共查询到20条相似文献,搜索用时 143 毫秒
1.
Objective To compare the effects of high, middle and low doses of enalapril in preventing left ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in ra ts, especially evaluating the efficacy of low dose enalapril.Methods AMI was induced by ligating the left coronary artery in 149 female SD rats. 48 hours after the procedure, the 97 surviving rats were randomized to one of the f ollowing four groups: (1) AMI controls (n=24),(2) high-dose (10mg·kg(-1)·d(-1), n=25), (3) middle-dose (1mg·kg·d[-1], n=23), and (4) low-dose (0.1mg·kg(-1)·d(-1), n=25) enalapril groups. I n addition, sham-operated (n=13) and normal rats (n=10) were randomly selected to serve as non-infarction controls. Enalapril was delivered by direct gastric gavage. After 4 weeks of therapy, hemodynamic studies were performed, then the rat hearts were fixed with 10% formalin and pathology analysis was performed. Exclusive of the dead rats and those with MI size <35% or >55%, complete experim ental data were obtained from 67 rats, which were comprised of (1) AMI controls (n=13), (2) high-dose enalapril (n=13), (3)middle-dose enalapril (n=12), (4) l ow-dose enalapril (n=12), (5) sham-operated (n=8) and (6) normal (n=9) groups .Results There were no significant differences among the four AMI groups in infarction si ze (all P>0.05). Compared with the sham-operated group, the left vent ricu lar (LV) end diastolic pressure (LVEDP), volume (LVV), absolute and relative wei ght (LVAW, LVRW) in AMI group were all significantly increased (all P<0.001 ), while maximum LV pressure rising and dropping rates (±dp/dt) and their corre cted values by LV systolic pressure (±dp/dt/LVSP) were all significantly reduce d in the AMI control group (P<0.01-0.001), indicating LVRM occurred and LV systoli c and diastolic functions were impaired. Compared with the AMI group, LVEDP, LV V, LVAW and LVRW were all significantly decreased in the three enalapril groups (control P<0.001), with the reduction of LVEDP, LVV and LVAW being mo re significant in high-dose than in low-dose enalapril groups (all P<0.05 ), and the ±dp/dt/LVSP were significantly increased only in the high and middle -dose enalapril groups (P<0.01).Conclusions High, middle and low doses of enalapril were all effective in preventing LVRM af ter AMI in the rat, with low dose enalapril being effective and high dose superi or. As for LV functional improvement, only high and middle-dose enalapril were effective. 相似文献
2.
《中国医学科学杂志(英文版)》2008,(4)
Objective To demonstrate the myocardial lesion associated with long-term administration of methamphetamine in rats. Methods The experimental models of intoxication of methamphetamine were established in Sprague-Dawley rats. Methamphetamine hydrochloride (3 mg·kg-1·d-1) was subcutaneously injected to rats in methamphetamine-treated group (n = 16), and normal saline at the same dose was injected to rats in control group (n = 16). After 1 week and 8 weeks of injection, 8 rats in each group were sacrificed and their hearts were examined with light microscopy and electron microscopy, respectively. Results After 1 week of methamphetamine exposure, foci of contraction band and cellular degeneration were present in subendocardial myocardium. Cellular degeneration, myocytolysis, and contraction band necrosis became prominent and extensive in methamphetamine-treated rats after 8 weeks. Hypertrophy, intracellular vacuolization, and fibrosis were also observed. The ultrastructural feature showed marked swelling and degeneration of mitochondria, enlargement of sarcoplasmic reticulum, and dissolution of myofilaments. No obvious cardiac myocyte lesions were observed in rats of control group. Conclusion Methamphetamine abuse daily for a long time may result in an increased risk of cardiovascular lesions similar to cardiomyopathy. 相似文献
3.
The levels of vasoactive intestinal peptide(VIP)in three regions of rat brain were assayed in 62 rats.Bilateral common carotid artery ligation was donein 50 rats.Half an hour before ligation 26 rats weregiven 10 g/kg of Radix Salviae Miltiorrhizae(RSM);24 rats were given same volume of normalsaline as controls.A sham operation wasdone in 12 rats.Half an hour(n=30)and 3hours(n=32)after operation,the rats were quicklydecapitated.VIP levels were assayed in cerebralcortex,hippocampus and caudate nucleus,in salin-treated animals,VIP levels of cerebral cortex andcaudate nucleus at 3 hour group were significantlydecreased compared with the sham-operated group.No significant difference was found between RSM-treated and sham-operated groups.The preliminaryresults suggest that VIP may be involved in thepathophysiological procedures of cerebral ischemiaand RSM may attenuate the dysfunction of VIPduring cerebral ischemia. 相似文献
4.
