic for MC. The actions eluted in 1.4～1. 6 mol· L~(-1) NaCl from the heparin Sepharose were mitogenic for 3T3 cells, and the ~3H-TdR incorporation values were 2～3 times as much as the control. The purified molecule had a molecular weight of about 18.4 kDa as determined by SDS-PAGE. Immunoblot analysis showed that this purified protein was positively immunoreactive to an anti-bFGF polyclonal antibody.Conclusions The purified protein from the present experiment is bFGF. It suggests that the SMC which have migrated in the intima may release bFGF when injured. Basic FGF may play a role in atherogenesis through inducing cell migration and proliferation.

Abstract:We reported the effect of L-arginine on lipoprotein, nitric oxide(NO), lipid peroxide (LPO) and superoxide dismutase (SOD) in hypercholesterolaemic rabbit. The results showed that 2% L-arginine fed in company with 2% cholesterol for 90 days and 4%L-argine orally administrated for 90 days after 2%L-arginine and 2% cholesterol could significantly protect the activity NO and SOD, decrease the LPO content. L-Arg/NO may reduce the oxidative modification of LDL of hypercholesterolaemic rabbit.

Abstract:Vascular smooth muscle cells (VSMC) cultured from the rat aorta at 3 and 10 days after balloon denudation. Results showed that activity of VSMC proliferation increased significantly, synthesis of DNA and protein accelerated, and cell count increased. During VSMC proliferation, calcium influx increased, calcium content elevated. 10 μmol·L~(-1) Verapamil inhibited not only the changes of calcium homeostasis, but also vascular injury induced SMC proliferation. These findings indicated that vascular injury induced VSMC proliferation. Disturbances of calcium homeostassis might be one of cellular mechanisms of vascular injury induced VSMC proliferation.

Abstract:Although ultrasonic therapy on the coronary heart disease have been identified as in effect, no studies have evaluated the capability of the ultrasound eliminating atherosclerotic lesions. The purpose of the present study was to elucidate the roles of the ultrasound in the hyperlipedemia reduction and the plaque ablation on the basis of the experimental animal models.Abstract: Methods Thirty Chinese white rabbits were divided into 3 groups: model, natural eliminating and ultrasonic therapeutic group, according the age and the body weight. In every group the experimental hyperlipedemia and atherosclerosis were produced by feding high lipid diets for 110 days. Then model group served as contral to assess on the atherosclerotic lesions, other two groups were given to normal diets maintaining 63 days so as to evalurate the role of ultrasonic plaque ablation. In the therapeutic group ultrasound was irritated every day for 15 min in front of the heart area, using pulsed mode, frequency 800 kHz and intensity 1. 0 W·cm~(-2). At the all experimental process the serum total cholesterol level was measured once every twenty days. At the end of experiment samples from coronary arteries and aortae were taken using different sections. Light sections were stained with hematoxylin-eosin and weigert and examined by light microscopy lesions with point lattice test system. Ultrathin sections were only to qualitative investigation. Results in the experimental handred-tenth days the serum total cholesterol level of the three groups was distinctly higher than that of the beginning of experiment. By the end of experiment the serum total cholesterol level; the incidence of coronary arterial sections with lesion, and the volume density of atherosclerotic lesions of coronary arteries and aortae in the therapeutic groups were 26.01±8. 15 mmol·L~(-1), 7.86%, 36.59%±6. 98%, 7. 95%±13. 16%, respectively. These results were remarkably lower than those of the natural eliminating groups (P=0. 05 ～0.01). Conclutions Our results suggest that the ultrasound has the significant effects to decrease concentrations of the serum total cholesterol and to eliminate the atherosclerotic pleques. This study was provided the theoretical base to treat coronary heart diseases with the ultrasound.

