汉防己甲素对硫唑嘌呤致大鼠肝损伤的保护作用

研究汉防己甲素(Tet)对硫唑嘌呤(Aza)致大鼠肝损伤的保护作用。方法大鼠分为三组 :①对照组 ;②Aza组 ;③Aza Tet组。给药量分别为Aza25mg/kg·d。Tet30mg/kg·d,测定用药1wk和2wk时大鼠血清谷丙转氨酶(ALT)、碱性磷酸酶(AKP)、总蛋白(TP)和白蛋白(Alb)等肝功能指标以及血清中丙二醛(MDA)、超氧化物歧化酶(SOD)和全血谷胱甘肽含量(GSH) ,并作病理观察。结果用药1wk及2wk后 ,Aza组大鼠血清ALT、AKP、MDA含量均显著升高 ,TP、Alb、SOD、GSH含量均显著降低 ;合用Tet组则上述变化不明显 ,与对照组比较无显著性差异。病理学检查发现合用Tet组病理改变较轻微。结论Tet对Aza致大鼠肝损伤有保护作用 ,推测此作用与其抗脂质过氧化物、增加内源性解毒物质有关。     

血管内皮细胞在门静脉高压性结肠病形成中的作用

目的探讨血管内皮细胞在门静脉高压性结肠病(PHC)形成中的作用。方法成年雄性Wistar大鼠19只,随机抽取8只作为正常组,其余大鼠按复合因素法制作肝硬化模型,10周后门静脉取血测定一氧化氮(NO)、肿瘤坏死因子(TNF)-α含量,取大鼠降结肠全层行免疫组织化学染色,观测黏膜下层血管内皮细胞,测定一氧化氮合酶(NOS)、TNF-α表达量。另取结肠组织行电镜观察。结果电镜下观察模型组可见内皮细胞分泌小泡增多,肌微丝形成。诱导型NOS(iNOS)、TNF-α在血管内皮细胞高度表达,与正常组相比差异有统计学意义(P<0.05)。血清NO、TNF-α显著增高,与正常组相比差异具有统计学意义(P<0.05)。结论肝硬化时,血管内皮细胞成为生成NO、TNF-α的主要细胞,这些炎症因子直接参与了PHC的形成。     

芸香苷对急性胰腺炎大鼠血浆TXB_2/6-keto-PGF1α值及胰腺组织NO的影响

目的:研究芸香苷(Ru)对大鼠急性胰腺炎模型(AP)血浆血栓素B(2TXB2)与6-酮基-前列腺素F1α(6-keto-PGF1α)及胰腺组织一氧化氮(NO)的影响。方法:SD大鼠48只,随机分为假手术、模型、丹参及Ru高、中、低剂量组。以牛磺胆酸钠溶液复制大鼠急性胰腺炎模型,测定各组大鼠血浆TXB2/6-keto-PGF1α值、酶学及胰腺组织NO,并做病理检查。结果:Ru能够有效降低AP模型大鼠血浆TXB2/6-keto-PGF1α值,降低胰腺组织的NO含量,减轻胰腺组织水肿、坏死炎症及空泡形成,明显改善胰腺的病理组织学变化。结论:Ru对胰腺组织有一定的保护作用。     