Objective:To investigate the effects of panax notoginseng saponins(PNS) on homing of C-kit+ bone mesenchymal stem cells(BMSCs) to the infarction heart.Methods:The acute myocardial infraction(AMI) model was established in 140 Wistar rats,105 model rats survived after operation,and the model rats were randomly divided into five groups,21 rats in each group:Western medicine group mobilized by subcutaneous injection of human granuloctye colony stimulating factor(G-CSF) 50 μg·kg-1·d-1;sham operation group and a model group treated by subcutaneous injection of normal saline 50 μg·kg-1·d-1;Chinese medicine group mobilized by intraperitoneal injection of Xuesaitong(血塞通)(ingredients of PNS) 150 mg·kg-1·d-1;integrative medicine group mobilized by subcutaneous injection of G-CSF 50 μg·kg-1·d-1 and intraperitoneal injection of Xuesaitong 150 mg·kg-1·d-1.Except for the sham-operated group,each group was divided into three sub-groups by three time points of 1 d,7 d and 14 d.G-CSF was injected once a day for 7 d.Xuesaitong was injected once a day until the rats were killed.The flow cytometry was used for detection of C-kit + cells in the peripheral blood in different time points,and immunohistochemical method was used for detection of the changes of C-kit + cell and Ki-67+ cell numbers in the marginal zone of AMI.Results:Twenty-four hours after the operation,C-kit + cells had a slight increase in the model group compared with the sham operation group(P>0.05).The peripheral blood C-kit+ cells in the integrative group increased significantly compared with the other groups on 7 d and 14 d(all P<0.05).Meanwhile the expression of C-kit + cells and Ki-67+ cells in the marginal zone of AMI in the integrative group increased significantly compared with the Chinese medicine group,the western medicine group and the model group on 1 d,7 d and 14 d(all P<0.05),and the cells in the integrative group decreased significantly on 14 d compared with that on 7 d(P<0.05).Conclusion:PNS can cooperate with G-CSF to mobilize C-kit+ BMSCs from the marrow into the peripheral blood and promote them "homing" to the infarction heart. 相似文献
5.
6.
Objective To optimize the therapeutic dosage of tetrandrine (Tet) in rat hepatic fibrosis mod- el. Methods 50 Wistar rats were divided into 5 groups at random including normal control, model control, Tel-treated model groups of 10mg·kg-1·d-1, 5mg·kg-1·d-1 and 2. 5mg·kg-1·d-1(n =10 in each group). All rats, except for the normal controls, were injected with axenic porcine serum (0. 5ml each time, twice a week) intraper-itoneally for 8 weeks to establish hepatic fibrosis. After the 8th week, rats of Tet-treated model groups were given by gavage once a day with different doses of Tet for another 8 weeks. Then the liver function, serum levels of hyaluronic acid (HA) , laminin (LM) , and procollagen type III(PCIII) were tested. Collagen type I and III pathological changes in liver tissue were also assessed. Results Most indices of liver function including alanine minotrans-ferase (ALT) , aspartate aminotransferase (AST) , albumin (ALB) , albumin /globulin ratio (A/G) and alkaline phosphatase (ALP) improved significantly in Tet-treated groups with the exception of γ-glutamyl transpeptidase (γ-GT) and total bilirubin ( TBIL). Secondly, markedly lowered levels of HA, LM and collagen type I, III were also detected by Tadioimmunology and immunohistochemistry in the 5mg·kg-1·d-1Tet-treated model group. Moreover, pathological findings confirmed the statistically significant improvement in hepatofibrotic degree resulted from the treatment of 5mg ·kg-1·d-1 rather than other doses of Tet. Conclusion For experimental Wistar rats, Tet exhibited an anti-hepat-ofibrotic action in doses within the range of 2. 5mg·kg-1·d-1to 10mg·kg-1·d-1,and 5mg·kg-1·d-1may be the optimum one among all doses. 相似文献
7.
