神香草精油对豚鼠和兔离体肠的松弛作用

单花鼠曲草(拟)Culcitium reflexure H.B.K.(即 Gnaphalium unifloruum Lam.)生长于南美。作者研究了该植物叶乙醇提取物及主要黄酮类化合物的体外抗氧化及体内光防护作用。将该植物叶切成小片风干,室温下用乙醇一水(7:3)提取3次,水溶部分冻干得乙醇提取物(ECR)。将 ECR 溶于乙醇(7:3)用于体外实验;将 ECR 凝胶用于体内实验。植化分析显示,ECR 中主要黄酮类成分为芦丁     

缬草抗心律失常活性部位的筛选

目的：筛选缬草抗心律失常的活性部位。方法：建立以氯仿诱导心律失常的小鼠模型,分别灌胃给予缬草不同的提取部位,以小鼠室颤发生率为观察指标。结果：缬草提取物中水液部位和缬草油部位分别在5g（生药）·ml^-1和2．5g（生药）·ml^-1能显著降低氯仿所致小鼠室颤发生率,且水液部位的90％乙醇洗脱物和水洗脱物能显著降低氯仿所致小鼠室颤发生率（P〈0．05）。结论：缬草提取物中水液部位和缬草油有抗心律失常作用。     

01095 新缬草黄酮类化合物有CNS活性

缬草根(Valeriana)提取物可用作镇静剂和睡眠辅助药。一般认为缬草中有许多物质有镇静作用，包括缬草酸衍生物，缬草醚酯及baldrinals。最近，一种称为6-甲基芹菜素(6-methylapigenin，MA)的黄酮类化合物从缬草wallichii中分离出来，也在缬草officinalis中有发现。本文描述了一种称为橙皮式(hesperidin，HN)的另一种缬草黄酮类化合物，并评估了这二种黄酮化合物的生化和药理学性能。     

油橄榄叶提取物对L-NAME诱导的大鼠高血压的降压作用

作者将油橄榄叶用80％(m/m)乙醇提取,再用专利方法精制得实验用提取物。HPLC分析显示该提取物含18％-26％的橄榄苦苷。对以NG-硝基-L-精氨酸甲酯(L-NAME)造成的Wistar大鼠高血压模型进行了以下实验。1)油橄榄叶提取物对高血压的预防作用。将大鼠随机分为5组,空白对照组     

正交试验法优选缬草总黄酮的提取工艺

目的研究缬草的提取工艺。方法以总黄酮含量作为考察指标,采用正交试验法对缬草提取工艺进行优选。结果乙醇浓度和乙醇用量对考察指标具有显著性影响。结论以总黄酮含量为考察指标的缬草提取最佳工艺为A2B3C1D2。     

超临界二氧化碳萃取法与水蒸气蒸馏法提取缬草油的化学成分比较

摘要目的对不同提取方法提取的缬草油化学成分进行比较研究。方法采用超临界二氧化碳（CO2）萃取法和水蒸气蒸馏法从缬草中提取缬草油,用气相色谱 质谱联用（GC MS）法进行化学成分定性与相对含量的比较。结果共鉴定了118种成分,超临界CO2萃取法提取物共鉴定98种,水蒸气蒸馏法提取鉴定了67种,共有成分47种;超临界CO2萃取所得缬草油的收率约为水蒸气蒸馏收率的1.8倍。结论超临界CO2萃取法是缬草油较好的提取方法。     

松生等总黄酮提取工艺及镇痛抗炎作用研究

目的：研究松生等总黄酮的最佳优化提取工艺,并对不同极性溶剂提取部分的镇痛抗炎作用进行研究。方法通过单因素实验和正交实验,考察提取时间、料液比、乙醇浓度和提取次数对松生等总黄酮提取率的影响;采用小鼠冰醋酸扭体法及二甲苯致小鼠耳肿胀模型筛选松生等不同溶剂提取部分镇痛抗炎作用。结果回流提取法提取松生等总黄酮的最佳条件为：提取时间3 h、料液比1：30、乙醇浓度60%、提取2次,黄酮提取率最高5.63%;松生等乙醇提取物、正丁醇提取物和乙酸乙酯提取物均能够抑制冰醋酸引起的小鼠扭体反应和二甲苯引起的小鼠耳肿胀。结论该工艺提取松生等总黄酮提取率高,方法简便,重复性好。松生等乙醇提取物、正丁醇提取物和乙酸乙酯提取物均具有明显镇痛抗炎作用。     