熊果酸对四氯化碳所致大鼠肝纤维化及门静脉高压的影响

目的 研究熊果酸(UA)对四氯化碳(CCl4)所致大鼠肝纤维化及门静脉高压的影响及其机制.方法 取120只实验用大鼠运用随机数字表法分为正常对照组、模型对照组、UA(10、20、40 mg·kg-1)组和秋水仙碱(0.1 mg·kg-1)组,每组20只;采用CCl4复合法复制肝纤维化门静脉高压大鼠模型;自造模第1天各组开始腹腔注射给药(正常对照组和模型对照组均给予等体积生理盐水),每天1次.6周后,测定血清中转氨酶和总胆红素(TBIL)含量,测定血清中肝纤维化四项指标[透明质酸(HA)、层黏蛋白(LN)、Ⅳ型胶原(CⅣ)、Ⅲ型前胶原(PCⅢ)]含量和肝组织中羟脯氨酸(HYP)水平;通过生理记录仪测定门静脉压(PVP)、门静脉血流量(PVF)、平均动脉压(MAP)并测定心率(HR);HE染色法观察肝脏组织形态结构变化;硝酸还原酶法测定肝脏组织中一氧化氮(NO)含量、放射免疫法测定环鸟苷酸(cGMP)含量;测定肝脏组织中抗氧化酶活性和丙二醛(MDA)含量.结果 较模型组对照组大鼠,UA(20、40 mg·kg-1)组血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)和TBIL含量显著降低,血清中CⅣ、PCⅢ、HA、HYP含量显著降低,其中UA 40 mg·kg-1组LN含量显著降低;UA(20、40 mg·kg-1)组PVP、PVF均显著降低,40 mg·kg-1组MAP显著升高、HR显著降低;UA(10、20、40 mg·kg-1)组肝纤维化门静脉高压大鼠肝脏组织病理性形态学变化呈不同程度改善,呈一定剂量依赖性;UA(20、40 mg·kg-1)组肝脏组织NO含量和超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性显著升高,40 mg·kg-1组cGMP含量和谷胱甘肽过氧化物酶(GSH-Px)活性显著升高,上述均差异有统计学意义(P<0.05或P<0.01).结论 UA对CCl4所致大鼠肝纤维化及门静脉高压具有一定的抑制作用,机制可能与UA能够有效保肝降酶,抑制氧化应激损伤,提高NO含量有关.     

汉防己甲素对硫唑嘌呤致大鼠肝损伤的保护作用

目的 研究汉防己甲素（Tet)对硫唑嘌呤（Aza)致大鼠肝损伤的保护作用。方法 大鼠分为三组：①对照组；②Aza组；③Aza Tet组。给药量分别为Aza 25mg/kg·d。Tet 30mg/kg·d,测定用药1wk和2wk时大鼠血清谷丙转氨酶（ALT）、碱性磷酸酶（AKP）、总蛋白（TP）和白蛋白（Alb）等肝功能指标以及血清中丙二醛（MDA）、超氧化物歧化酶（SOD）和全血谷胱甘肽含量（GSH），并作病理观察。结果 用药1wk及2wk后，Aza组大鼠血清ALT、AKP、MDA含量均显升高，TP、Alb、SOD、GSH含量均显降低；合用Tet组则上述变化不明显，与对照组比较无显性差异。病理学检查发现合用Tet组病理改变较轻微。结论 Tex对Aza致大鼠肝损伤有保护作用，推测此作用与其抗脂质过氧化物、增加内源性解毒物质有关。     

山茱萸配伍组分对糖尿病大鼠心血管病变的保护作用

目的通过观察糖尿病大鼠血脂、血管损伤相关因子及病理变化,分析山茱萸配伍组分保护糖尿病心血管病变的作用机制。方法链脲佐菌素(STZ)复合高脂饲料造成糖尿病大鼠模型,取造模成功大鼠按血糖值随机分组,设立模型组、格列美脲(GLMN)组(0.4 mg.kg-1)、山茱萸配伍组分低剂量(PC-L)组(60 mg.kg-1)、高剂量(PC-H)组(120mg.kg-1),灌胃给药12周,另设空白对照组,模型组与空白组大鼠以蒸馏水灌胃。试剂盒测定血清中TC、TG、HDL-C、LDL-C、NO、T-NOS;放射免疫测定血清中TXB2和6-keto-PGF1α及血浆中ET含量。取大鼠心脏并计算脏器系数,同时观察大鼠心脏和胸主动脉病理组织学变化。结果 PC-L、PC-H组大鼠血清中TC、TG、LDL-C、TXB2含量减少,LDL-C/HDL-C、TXB2/6-keto-PGF1α值降低,与模型组比较差异有显著性(P<0.05,P<0.01)。PC-L组NO、T-NOS含量有增加的趋势,而ET含量减少、NO/ET值升高,与模型组比较差异有显著性(P<0.05);PC-H组NO、T-NOS含量增加、ET含量减少、NO/ET值升高,但与模型组比较差异无显著性。结论山茱萸配伍组分可调节血脂,恢复血管收缩与舒张的动态平衡,改善血液流变性和减轻心脏及胸主动脉病变,具有保护糖尿病大鼠心血管病变的作用。     