《上海医学》2007,30(Z1)
Objectives To explore changes of myocardial pro-inflammatory and fibrogenic cytokines after coronary microembolization (CME) in rats. To observe effects of carvedilol at different doses on myocardial cytokines expression and ventricular remodeling. Methods A rat model of CME was created by injecting a suspension of microthrombotic particles generated from rat clots into left ventricle when clamping the ascending aorta. Forty SD rats were randomly divided into 4 groups(n=10 per group): sham-operation group(SO), CME group(ME), low-dose carvedilol intervention group (LCAR,1.0 mg·kg-1·d-1) and high-dose carvedilol intervention group (HCAR, 10.0 mg·kg-1·d-1). A microscopy incorporated with an image analysis software was employed to calculate the number of micro-myocardial infarction (Nmmi) and the area of micro-myocardial infarction (Ammi) in sections with HE-staining, to measure the collagen volume fraction(CVF) in sections with Sirius-Red-staining, to detect the density of expressions of TNF-α, IL-1β, TGF-β1 and MMP-9 in sections with immunohistchemical staining, to calculate the myocyte apoptosis rate (Rapo) in sections with TUNEL-staining. Two-dimensional Echocardiography was performed to monitor left ventricular end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD), left ventricular fraction shortening (LVFS) and ejection fraction (LVEF); and electrophysiolography was utilized to measure left ventricular systolic pressure(LVSP), maximal positive dp/dt ( LVdp/dtmax), and end diastolic pressure(LVEDP). Four weeks after operation, comparing measurements in ME with those in SO, both Nmmi and Ammi were increased(P<0.01, each); all of the expressions of TNF-α, IL-1β, TGF-β1 and MMP-9 were increased (P<0.01,each), both CVF and Rapo were increased (P<0.01,each), both LVEDD and LVESD were increased but LVFS and LVEF were reduced(P<0.01,each), both LVSP and LVdp/dtmax were increased (P<0.01,each), but LVEDP was increased (P<0.01). Comparing with measurements in ME, the expression of TNF-α, IL-1β, TGF-β1 and MMP-9 were decreased(P<0.01,each), both CVF and Rapo were decreased(P<0.01,each), LVEDD and LVESD were smaller(P<0.01,each), LVEF and LVFS was higher(P<0.01,each), LVdp/ dtmax were increased and LVEDP was decreased(P<0.01,each), heart rate were slower (P<0.01,each) both in LCAR and HCAR. Except for LVSP, the above-mentioned changes were more remarkable in HCAR than in LCAR(P<0.05). Myocyte interstitial CVF was positively correlated with the expression of IL-ip and TGF-β1(r=0.81 and 0.93, P<0.01), the activity of MMP-9 was obviously positively correlated with the expression of TNF-αand IL-β1(r=0.90 and 0.91, P <0.01), and Rapo was positively correlated with the expression of TNF-α(r=0.88, P<0.01). Conclusions Left ventricle is undergoing progressive remodeling after CME due to abnormal expressions of pro-inflammatory and fibrogenic cytokines leading to myocyte apoptosis and interstitial collagen proliferation. Via down-regulating the expressions of these cytokines, Carvedilol intervention decreases myocyte apoptosis, interstitial collagen proliferation and improve ventricular function. 相似文献
8.
The expression of AT1 receptor on hepatic stellate cells in rat fibrosis induced by CCl4 总被引:13,自引:1,他引:12
Objectives To assess the effect of an ACE inhibitor and an Ang Ⅱ type 1 (AT1) receptor an tagonist on preventing hepatic fibrosis induced by CCl(4) in rats and to investi gate whether there is the expression of AT1 receptors on hepatic stellate cell s. Methods Studies were conducted in male Sprague-Dawley rats. Except for model group and control group, in three treated groups, either enalapril (5 mg/kg), or losarta n (10 mg/kg), or enalapril+losartan were given to the fibrotic rats (daily gava ge). Saline vehicle was given to the control group. After 6 weeks, liver fibro sis was assessed directly by hepatic morphometric analysis. The expression of A T1 receptors and α-smooth muscle actin (α-SMA) in liver tissue and isolated hepatic stellate cells (HSC) were detected by immunohistochemical techniques. Results Compared with the fibrosis in rats of the model group, rats treated with either enalapril or losartan, or a combination of two drugs, showed a limited expansion of the interstitium (P<0.05), but no significant difference was observed a mong the three treated groups (P>0.05). The expression of AT1 receptors w as found in abundance in the fibrotic interstitium of the fibrotic rats, whereas in the normal control rats they were limited to the vascular wall. AT1 recept ors were also expressed on activated HSC in culture plates. Conclusions Angiotensin-converting enzyme inhibitors and AT1 blockers might slow the progr ession of hepatic fibrosis. Activated HSCs expressed AT1 receptors. Activatio n of RAS might be related to hepatic fibrogenesis induced by CCl(4). 相似文献
9.