含铁青树科植物的药物

用溶剂提取粉碎的铁青树科植物Heiste-ria paliida的皮得到一种新的植物提取物。特定的提取法是用乙醇将植物皮浸渍0.2～5周,每公斤皮用3～9L(最好是6L)水和3～9L(最好是6L)95％的乙醇。用提取物制得药剂可治疗或预防炎症(如风湿病和关节炎)、痛风和发热。也可用作     

刺痒黎豆提取物的制备

刺痒黎豆Mucuna pruriens DC.子叶粉脱脂后,用含水乙醇提取,分离得到含水乙醇提取物,将该提取物脱脂,移去乙醇得一含水提取物。该提取物由烟酰胺腺嘌呤二核苷酸(NADH)(2.59±0.32)μg、多酚(35.81±0.01)μg、巯基(100.69±13.25)μg、辅酶Q10(13.39±1.37)μg、左旋多巴(51.35     

用灰树花制备糖蛋白治疗肥胖症

本专利的新颖性在于提供了一种制备具有生物活性、分子量≥1400的糖蛋白的方法。该方法包括将多孔菌科植物灰树花Grifola frondosa(Fr.)S.F.Gray用乙醇于室温下提取,移去乙醇提取物,残余物在热水100~120℃中提取,加入乙醇至热的提取物中,使乙醇终浓度为50%~75%,于4~10℃放置8~1     

三七绒根提取物(76017)对心血管的作用

三七绒根提取物(76017)为三七绒根乙醇提出物的有效成分,毒性较低,给小白鼠静注LD₅₀为836±17mg/kg。给麻醉猫静注76017 25～50 mg/kg,3～5分钟内冠脉流量最高增加79%(P<0.05),血压呈暂时性下降,心率也略减慢,心肌耗氧量减少,比给药前平均降低24.3%(P<0.05)。在家兔离体心脏灌流实验中,当2%76017 0.1和0.2ml注入灌流系统时,小剂量组给药后1分钟,冠脉流量平均增加17.5%;大剂量组给药后5分钟和7.5分钟分别增加48%和43%,(P<0.05),心率也稍减慢(P>0.05)。小剂量组心肌收缩振幅在5分钟内最高增加48%(P<0.05)。在家兔离体器官血管灌流的实验中,当2%76017 0.1和0.2ml注入灌流系统,记录5分钟内的峰值,小剂量组兔肾、耳及后肢的流量分别增加50,57和32%;而大剂量组分别增加70,64和33%。     

Haemodynamic and coronary actions of ouabain during coronary infusion

Summary The investigations were carried out on 24 mongrel dogs which were anaesthetized with chloralose or sodium pentobarbital. Ouabain was added to the coronary blood (50, 100 and 200 ng/ml coronary blood or 0.7, 1.4 and 2.8×10^–7 M) over periods of 30 or 60 min by intracoronary infusion of the glycoside.Under chloralose anaesthesia, ouabain at concentrations of 100 and 200 ng/ml coronary blood augmented left ventricular dp/dt significantly. No significant changes were observed in coronary resting flow and flow per beat at the same time. Likewise, the maximum reactive hyperaemic blood flow remained constant, indicating the absence of any changes in the tone of the large extramural arteries.Under sodium pentobarbital anaesthesia small decreases in heart rate and increases in left ventricular dp/dt were seen only at the highest ouabain concentration (200 ng/ml). All flow parameters remained unchanged.These experiments provide evidence that concentrations of ouabain which 100- and 200-fold exceed therapeutic maintenance levels and 10- and 20-fold exceed the concentrations that produce constriction of helically cut pig and rabbit coronary arteries in vitro, do not diminish the coronary blood supply of the anaesthetized dog in vivo     

Cardiovascular effects of human and rat CGRP compared in the rat and other species

In the anaesthetised rat, human and rat CGRP (calcitonin gene-related peptide) which differ by 4 out of 37 amino acids, when given intravenously, lowered blood pressure and increased heart rate. The effects of human CGRP were unaltered by either propranolol or by mepyramine plus cimetidine. In the rat isolated perfused heart the peptides decreased coronary perfusion pressure and evoked a tachycardia. The latter effect was not seen in the rabbit isolated heart, although human CGRP increased coronary flow. The two peptides were equipotent at increasing the rate and force of contraction in the rat isolated right atrium, effects unaltered by propranolol. In the guinea-pig isolated atrium, rat CGRP was 10 times as potent as a chronotropic agent than as an inotrope, unlike human CGRP which was equipotent. In conclusion, human and rat CGRP probably acted directly on the cardiovascular system to produce their qualitatively similar effects.     