一氧化氮供体型齐墩果酸衍生物ZCⅡ2对早期实验性肝纤维化的保护作用

目的:观察一氧化氮供体型齐墩果酸衍生物ZCⅡ2对早期实验性肝纤维化的保护作用。方法:用CCl4诱导大鼠肝纤维化模型,ZCⅡ2以128mg·kg-1和64mg·kg-1的剂量给大鼠连续灌胃给药30d,测定血清总蛋白(TP)、白蛋白(ALB)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、一氧化氮(NO)以及血清透明质酸(HA)、层粘蛋白(LN)和Ⅲ型前胶原(PCⅢ)的含量,计算白蛋白与球蛋白的比例(白球比例);测定肝组织中丙二醛(MDA)和谷胱甘肽过氧化物酶(GSHPx)及一氧化氮合酶(NOS)的含量,并行肝组织病理组织学检查。结果:与模型组相比,ZCⅡ2高剂量能显著降低谷丙转氨酶、谷草转氨酶含量,增加白蛋白含量,提高白球比例,显著降低血清透明质酸、层粘蛋白和Ⅲ型前胶原含量,明显改善肝组织病理损伤。结论:一氧化氮供体型齐墩果酸衍生物ZCⅡ2对大鼠早期实验性肝纤维化具有一定的保护作用。     

通络逐瘀汤对脑缺血/再灌注损伤的临床研究

目的 观察通络逐瘀汤对脑缺血/再灌注损伤的保护作用,并对其机制作初步探讨.方法 对大鼠大脑中动脉缺血2h /再灌注22h模型采用不同方案治疗,比较其神经病学评分、脑梗死范围及抗脑缺血/再灌注损伤的效果;放射免疫法检测患侧皮质内皮素(ET)、血栓素B2 (TXB2 )、6-酮-前列腺素F1α(6-keto-PGF1α)含量的变化.结果 大鼠脑缺血2h/再灌注22h后,假手术组大鼠神经病学评分均为0分,无脑梗死;尼莫地平组和通络逐瘀汤30、60mg/kg组神经病学评分和脑梗死范围均小于生理盐水组,差异有统计学意义(P<0.05).生理盐水组ET及TXB2 含量高于假手术组,6-Keto-PGF1α活性低于假手术组,差异均有统计学意义(P<0.05); 尼莫地平组和通络逐瘀汤30、60mg/kg组ET及TXB2 含量低于生理盐水组,6-Keto-PGF1α活性高于生理盐水组,差异均有统计学意义(P<0.05).结论 通络逐瘀汤对脑缺血/再灌注损伤有保护作用,其作用机制与抑制ET、TXB2含量,提高6-keto-PGF1α活性,维持TXB2/6-keto-PGF1α动态平衡有关.     

肝硬化门脉高压性胃病173例分析

门静脉高压性胃病(Portal hypertensive gastropathy,PHG)是指门静脉高压患者发生的胃黏膜的特殊病变[1].与非门静脉高压性胃病情况不同,胃黏膜组织内无明显炎症,而黏膜下血管可见扭曲和扩张.近年来,PHG越来越受到重视.现将近10年来经胃镜检查确诊的173例门静脉高压性胃病报告分析总结如下.     

丹参醇提物对大鼠肝硬化门脉高压性胃病和肝功能的影响

目的：研究丹参醇提物对大鼠肝硬化门脉高压性胃病和肝功能的影响。方法：采用左肾上腺静脉结扎并按体重变化调节硫代乙酰胺（TAA）的浓度,建立肝硬化门脉高压大鼠动物模型。灌胃给予丹参醇提物,给药8周后检测大鼠门静脉压力、血清丙氨酸氨基转氨酶（ALT）、天冬氨酸氨基转移酶（AST）、总胆红素（TBIL）、碱性磷酸酶等;观察大鼠胃组织形态病理学和免疫组化变化。结果：与模型组相比,丹参醇提物各剂量组大鼠门静脉压力、血清ALT、AST、TBIL水平均显著下降（P<0.05,P<0.01）。病理结果显示,模型组大鼠胃黏膜面有溃疡及糜烂形成,黏膜层上皮细胞可见变性、坏死、脱落、炎细胞浸润,黏膜下层、肌层、外膜组织结构不完整;丹参醇提物各剂量组大鼠胃黏膜面有轻度溃疡及糜烂形成,黏膜层上皮细胞见少量炎细胞浸润现象。免疫组化结果显示,丹参醇提物各剂量组阳性细胞染色较弱,呈弥漫性表达,较模型组表达均有不同程度的降低。结论：丹参醇提物对大鼠肝硬化门脉高压性胃病和肝功能损害有显著的治疗作用。     