Granulocyte colony-stimulating factor (G-CSF) has been demonstrated to have neuroprotective effects in rat model with focal cerebral ischemia through anti-apoptotic pathways and by promoting proliferation of neural stem cells. In the present study, we examined the neuroprotective effect of G-CSF in an acute focal cerebral ischemia rat model with lipid metabolism disorder. Eighty male SD rats were randomly divided into normal diet control group (NC group) and high-fat diet group (HFD group) (n = 40 in each). In HFD group, rats were fed on high fat diet to induce atherosclerosis. After 29 days, 4 rats from each group were sacrificed to evaluate the effects of different diets, and the middle cerebral artery occlusion (MCAO) was performed in the rest of the rats. MCAO rats received either G-CSF (50 μg·kg-1·mL-1) or phosphate buffered saline (PBS) injection through the external jugular vein for 5 days, which was followed by 5-bromo-deoxy uridine (BrdU, i.p., 50 mg/kg) injection for another 7 days. To evaluate the effects of G-CSF treatment on neurological function, the modified neurological severity score (mNSS) was calculated. The vascular distribution, ischemic cells proliferation, cell apoptosis and the expression of vascular endothelial growth factor (VEGF) were measured to determine the effects of G-CSF treatment. Our results showed that G-CSF-treated rats had a lower mNSS than PBS-treated rats in both NC group and HFD group. G-CSF injection promoted endothelial cell proliferation and vascular regeneration, and inhibited cell apoptosis. The serum and tissue levels of VEGF were significantly increased after G-CSF treatment. It is concluded that G-CSF exerts its neuroprotective effect in focal cerebral ischemia rats with hyperlipidemia by enhancing angiogenesis, promoting cells proliferation, decreasing cell apoptosis, and increasing local VEGF expression. 相似文献
10.
Objective. To determine the effecm of losarcan and captoptil treatment on ventricular remodeling and function after myocardial infarction in rats. Methods. Thirty-two rats with MI induced by coxortary llgation after seven days were divided into four groups randomly and treated with eaptopri1(2 g. liter^-1 , group A), loaartan(10mg. kg^-1. d^-1 , group B),losartsn(30 rag. kg-l.d-l,group C) and placebo (no drug,group D) for six weeks, respectively. Shamoperated rats(group E)served as ccmtrols. Echccardiography was performed at 1 and 7 weeks after MI, respectively. Results. Compared with the results before treazment,both LV end-diastollc inzemal diameter and volume decreased significantly and the thickened posterior wall was reversed in group A, B and C; the peak early filling velocity decreased whereas the peak velocity was increased in these three groulm. There are no significant difference among the three treated groups. However ,LV end-diastolic interned diameter and the E/A were still increasnd,whereas the thickness of anterior wall and the peak velocity of LV outflow were decreased in group A,B,and C after treatment comparing with group E. Conclusion. Both angiotensin converting enzyme inhibitor and angiotensin I receptor antagonist can prevent the ventricular remodeling and improve the ventricular function. 相似文献
11.
大、中、小剂量依那普利防治大鼠AMI左室重构的作用对比 总被引:1,自引:0,他引:1
目的 对比大、中、小剂量依那普利 (Enla)对大鼠AMI左室重构 (LVRM)的防治作用 ,并评价其量效关系。方法 97只雌性SD大鼠 ,AMI术后 4 8小时随机分成 :(1)AMI对照 ,(2 )Enla大剂量 (10mg·kg 1·d 1) ,(3)Enla中剂量 (1mg·kg 1·d 1)和 (4)Enla小剂量 (0 1mg·kg 1·d 1)四组。另设 :(5 )假手术和 (6 )正常组作对照。给药治疗 4周后均行血流动力学测定、心脏标本固定及病理分析。最终 6 7只大鼠获完整资料 ,在上述各组中的数目分别为 13、13、12、12、8和 9只。结果 AMI各组间梗塞面积均无显著差异 (45 4 % - 4 7 4 % ,P均 >0 0 5 )。与假手术组相比 ,AMI组左室舒张未压 (LVEDP)、容积 (LVV)、长 (L)、短 (D)轴长度和左室实际 (LVAW )及相对重量 (LVRW)均显著增加 (P均 <0 0 0 1) ,发生了LVRM ;而左室内压最大上升和下降速率 (±dp/dt)及其校正值均显著降低 (P <0 0 1- 0 0 0 1)。与AMI组相比 ,Enla大、中、小剂量三组的LVEDP、LVV、L以及LVAW和LVRW均显著降低或减小 (P <0 0 5 - 0 0 0 1) ,其中LVEDP、LVV、L和LVAW在大剂量组均比小剂量组降低或减小更显著 (P均 <0 0 5 ) ;而±dp/dt校正值在大、中剂量二组显著恢复 (P <0 0 5 - 0 0 1)。结论 1 Enla大、中、小剂量均能有效防治AMI大 相似文献
12.