Felodipine, pharmacodynamics and pharmacokinetics in the isolated rabbit heart

Myocardial pharmacodynamics of the Ca2+-antagonist felodipine, a structural analogue of nifedipine, were studied in isolated, spontaneously beating and retrogradely perfused rabbit hearts. The concentration of felodipine in the Krebs-Henseleit perfusion liquid was stepwise increased from 0.7 ng/ml to 90.4 ng/ml (1.8 to 235.3 nmol/l). Increasing felodipine concentrations from 0.7 to 3.6 ng/ml produced an increase of up to 115% in coronary flow rate, which then decreased at higher concentrations to 84% of the control value. Oxygen consumption decreased progressively to 28% at concentrations from 3.6 to 90.4 ng/ml. Myocardial contractility measured by amplitude and rate of contraction decreased progressively to 45.7 and 41.5%, respectively, at concentrations from 0.7 to 9.4 ng/ml and further to 4.0 and 3.0%, respectively, at 90.4 ng/ml. Myocardial efficiency expressed as the percentual ratio of contraction amplitude times frequency to oxygen consumption decreased to 11% at the highest concentration of felodipine. Heart beat frequency decreased simultaneously to 45.6%. The electrocardiographic PQ and QRS intervals increased at the highest concentration to 174 and 111%, respectively, whereas the QT interval decreased to 86.6%. Asystolia occurred in several cases at felodipine concentrations of 90.4 ng/ml. Both myocardial accumulation and disposition pharmacokinetics of the drug showed one-compartment characteristics with half-lives of about 97 min. for both processes. Apparent Vd was about 480 ml/g myocardial tissue, which expresses a very pronounced binding and accumulation of felodipine in the rabbit myocardium in vitro. The findings demonstrate that lower concentrations of felodipine produces coronary vasodilation in the isolated rabbit heart accompanied by a marked negative inotropic effect and a less than proportional reduction in oxygen consumption. The drug seemed to cause direct cardiotoxic effects at higher concentrations.     

Effects of intravenous diltiazem on cardiocirculatory dynamics and cardiac output distribution in conscious spontaneously hypertensive rats

The effects of the calcium channel blocker, diltiazem hydrochloride (DZ), on conscious, resting spontaneously hypertensive rats (SHR) were evaluated and compared with results from parallel studies on Wistar-Kyoto (WKY) controls. DZ was administered as a continuous, cumulative infusion at rates equal to 0.40, 2.00, and 10.00 mg/kg/h (each dose was administered for 15 min). Parallel volume infusion (saline) controls were simultaneously conducted using volume infusion rates identical to those used in DZ studies (0.015, 0.100, and 0.500 ml/min). Three hours prior to study, animals were instrumented under halothane anesthesia for measurement of left ventricular, arterial, and central venous pressures; heart rate and arterial blood gases; and for injection of radioactive microspheres and subsequent determination of cardiac output, regional blood flows, and cardiac output distribution. All data were collected at control (C) before initiation of infusion, and at the end of each 15-min infusion period in each animal. At C and compared with WKY, SHR had increased heart rate (392 vs. 280 beats/min), mean arterial pressure (155 vs. 100 mm Hg), left ventricular peak systolic pressure (200 vs. 132 mm Hg), and systemic vascular resistance (0.3 vs. 0.2 mm Hg/ml/min/kg), and reduced stroke volume (1.8 vs. 2.2 ml/beat/kg); but no difference in cardiac output, left ventricular end diastolic pressure, or central venous pressure was found. At C, SHR tended to have increased blood flow and reduced vascular resistance in the coronary circulation and increased vascular resistance in the cutaneous, renal, bronchial arterial, hepatic arterial, testicular, and cerebral circulations. Infusion of DZ increased cardiac output and stroke volume and decreased heart rate, left ventricular and arterial pressures, and systemic vascular resistance in SHR. Similar changes of substantially smaller magnitude were observed in WKY. DZ increased flow and reduced resistance in the coronary and skeletal muscle circulations of SHR to a greater extent than in WKY. DZ also normalized vascular resistance in previously elevated regions. These results suggest that acute intravenous infusion of DZ at doses ranging between 2 and 5 mg/kg is capable of normalizing cardiovascular hemodynamics and regional blood flow distribution in SHR.     