Abstract:It is very clear that hyperlipemia is a risk factor of atherosclerosis. To further understand the role of lipoproteins, especially oxidized lipoproteins in atherogenesis, we examined the effects of oxidized low density lipoprotein (OLDL) and very low density lipoprotein (OVLDL) on platelet-derived growth factor Bchain (PDGF-B) expression in monocytes. Methods Low density lipoprotein (LDL) and very low density lipoprotein (VLDL) were isolated from normal blood donors by density gradient ultracentrifugation. After exposed to LDL, OLDL, VLDL, and OVLDL for 24 hours and subsequently exposed to lipoprotein-free media for 24 hours, respectively, monocytes were used to immunocytochemical staining by anti-PDGF-B antibody, meanwhile the conditioned by cultured monocytes media were collected. and their influences on 3H-TdR incorporation into DNA of smooth muscle cells were observed.Results Monocytes can express PDGF-B, and OLDL and OVLDL enhance the expression; the monocyte conditioned media also can promote the 3HM-TdR incorpation into DNA of smooth muscle cells. Conclusions OLDL and OVLDL may play an important role in pathogenesis of atherosclerosis through stimulating the secreation of PDGF-B in monocytes, that promotes the proliferation of smooth muscle cells.

Abstract:Previous study proved that it generated an in vitro model of macrophage-derived foam cell, namely, the characteristic pathological cell in the early atherosclerotic lesion to incubate C₅₇ BL/6J mouse peritoneal macrophages with 10 mg·L~(-1) oxidized low density lipoprotein for 4 days. With the Ca~(2+) fluorescent indicator technique and NADH-oxidizingcoupling-spectrum-analysis method, we determined the intracellular Ca~(2+)-ATPase of the above cultured foam-like cell. The results indicated that the [Ca~(2+)]i level was 2. 7 times higher than that of control group cells, and the activity of Ca~(2+)-ATPase was 24% of that of the later cells. This supported that macrophage-derived foam cell formation is connected with the slow Ca~(2+) entry or release, which possibly derived from long-lasting openings of membranous Ca~(2+) channels and the inactivating of Ca~(2+)-ATPase at the late stage.

Abstract:Vascular endothelial cell damage and excessive smooth muscle cell (SMC) proliferation are considered to paly a key role in the development of a atherosclerotic disease. In present study, it was Observed that nitric oxide-generating vasodilator-sodium nitroprosside (SNP) induced endothelium-independent relaxation on porcine coronary arterial rings and inhibited mitogenesis and proliferation of cultured procine vascular smooth muscle cells in dose-dependent manner with MTT colorimetric assay. The results suggest that endogenous nitric oxide (NO) may play an important role as medulator of smooth muscle cell growth, and the long-term administration of SNP and other nitrovasodilators which release NO in the body favors inhibiting the development of atherosclerosis to patients with atherosclerotic disease.

Abstract:In order to study expression of human leukocyte antigen-DR (HLA-DR) and chondroitin sulfate proteoglycan (CS-PG) in human coronary artery , 13 coronary arieries including normal group (n=6) and lesion group (n=7),which were fixed with formalin, embedded in paraffin and slided successively (4μm ), were stained with HLA-DR and CS-PG microwave immunohistochemistry. Then the slides were quantitated with image analyzer. Results indicated that the numerical density of HLA-DR positive cells and the area density of CS-PG in the intima of lesion group were evidently higher than that of normal group, and were significantly correlative with that of normal group. One of lesion group was stained with proliferative cell nuclear antigen (PCNA) and CD68. Similar localization of CD68 and HLA-DR was found in intima. Menatime, positive cells of HLA-DR mostly were positive ones of PCNA. These results indicated that expression HLADR in earlier As lesion was closely related with formation of foam cells, proliferation of SMC and increase of CS-PG.

Abstract:In order to investigate the mechanism of serum low level of high density lipoprotein cholesterol (HDLC) under the condition of hypeririglyceridemia (HTG), we studied 93 patients with non-insulin dependent diabetes.Abstract: Methods All of patients were divided into a HTGgroup (n=24) and a anormotriglyceridemia (NTG) group (n=69). The serum lipids and the apolipoprotein levels that were concerned with HDLC were meassured in all of these patients.Results in HTG group, the level of HDLC, HDL2C and the ratio of apolipoprotein A_Ⅰ(apo A_Ⅰ)/apolipoprotein Al (apo A_Ⅱ) and HDLC/apo A_Ⅱ were all significantly decreased however ,apo A_Ⅱ was significantly increased　contrasting with NTG group. The multiple regression analysis showed that all above mentioned serum lipids, apolipoprotein and its ratio had a linear regression relationship with triglyceride (TG). But there were not significant difference in the HDL3C and apo AI levels between this two group. The HDL3C and apo AI had not also a linear regression relationship with TG. Conclusions All above results indicated that in HTG, the main was that the serum HDL2C level was decreased. According to no apperently changed apo AI level and decreased HDLC/apo AI retio in HTG group. When we estimated the HTG, the numbers of the high density lipoprotein (HDL) particles didn't reduce, but the combination of the apolipoprotein with the cholesterol may be influenced. In addition, according to the significant increase of apo A_Ⅱ and the significant decrease of apo AI/apo A_Ⅱ in HTG, we a also estimated that the estirizing speed of cholesterol in HDL maybe slow in HTG. Both of above mentioned reasons may lead to the serum HDL2 C level decreasing, therefore, presented a serum low level of HDLC in patients.