目的 对比大、中、小剂量依那普利(Enla)对大鼠AMI左室重构(LVRM)的防治作用,并评价其量效关系.方法 97只雌性SD大鼠,AMI术后48小时随机分成:(1)AMI对照,(2)Enla大剂量(10?mg*kg-1*d-1),(3)Enla中剂量(1?mg*kg-1*d-1)和(4)Enla小剂量(0.1?mg*kg-1*d-1)四组.另设:(5)假手术和(6)正常组作对照.给药治疗4周后均行血流动力学测定、心脏标本固定及病理分析.最终67只大鼠获完整资料,在上述各组中的数目分别为13、13、12、12、8和9只.结果 AMI各组间梗塞面积均无显著差异(45.4%-47.4%,P均>0.05).与假手术组相比,AMI组左室舒张未压(LVEDP)、容积(LVV)、长(L)、短(D)轴长度和左室实际(LVAW)及相对重量(LVRW)均显著增加(P均<0.001),发生了LVRM;而左室内压最大上升和下降速率(±dp/dt)及其校正值均显著降低(P<0.01-0.001).与AMI组相比,Enla大、中、小剂量三组的LVEDP、LVV、L以及LVAW和LVRW均显著降低或减小(P<0.05-0.001),其中LVEDP、LVV、L和LVAW在大剂量组均比小剂量组降低或减小更显著(P均<0.05);而±dp/dt校正值在大、中剂量二组显著恢复(P<0.05-0.01).结论 1.Enla大、中、小剂量均能有效防治AMI大鼠LVRM,且大剂量更优.2.Enla大、中剂量能明显改善AMI大鼠的左室功能,而小剂量则无效. 相似文献
13.
不同剂量卡维地洛防治大鼠急性心肌梗死左室重构的研究 总被引:14,自引:1,他引:13
目的对比观察不同剂量卡维地洛对大鼠急性心肌梗死(AMI)左室重构(LVRM)的防治作用。方法雌性SD大鼠AMI术后成活142只,分为AMI对照组(n=35),和卡维地洛大剂量(10mg·kg-1·d-1,n=37),中剂量(1mg·kg-1·d-1,n=35),及小剂量(0.1mg·kg-1·d-1,n=35)四组。另设假手术组对照。直接灌胃给药4周后行血流动力学测定、心脏标本固定及病理分析。去除梗死面积<35%或>55%者,最终58只大鼠资料完整。结果AMI各组间梗死面积均无显著差异(44.5%~46.3%,P均>0.05)。与假手术组相比,AMI组的左室舒张末压(LVEDP)、容积(LVV)、实际左心室重量(LVAW)及相对重量(LVRW)均显著增加(P均<0.01),左室球形指数和左室内压最大上升和下降速率(±dp/dt)及其校正值(±dp/dt/LVSP)均显著降低(P均<0.01)。与AMI组相比,卡维地洛大、中、小剂量组的LVEDP、LVV、LVAW和LVRW均呈剂量相关性显著降低(LVEDP7.7mmHg±1.9mmHg,12.1mmHg±2.0mmHg,14.5mmHg±4.6mmHg对24.5mmHg±5.3mmHg;LVV0.72ml±0.10ml,0.79ml±0.08ml,0.82ml±0.10ml对0.92ml±0.11ml;LVAW589mg±57mg,622mg±70mg,666mg±57mg对730mg±79mg;P<0.05~0.001),±dp/dt及±dp/dt/LVSP均显著增加(P<0.05~0.01),但各剂量组间均无显著差异,左室球形指数仅在大剂量组显著改善(P<0.05)。结论卡维地洛大、中、小剂量均能有效地防止大鼠AMI左室重构,改善血流动力学和左室功能;小剂量有效,大剂量更好。 相似文献
14.