Effects of intravenous epinine administration on left ventricular systolic performance, coronary hemodynamics, and circulating catecholamines in patients with heart failure.

Twenty-six patients with mild to moderate heart failure were studied to determine the effects of epinine infusion (at a rate producing plasma levels similar to those measured after oral administration of 100 mg of the prodrug ibopamine) on left ventricular (LV) function (14 patients), and coronary flow and circulating catecholamines (12 patients). The only significant hemodynamic change at an infusion rate of 0.5 microgram/kg/min was a 9% (p less than 0.05) decrease in systemic vascular resistance (SVR). At an infusion rate of 1 microgram/kg/min (mean free epinine plasma levels 14.3 +/- 3.7 ng/ml), heart rate (HR), dP/dtmax (1,405 +/- 255 to 1,490 +/- 320 mm Hg, NS), (dP/dt)/DP40, and the relaxation rate remained unchanged, but the ejection fraction (EF) increased from 32 to 38% (p less than 0.001), cardiac output (CO) increased, and SVR decreased by 22% (p less than 0.05). In a separate group of 12 patients, epinine infusion at rates of 0.5-1 microgram/kg/min produced no significant changes in coronary blood flow or myocardial oxygen uptake. At these infusion rates, arterial norepinephrine (NE) and dopamine (DA) levels decreased slightly and arterial and coronary sinus epinephrine increased. In conclusion, epinine, at concentrations similar to those achieved during therapeutic use of ibopamine, had negligible effect on myocardial contractility and relaxation rate in heart failure patients. Cardiac pump function was improved by a decrease in SVR rather than by inotropic stimulation. The data also suggest that these low concentrations of epinine may modulate the sympathetic nervous system, but further studies are needed to determine whether this effect could have clinical significance.     

Vasodilator action of KB-944, a new calcium antagonist

Vasodilator action of diethyl 4-(benzothiazol-2-yl)benzylphosphonate (KB-944) was mainly examined in comparison with papaverine in isolated perfused heart and anesthetized or conscious dogs. In isolated perfused heart, KB-944 (1-30 micrograms/heart i.a.) and diltiazem (1-30 micrograms/heart i.a.) produced a dose-dependent increase in coronary flow, and dose-dependent decrease in the heart rate and the myocardial contractile force. On the other hand, papaverine (3-100 micrograms/heart i.a.) produced a dose-dependent increase in coronary flow and heart rate, and did not practically affect the myocardial contractile force. KB-944 was about 3 times as active as papaverine and diltiazem on the percent increase of coronary flow. In anesthetized dogs, KB-944 (0.03-0.3 mg/kg i.v. or 10 mg/kg i.d.), diltiazem (0.03-0.3 mg/kg i.v. or 10 mg/kg i.d.) and papaverine (0.1-1 mg/kg i.v.) significantly increased the coronary blood flow with hypotension. Simultaneously, KB-944 and diltiazem decreased the heart rate, whereas papaverine increased it. Furthermore, KB-944 and diltiazem selectively increased the coronary blood flow more than the carotid blood flow, though papaverine increased the carotid blood flow more than the coronary blood flow. In case of i.v. route, KB-944 and diltiazem were about 5 times as active as papaverine on the percent increase of coronary blood flow. In case of i.d. route, the effect on coronary blood flow and heart rate induced by KB-944 was quantitatively similar to that induced by diltiazem, although the decrease in blood pressure induced by diltiazem was lesser than that produced by KB-944. In conscious dogs, KB-944 (0.03-0.3 mg/kg i.v. or 10-100 mg/kg p.o.) produced a dose-dependent increase in coronary blood flow and heart rate. In case of i.v. route, this vasodilator activity of KB-944 was 10 times as potent as that of papaverine. Thus, KB-944 is a more potent coronary vasodilator. Furthermore, KB-944 is well absorbed from the intestinal tract, and produces a long-acting increase in the coronary blood flow.     

Prostacyclin inhibits the platelet-dependent effects of platelet-activating factor in the rabbit isolated heart.