The role of nitric oxide in systemic and hepatic haemodynamics in the rat in vivo

The physiological role of nitric oxide (NO) in portal venous and hepatic arterial haemodynamics in the rat in vivo during healthy and diseased conditions remains unclear. The present study determined the physiological role of nitric oxide in hepatic haemodynamics in the rat in vivo during healthy conditions as a basis for future pharmacological work. Male Wistar rats (300–350 g) were anaesthetised with fentany/fluanisone (0.3 mg/kg s.c.) and midazolam (0.3 mg/kg s.c.) and heparinised (30 U/100 g i.v.) via a cannulated left carotid artery for measurement of heart rate, mean arterial pressure, and the difference between systolic and diastolic blood pressures (P_S-D). Following laparotomy, two distal ileocolic veins were cannulated, one catheter introduced to a distance of 1 cm and used for intraportal drug injections and the other to the main trunk of the portal vein for continuous measurement of portal venous pressure. The portal venous trunk and hepatic artery were carefully isolated and electromagnetic probes placed around each of them for measurement of portal venous flow and hepatic arterial flow. Augmentation of NO production was achieved by intraportal injection of 0.2, 0.4, 0.6 and 0.8 g/kg L-arginine and the NO donor, 3-morpholinosydnonimine (SIN-1), was injected intraportally at 0.2, 0.4, 0.6 and 0.8 mg/kg. L-NAME, the non-selective NOS inhibitor, was injected intraportally in increasing doses of 5, 10, 15 and 20 mg/kg in the absence or presence of L-arginine in doses of 0.2 and 0.5 g/kg. L-arginine increased portal blood flow by 25% without significant changes in systemic haemodynamics. SIN-1 decreased mean arterial pressure by 33% with no effect on portal blood flow. Both L-arginine and SIN-1 reduced portal venous pressure by 25% in a dose-dependent manner. L-NAME had no effect on portal haemodynamics despite a significant increase in systemic arterial pressure of 60% that was reduced dose-dependently by L-arginine. Hepatic arterial flow increased by 88% and 49% at the second and third doses of L-arginine and by 68% and 27% at the first two doses of L-NAME. No significant changes in hepatic arterial flow were found when L-NAME and L-arginine were given together. It is concluded that augmented endogenous NO production increased portal flow. Inhibition of endogenous NO had no effect on portal haemodynamics. Endogenous NO may not play a major role in regulation of portal haemodynamics in the rat in vivo.     

Inhibition of platelet aggregation by polyaspartoyl L-arginine and its mechanism

AIM: To observe the oral anti-platelet efficacy and the potential action mechanism of polyaspartoyl L-arginine (PDR), a new L-arginine rich compound. METHODS: Platelet aggregation was conducted by Born's method; bleeding time was determined using tail's bleeding time in mice; platelet adhesion was carried out with glass bottle method; nitric oxide (NO) was tested with Griess's method; and cAMP, thromboxane B(2) (TXB(2)) and 6-keto-PGF(1 alpha ) were assessed with commercial kits. RESULTS: The inhibition by PDR (15-60 mg/kg i.g. or 10 mg/kg i.v.) of platelet aggregation induced by adenosine diphosphate (ADP), collagen or thrombin at 1 h after oral administration or at 20 min after i.v. injection for rats (P<0.01), and its (15 mg/kg, i.g.) inhibition of ADP-induced platelet aggregation for rabbits during 6 h after administration were observed. PDR (15-60 mg/kg) prolonged the bleeding time of mice (P<0.05) and (30 mg/kg) increased NO concentration in plasma. On the other hand PDR did not change the contents of cAMP in platelet and TXB2 or 6-keto-PGF(1 alpha) in plasma. CONCLUSION: PDR is a novel, oral effective platelet aggregation inhibitor and its action mechanism possibly related to increasing NO generation.     