卡维地洛与倍他乐克防治大鼠AMI左室重构作用的比较 总被引:1,自引:0,他引:1
Tang YD Yang YJ Zhang P Ruan YM Lu SQ Sun RC Wang PH Gao RL Chen JL Chen ZJ 《中国医学科学院学报》2001,23(5):476-480
目的对比卡维地洛及倍他乐克对大鼠急性心肌梗死(AMI)左室重构(LVRM)的防治作用.方法 105只AMI术后成活的雌性SD大鼠随机分成AMI对照(n=35)、卡维地洛1 mg/(kg@d)(n=35)和倍他乐克2 mg/(kg@d)(n=35)三组.另设假手术组.给药4周后行血流动力学测定和病理分析.去除死亡及梗死面积<35%或>55%者,最终46只大鼠资料完整,在以上各组分别为11,12,11和12只.结果与假手术组相比,AMI组的左室舒张末压(LVEDP)、容积(LVV)、重量(LVW)显著增加(P<0.05~0.111),左室内压最大上升和下降速率(±dp/dt)及其校正值(±dp/dt/LVSP)显著降低(P<0.01~0.001).与AMI组相比,卡维地洛和倍他乐克组的LVEDP及LVV均显著降低(P均<0.001),±dp/dt及±dp/dt/LVSP均显著升高(P<0.05~0.001),而LVW和RVW仅在卡维地洛组显著减轻(P均<0.05~0.01).结论 1、卡维地洛能有效抑制大鼠AMI左室重构并改善血流动力学和左室功能,2、倍他乐克与卡维地洛的作用相似,但对心室肥厚似无抑制作用. 相似文献
15.
强力霉素、氯沙坦及其合用防治大鼠急性心肌梗死后左室重构的作用 总被引:2,自引:0,他引:2
目的对比强力霉素、氯沙坦及其合用对大鼠急性心肌梗死(AMI)左室重构的防治作用.方法461只雌性SD大鼠,其中30只设为假手术组(仅在冠脉下穿线,不结扎);另外431只大鼠行冠脉前降支结扎致AMI,术后24 h存活的254只大鼠随机分为下列各组:(1)AMI对照组64只;(2)强力霉素组(30 mg·kg-1·d-1)63只;(3)氯沙坦组(10 mg·kg-1·d-1)62只;(4)强力霉素(30 mg·kg-1·d-1)和氯沙坦(10 mg·kg-1·d-1)合用组65只.依疗程不同,将上述各组再均随机分为1、2和4周3个亚组.给药满疗程后各组均行血流动力学测定、心脏标本固定和病理分析.结果最终157只大鼠获完整资料.AMI对照及3个治疗组各亚组间的梗死面积差异均无显著性(P>0.05).与假手术组相比,AMI对照组的左室舒张末压(LVEDP)、实际和相对重量(LVAW和LVRW)在各时间亚组均显著增加(P<0.05,P<0.01,P<0.001),且LVEDP在4周比1和2周时升高更显著(P<0.01);而左室内压最大上升和下降速率及其与左室收缩压的比值仅在4周时显著降低(P<0.001).与AMI对照组相比,强力霉素、氯沙坦及其合用3个治疗组的LVEDP在各时间亚组均显著降低(P<0.05,P<0.01,P<0.001);LVAW和LVRW仅在氯沙坦和合用组的2和4周亚组,以及强力霉素组的4周亚组显著减轻(P<0.05,P<0.01,P<0.001);而左室内压最大下降速率和左室内压最大上升和下降速率与左室收缩压的比值仅在3个治疗组的4周亚组显著增加(P<0.05,P<0.01).上述各指标在3个治疗组的各时间亚组间差异均无显著性(P>0.05).结论强力霉素和氯沙坦均能有效防治大鼠AMI左室重构,改善左室收缩和舒张功能,且作用相当,而两药合用似无叠加效应,值得进一步研究. 相似文献
16.
刺五加叶皂苷对急性心肌梗塞大鼠心室重构的作用 总被引:12,自引:1,他引:11
目的:通过大鼠急性心肌梗塞心室重构模型观察刺五加叶皂苷(ASS)对急性心肌梗塞大鼠心室重构的作用。方法:大鼠结扎左冠状动脉前降支造成急性心肌梗塞心室重构模型,同时应用ASS,给药4周后测定心室重构大鼠血液动力学、生化学及形态学参数。
结果: ASS对急性心肌梗塞心室重构大鼠,能明显升高左心室内压最大上升和下降速率(±dp/dtmax)及其校正值(±dp/dtmax/LVSP),降低左心室舒张末压(LVEDP),亦能明显降低左心室容积(LVV)、左心室长轴(LVLA)长度、左心室短轴(LVSA)长度、左心室绝对重量(LVAW)、左心室相对重量(LVRW),但对右心室绝对重量(RVAW)、右心室相对重量(RVRW)、心率(HR)、左心室收缩压(LVSP)、平均动脉压(MAP)及体重(BW)均无明显影响。ASS可明显降低血清脂质过氧化物 (LPO)及心肌血管紧张素Ⅱ(AngⅡ)和肾上腺素(E) 含量,提高超氧物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性。
结论:ASS能有效抑制急性心肌梗塞大鼠的心室重构。 相似文献
17.