In a previous study we showed that platelet-activating factor (PAF) is released in the coronary effluent early after reperfusion of ischemic, isolated rabbit heart. The amounts released were sufficient to induce intracoronary platelet activation and release of secondary mediators, suggesting a relevant contribution of this mediator to the cardiac dysfunction during reperfusion. We examined the modulatory effect of prostaglandin I2 (PGI2) on the cardiac alterations caused by infusion of PAF and autologous platelets in rabbit isolated heart. The intra-coronary infusion of PAF (10 ng-1 microgram) in the presence of autologous platelets induced marked alterations in the electrical and mechanical activities in rabbit heart, characterized by a transient positive inotropic effect (mean +/- SD = 113 +/- 6.1% of the control at 10 ng, 116 +/- 11.6% at 1 microgram), followed by a decrease in coronary flow (76 +/- 6.5 and 57 +/- 8.1%), contractile force (88 +/- 2.5 and 56 +/- 10.6%), and action potential duration (APD, 87 +/- 2.5 and 83 +/- 4.9%), and by conduction arrhythmias (75 and 100% of cases). The infusion of adenosine (1 x 10(-5) M) to increase coronary flow maximally abolished PAF and platelet-dependent reduction in coronary flow (CF) and contractile force, as well as conduction arrhythmias, but not the early transient positive inotropic effect. The alterations induced by platelets and PAF infusion were not affected by treatment of hearts with aspirin (3 x 10(-4) M), indicating that endogenous PGI2 generation did not affect the platelet-dependent response of the rabbit heart to PAF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blockade of angiotensin II type 1 receptors suppressed free radical production and preserved coronary endothelial function in the rabbit heart after myocardial infarction.

The hypothesis that blockade of angiotensin II type 1 (AT1) receptors after myocardial infarction prevents coronary endothelial vasomotor dysfunction by suppressing oxygen free radical production was examined. Rabbits underwent coronary ligation or a sham operation with or without infusion of valsartan, an AT 1 receptor blocker. Two weeks after the operation, the heart was isolated from each rabbit and perfused with buffer in the Langendorff mode, and coronary flow responses to acetylcholine and sodium nitroprusside were assessed. The ratio of heart weight to body weight and the lipid peroxide level in the myocardium were increased by 30 and 50%, respectively, 2 weeks after infarction. The coronary flow response to acetylcholine (10(-8) to 10(-5) M) was reduced by 50% in the hearts with infarction compared with the sham controls, although coronary flow responses to sodium nitroprusside were similar. The coronary flow response to acetylcholine in the hearts with infarction was restored by concurrent infusion of N -2-mercaptopropionyl-glycine, a free radical scavenger. Valsartan (10 mg/kg/d) infused after infarction prevented both ventricular remodeling and elevation of the tissue lipid peroxide level and preserved coronary flow response to acetylcholine. In conclusion, long-term AT1 receptor blockade after infarction protects the coronary arteries from endothelial vasomotor dysfunction through suppression of free radical production.     

Effects of nipradilol, a new beta-adrenoceptor blocking agent with vasodilating properties, on transmural energy metabolism in the underperfused canine heart

Effects of nipradilol on hemodynamics and transmural energy metabolism of underperfused (ischemic) canine hearts were investigated. The ischemic heart was prepared by constricting a tube connecting the circumflex coronary artery with the carotid artery for 10 min so that the perfusion pressure (CPP) was reduced to 30 mmHg. The reduction in CPP resulted in decreases in coronary blood flow (CBF) by 70%, regional myocardial contractile force (MCF) by 30%, myocardial ATP contents by 32% (inner layer)-22% (outer) and creatine phosphate by 75% (inner)-60% (outer). Increases in the left ventricular end diastolic pressure (LVEDP) by 4.8 mmHg, myocardial inorganic phosphate contents by 1.9 times (inner)-1.3 (outer) and lactate by 4.3 times (inner)-2.4 (outer) were also observed. In dogs with normal hearts, an infusion of nipradilol (10 micrograms/kg/min, i.v., for 15 min) decreased CPP by 25%, CBF by 40%, cardiac effort index by 45% and MCF by 30 to 40%, and it slightly increased LVEDP without affecting myocardial high-energy phosphate and lactate levels. In ischemic hearts, nipradilol infusion starting 5 min before ischemia attenuated the ischemia-induced elevation of LVEDP to 1.8 mmHg, and the ischemia-induced changes in high-energy phosphate contents to 1/2 (inner)-1/3 (outer) and changes in lactate to 1/6 (inner)-1/10 (outer). These results indicate that nipradilol improves the ischemic derangement of both transmural energy metabolism and hemodynamics.