Abstract:Macrophages were incubated with apolipoprotein B-containing lipoproteins, the complexes of lipoprotein with dextran sulfate (DS) or antibodies (lipoprotein cholesterol 200 mg·L~(-1), dextran sulfate 0.4 mg or antibodies 0.1 ml) for 24 h. The cholesteryl esters (CE) in macrophages were determined by thinlayer chromatography. The results that native lipoprotein (a) did not give rise to any significant storage of intracellular cholesteryl esters (0. 9 mg·g~(-1) cell protein,p>0. 05); low density lipoprotein (LDL)increased CE formation in macrophages ( 4.0 mg·g~(-1) cell protein, p<0. 05); lipoprotein (a)-DS or LDL-DS complexes caused a significant enhance in CE formation in macrophages, which were 7. 7 ,and 8. 7 mg·g~(-1) cell protein ,respectively (P < 0. 01 ); similar result were observed when macrophages were incubated with both the complexes of lipoprotein (a) with antibodies against apolipoprotein (a) or apolipoprotein B and LDL with antibodies against apolipoprotein B,which were 19.9, 18.3 and 17. 4 mg·g~(-1) cell protein, respectively (p<0. 01 ) . The above data showed that the complexes of apolipoprotein B-containing lipoproteins with DS or antibodies could cause lipid accumulation in macrophages.

Abstract:Hybridoma cell lines secreting monoclonal antibodies to human serum apo (a) were produced by lymphocyte hybridoma technique. Sandwich enzyme-linked immunosorbent assay (ELISA) for determining lipoprotein (Lp) (a) concentration were established with monoclonal or polyclonal antibodies: the first ELISA was performed by using polyclonal antibody to apo (a) as the capture and quantitating antibody, the second by using polyclonal antibody to apo B as the capture antibody and quantitating the bound Lp (a) particles with antibody to apo (a). ELISA by using a single and mixed monoclonal antibodies were established also. We measured and analysed the serum Lp (a) levels, the results indicated that differences between the values obtained by different methods are dependent on the size of the apo (a ) isoform in the sample.

Abstract:To investigate the associtation of heart rate variability with myocardial ischemia we observed the 24 h dynamic electrocardiogram in 35 cases of coronary heart disease. Heart rate variability was obtained statistically by a measure of the standard deviation of the set of all R-R intervals in a 24 h period while myocardial ischemia was estimated by the total time of the myocardial ischemia attack recorded in the 24 h dynamic electrocardiogram. The 35 patients were divided into high and low standard deviation group (high group standard deviation>50 ms ,low standard deviation≤50ms). 22 patients were in high group and 13 patients were in low group. Comparison was made between the 2 groups in the number of transient myocardial ischemia attack and the total time of the myocardial ischemia in a 24 h period. The study showed significant differences existed between the 2 group both in numbers and in the total time of transient myocardial ischemic attack (p<0. 01,p<0.05). Negative correlation of low degree was observed between heart rate variability and total ischemic time (r=-0.29 , p<0. 05 ). Significant difference could also be seen between the 2 groups in the numbers of nonsustained ventricular tachycardia (p<0. 05). Our study indicated that low heart rate variability associated with myocardial ischemia and might be predisposed to serious arrhythmia.

Abstract:The essay reported our hospital treated coronary heart disease used percutaneous transluminal coronary angioplasty (PTCA) in 18 cases (men 13, 58. 6±9.2 yrs) and percutaneous transluminal coronary rotational ablation (PTCRA) for 10 cases (men 9, average age 54 yrs) from July 1992 to September 1995. PTCA were performeed in 25 lesions of 23 vessels, resulting in a reduction of diameter stenosis from 81%±12% to 18%±12%. PTCRA were initially successful in 25 lesions of 9 patients and the diameter stenosis were reduced from 86. 2% to 20.2% averagely.