复方甘草酸苷治疗慢性乙型肝炎肝硬化疗效和对一氧化氮的影响

目的:观察复方甘草酸苷对慢性乙型肝炎肝硬化的临床疗效和对NO的影响。方法:选择110例慢性乙型肝炎肝硬化患者,随机分为治疗组55例,对照组55例。对照组进行保肝综合治疗,治疗组在保肝综合治疗的基础上加用复方甘草酸苷,12周为一疗程。观察患者临床症状,检测肝功能、Child-pugh计分、肝纤维化指标,行超声检查,检测血清中NO、cNOS、iNOS含量。结果:治疗组患者ALT、AST、ALB、TBIL,Child-pugh计分,肝纤维化指标HA、LN、PCⅢ、IVC改善明显优于对照组;B超检查,门静脉内径和脾脏厚度改善优于对照组;血清中NO和iNOS含量明显降低。结论:复方甘草酸苷可用于慢性乙型肝炎肝硬化患者的治疗。     

Sildenafil prevents indomethacin-induced gastropathy in rats: role of leukocyte adherence and gastric blood flow

Nitric oxide (NO) is an important mediator of gastric mucosal defense. Sildenafil (SILD), a cyclic GMP-specific phosphodiesterase inhibitor, promotes an increase in cGMP concentrations in the gastrointestinal tract. cGMP mediates many of the biological actions of NO. We tested the hypothesis that SILD could increase mucosal defense against indomethacin-induced gastropathy in rats. SILD (1, 4 or 10 mg kg(-1), p.o.) pretreatment significantly reduced (P < 0.01) the gastric damage and the increase in gastric myeloperoxidase (MPO) activity elicited by indomethacin (20 mg kg(-1) p.o.), with the maximal effect at the dose of 10 mg kg(-1). L-NAME (3, 10 or 20 mg kg(-1), i.p.) dose dependently reversed the protective effects of SILD, an effect not seen when L-arginine (L-ARG) (200 mg kg(-1), i.p.) was co-administered with L-NAME. Indomethacin-induced leukocyte adhesion, assessed by intravital microscopy, was decreased (P < 0.01) by SILD, and this effect was reversed by L-NAME cotreatment. Indomethacin elicited a decrease in gastric blood flow and in gastric PGE2 levels. SILD was able to prevent the decrease in gastric blood flow (P < 0.01), without diminishing the inhibitory effect of indomethacin on prostaglandin synthesis. These results indicate that SILD, acting via NO-dependent mechanisms, prevents indomethacin-induced gastropathy, possibly through a reduction of leukocyte adhesion and maintenance of gastric blood flow.     

波依定联合氟伐他汀对原发性高血压左室肥厚的影响

目的评价波依定合用氟伐他汀对原发性高血压左室肥厚的影响。方法将80例原发性高血压左室肥厚患者随机分为A、B两组,A组给予波依定5 mg/d;B组给予波依定5 mg/d+氟伐他汀40 mg/d。疗程6个月,治疗前后用放免法测定血清中Ⅲ型前胶原(PCⅢ)、NO含量。分别在用药前后用超声心动图检查评价心肌肥厚。结果两组患者药物治疗后血压降低的同时LVM I及血清PCⅢ浓度也较治疗前降低(P<0.01),B组血清PCⅢ浓度的降低较A组更明显(P<0.05),LVM I的降低在两组间差异有统计学意义(P<0.05),B组治疗后NO的变化明显高于A组(P<0.05)结论波依定合用氟伐他汀对原发性高血压左室肥厚逆转及舒张功能改善有协同作用,较单一用药疗效显著。     

Roles of endogenous prostacyclin and thromboxane A2 in the ischemic canine heart

The ability of the ischemic heart to release prostacyclin (PGI2) and thromboxane A2 (TXA2) was studied, together with the effects of these substances on the ischemic myocardium in open-chest dogs. We measured the plasma levels of 6-keto-PGF1 alpha and TXB2--which are stable metabolites of PGI2 and TXA2, respectively--as well as lactate and coronary venous blood flow. The dogs were divided into three groups of eight animals which received indomethacin (5 mg/kg), (E)-3-[4-l-imidazolylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate (OKY-046) (1 mg/kg), or the vehicle. A transient increase in 6-keto-PGF1 alpha was observed in the great cardiac vein 5 min after the ligation of the left anterior descending coronary artery (LAD). TXB2 and lactate increased 30 and 15 min, respectively, after the ligation. Indomethacin prevented significant increases in 6-keto-PGF1 alpha and TXB2, but accelerated the lactate release. OKY-046 prevented significant increases in TXB2 and lactate release, but did not counteract the increase in 6-keto-PGF1 alpha. Although coronary venous flow decreased significantly 5 min after the ligation in every group, the flow returned to the preligation level 15 min after the ligation in the OKY-046 and the vehicle groups. Thus, we have demonstrated the release of PGI2 and TXA2 from the ischemic heart and suggest beneficial effects of PGI2 and of a selective inhibitor of thromboxane synthetase on the ischemic myocardium.     