中药通心络对猪急性心肌梗死再灌注后无再流的影响 总被引:13,自引:0,他引:13
Yang YJ Zhao JL Jing ZC Wu YJ You SJ Yang WX Meng L Tian Y Chen JL Gao RL Chen ZJ 《中华医学杂志》2005,85(13):883-888
目的评价通心络防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪40只随机分成5组,每组8只:(1)AMI模型对照组(对照组),(2)通心络小剂量治疗组(0·05g·kg-1·d-1),(3)通心络中剂量治疗组(0·2g·kg-1·d-1),(4)通心络大剂量治疗组(0·5g·kg-1·d-1),(5)假手术组。通心络各组预给药3d后行冠状动脉结扎180min,松解60min制备AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定,心肌声学造影(MCE)检查和病理学分析。结果(1)与AMI前相比,对照组AMI后180min左室收缩压(LVSP)、心排量和左心室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0·05或P<0·01),左室舒张末压(LVEDP)显著升高(P<0·01);再灌注后60min仅LVSP显著恢复(P<0·05),然而±dp/dtmax继续显著下降(P<0·05)。小、中和大剂量通心络组AMI后180min各项指标变化与对照组相同;再灌注后60min仅大剂量通心络组LVEDP、±dp/dtmax和心排量均显著恢复(均P<0·05),且显著好于对照组(均P<0·05)。(2)对照组MCE和病理染色所测的冠脉结扎区心肌范围(LA)高度一致(P>0·05),再灌注后无再流区范围分别为78·5%和82·3%,心肌坏死面积占结扎区心肌面积的98·5%。3个通心络组LA与对照组相当(均P>0·05),但MCE和病理染色所测无再流范围在中及大剂量通心络组分别为41·1%、42·4%和24·1%、25·0%,坏死心肌范围分别为90·2%及81·2%,均显著小于对照组和小剂量组(P<0·05或P<0·01),大剂量组也显著小于中剂量组(P<0·05或P<0·01)。(3)对照组再灌注后即刻和再灌注后60min冠脉血流量仅占AMI前的45·8%和50·6%(均P<0·01),而大剂量通心络组冠脉血流量分别占AMI前的76·0%和73·5%,均显著高于对照组(均P<0·01)。结论通心络能有效地防治心肌梗死再灌注后无再流,缩小梗死面积;中剂量有效,大剂量更好。 相似文献
18.
地尔硫卓对猪急性心肌梗死再灌注后无再流的影响 总被引:5,自引:3,他引:2
Zhao JL Yang YJ You SJ Jing ZC Wu YJ Yang WX Meng L Tian Y Chen JL Gao RL Chen ZJ 《中华医学杂志》2005,85(10):679-683
目的评价地尔硫卓防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法实验动物随机分成对照组、地尔硫卓组(2mg/min冠脉内)和假手术组。前两组行冠状动脉结扎3h,松解1h制备AMI再灌注模型。AMI前、后和再灌注后均行血流动力学测定和心肌声学造影(MCE)检查,最终行病理学分析。结果与AMI前相比,对照组AMI后3h、左室收缩压(LVSP)、心排量(CO)和左心室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(均P<0.05,P<0.01),左室舒张末压(LVEDP)显著升高(P<0.01);再灌注后1h仅LVSP显著恢复(P<0.05),然而±dp/dtmax继续显著下降(P<0.05);而地尔硫卓组AMI后3h各项指标变化与对照组相同;但再灌注后1h LVEDP、±dp/dtmax和CO均显著恢复(均P<0.05),且比对照组更显著(均P<0.05)。对照组MCE和病理染色所测的冠脉结扎区心肌范围(LA)高度一致(P>0.05),再灌注后无再流范围(ANR)分别为78.5%和82.3%,心肌坏死范围(NA)占LA的98.5%;而地尔硫卓组两方法所测LA均与对照组相当(均P>0.05),但ANR仅分别为20.6%和19.9%,NA又与对照组差异无统计学意义(P>0.05)。对照组再灌注即刻和再灌注后1h冠脉血流量仅占AMI前的45.8%和50.6%(均P<0.01),而地尔硫卓组冠脉血流量分别提高到80.4%和79.3%,比对照组增加均有统计学意义(均P<0.01)。结论 相似文献
19.