白芍总苷对代谢综合征-高血压大鼠改善胰岛素敏感性、降压和抗氧化作用

目的：探讨白芍总苷（TGP）对代谢综合征-高血压（metabolic syndromic—hypertension,MS—Ht）大鼠血压的作用,检测胰岛素敏感性、细胞因子、血管活性物质以及氧化应激的改变,研究其作用机制。方法：采用高脂、高糖饮食喂饲SD大鼠,连续8周,当造模动物出现高血压、糖耐量减退,MS—Ht病理模型建立成功;然后将大鼠随机分为模型对照、二甲双胍（metformin,Met）200mg／kg和TGP150、50mg／kg两个剂量组;分别灌胃给药或蒸馏水,qd×4周,实验结束时,测定大鼠血压、空腹血糖（FBG）和口服糖耐量试验2h血糖（OGTT-2 hBG）、血浆胰岛素（Fins）,并计算胰岛素敏感性（ISI）和胰岛素抵抗指数（HOMA—IRI）;测定游离脂肪酸（FFA）、TNF—α、内皮素（ET-1）、肾素-血管紧张素（AngⅡ）、NO和丙二醛（MDA）含量以及一氧化氮合酶（NOS）和超氧化物歧化酶（SOD）活性。结果：与正常对照组比较,MS—Ht大鼠血压升高;FBG、OGTT-2hBG和Fins含量增高;ISI减弱、而HOMA—IRI增强;FFA、TNF—α、ET-1、肾素-AngⅡ和MDA含量增高（P〈0．05或P〈0．01）;NO含量和NOS及SOD活性降低（P〈0．05或P〈0．01）。Met和TGP150mg／kg增强ISI,而降低HO—MA—IRI,纠正高胰岛素血症（P〈0．05或P〈0．01）,降低FFA、TNF—α、ET-1、肾素-AngⅡ和MDA含量（P〈0．05或P〈0．01）,提高NO含量和NOS及SOD活性;而Met能降低FBG、OG—TT-2hBG含量（P〈0．05或P〈0．01）;与TGP150mg／kg组比较,差异无统计学意义（P〉0．05）;TGP50mg／kg组,除降低肾素、AngⅡ和FFA含量外（P〈0．05）,对其余指标,差异均无统计学意义（P〉0．05）。结论：TGP和Met能对抗MS—Ht大鼠胰岛素抵抗、增强胰岛素敏感性、纠正高胰岛素血症,拮抗ET-1、肾素-AngⅡ系统和氧化应激反应,提高NO和NOS功能,降低血压;TGP不具直接降血糖作用,与Met不同。TGP以上效应呈量效关系。     

Portal Hypotensive Effects of Tetrandrine and Verapamil in Portal Hypertensive Rats

The portal hypotensive effects of tetrandrine and verapamil (both calcium-channel blockers) were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague–Dawley rats. Both tetrandrine (4, 8, 16 and 24 mg kg^?1) and verapamil (0.5, 10, 1.5 and 2.0 mg kg^?1) induced dose-dependent decreases of portal venous pressure and mean arterial pressure after intravenous infusion. For example, infusion of tetrandrine (16 mg kg^?1) induced a maximum reduction of portal venous pressure and mean arterial pressure approximately 1 min after the start of infusion. Portal venous pressure decreased from baseline (12.5 mmHg) to 100 mmHg, and mean arterial pressure from baseline (90 mmHg) to 80 mmHg. Heart rate decreased from 250 to 240 beats min^?1. At 24 mg kg^?1, tetrandrine reduced portal venous pressure and mean arterial pressure to 20.3 ± 2.4% and 28.4 ± 1.4% of baseline, respectively. Our results show that both tetrandrine and verapamil induce portal pressure reduction in portal hypertensive animals.