目的:观察转染与未转染phVEGF165的骨髓单个核细胞(BM-MNC)移植对心肌梗死后心功能的影响。方法:结扎家兔冠状动脉左前降支,建立急性心肌梗死(AMI)模型。随机分为3组:①BM-MNC+ph-VEGF165组(n=7):梗死心肌边缘注射转染了phVEGF165的自体骨髓细胞;②BM-MNC组(n=7):梗死心肌边缘注射未转染phVEGF165的自体骨髓细胞;③AMI对照组(n=7):梗死心肌边缘注射等量无血清培养基;④假手术组(n=5):只穿线,不结扎。AMI后第3天抽取股骨骨髓,分离单个核细胞培养。并于AMI后14d进行细胞移植。细胞移植后28d,采用超声心动图,并结合心脏重量指数及血流动力学等参数评价转染与未转染ph-VEGF165的骨髓细胞移植对心功能的影响。结果:与假手术组相比,AMI组左室舒张末期压明显升高(P<0.05),而左室短轴缩短率、左室壁厚度/左室内径、射血分数以及左室收缩压、压力变化率最大值均显著降低(P<0.05),然而,与AMI对照组相比,细胞移植组左室舒张末期压显著降低,而左室短轴缩短率、左室壁厚度/左室内径、射血分数以及左室收缩压、压力变化率最大值明显升高。同时我们发现,与未转染phVEGF165的骨髓单个核细胞移植相比,转染了phVEGF165的骨髓单个核细胞移植对心肌梗死后心功能的改善更为显著。结论:骨髓单个核细胞移植能明显改善心功能,并防止AMI后左室重构发生。转染phVEGF165的骨髓单个核细胞移植更加有效。 相似文献
20.
OBJECTIVE: To evaluate the beneficial effects of early coronary reperfusion on left ventricular remodeling (LVRM) and systolic function in patients with acute myocardial infarction (AMI). METHODS: Eighty-one patients with first AMI in the convalescent stage and having undergone left ventriculography (LVG) and coronary arteriography (CAG) were divided into four groups: the anterolateral wall (ALW) myocardial infarction (MI) non-reperfusion (n = 20) and reperfusion (n = 21), and inferoposterial wall (IPW) MI non-reperfusion (n = 20) and reperfusion (n = 20), according to infarct location and early treatment with or without successful coronary reperfusion therapy within 6 hours after onset of symptoms. By LVG, the parameters of LVRM and systolic function in the four MI groups were analyzed and compared with those in normal group (n = 25) and between the two reperfusion and non-reperfusion MI groups. RESULTS: In both ALW and IPW MI non-reperfusion groups, the left ventricular (LV) end-diastolic volume (EDV), circumference (EDC), short-axis dimension (EDD), short to long axis ratio (ED-D/L), sphericity index (ED-SI) and end-systolic volume (ESV) were all significantly increased (P < 0.01-0.001), while LV ejection fractions (LVEF) were significantly decreased (both P < 0.001) when compared with those of normal group; and the increase in ESV and decrease in LVEF were both significantly greater in ALW than in IPW MI groups (both P < 0.01). In both ALW and IPW MI reperfusion groups, however, the EDV, EDD, ESV, as well as the extent and severity of regional wall motion abnormality (RW-MA) were significantly smaller (P < 0.05-0.001), while LVEF were significantly higher (P < 0.01-0.001) when compared with those in the two non-reperfusion MI groups respectively. There were no longer significant differences in LVEF and ESV between ALW and IPW MI groups (both P > 0.05). The EDC in IPW MI reperfusion group and the ED-D/L and ED-SI in ALW MI reperfusion group were also significantly reduced compared with those in the two non-reperfusion MI groups respectively (P < 0.05-0.001). All the above parameters in the two reperfusion MI group were decreased to the normal in comparison with normal group except ESV and LVEF, and ED-D/L and ED-SI in IPW MI group. CONCLUSION: It was indicated that in both ALW and IPW MI non-reperfusion groups, LVRM had occurred in convalescent stage of AMI with an increase in EDV and EDC, spherical change in LV shape, and accompanying reduction in LV systolic function; and early coronary reperfusion in AMI could reduce the extent and severity of RWMA, prevent from LV enlargement and remodeling, and preserve or improve LV systolic function with more prominence in ALW MI. 相似文献