野荆芥花挥发油化学成分分析

目的 研究采自河北承德地区的野荆芥(Elsholtzia stauntonii Benth)花挥发油化学成分。方法 采用GC-MS技术和NIST质谱库对野荆芥花挥发油的化学成分进行分析和鉴定,用色谱峰面积归一化法计算各成分的相对含量。结果 从该植物挥发油中分离出40个成分,鉴定了以4-异丙基-苯甲醇(48.32%),2-甲基-5-戊酮(3)基-呋喃(22.87%),2-甲基-5-异戊酮基-呋喃(6.40%),β-石竹烯(3.00%),2-乙基-5-异丁酮基-呋喃(3.56%),氧化-β-石竹烯(3.46%)等为主的36个成分。结论 这些成分为首次从该植物花挥发油中所发现。     

朝鲜苍术挥发油成分GC—MS分析

目的研究朝鲜苍术挥发油成分,为朝鲜苍术的药用价值及合理开发利用提供参考。方法采用水蒸气蒸馏法提取挥发油,GC毛细管柱色谱法进行分析,峰面积归-化法确定其相对含量,气相色谱-质谱联用技术辅助人工检索鉴定其化学成分。结果从朝鲜苍术的挥发油中分离出58种,鉴定出55种化学成分,鉴定出的挥发性化学成分占挥发油总量的79．94％,主要成分有苍术酮（31．1831％）、3-羟基-6β-环丙烷-5β-胆甾烷（12．3086％）、5α-螺甾烷（11．2161％）、巴伦西亚橘烯（7．05606％）、γ-榄香烯（4．24732％）、菜油甾醇（2．11089％）、石竹烯（1．44473％）、β-桉叶烯（1．43541％）、9,10-脱水-异长叶烯（1．21445％）、α-石竹烯（0．72132％）。结论朝鲜苍术挥发油的主要化学成分为倍半萜类化合物。     

浙产连钱草挥发油化学成分的分析

目的研究浙产连钱草挥发油的化学成分。方法水蒸气蒸馏法提取挥发油,应用气相色谱-质谱联用法（GC-MS）进行定性分析,按峰面积归一化法,求出挥发油中化学成分的百分含量。结果挥发油鉴定出33个化合物,主要成分为石竹烯及其氧化物（25．14％）、早熟素Ⅰ和Ⅱ（12．58％）、喇叭烯（10．6％）、异松蒎酮（10．5％）、β-荜澄茄油烯（6．34％）,且油中含有一定量的反式斯巴醇（4．53％）、γ-榄香烯（4．68％）、β-榄香烯（1．45％）和D-柠檬烯（0．39％）。结论浙产连钱草挥发油舍有丰富的药用活性成分。     

阿尔泰狗哇花挥发油的气相色谱-质谱联用分析

目的分析植物阿尔泰狗哇花的精油成分。方法采用常规水蒸气蒸馏法提取精油，运用气相色谱质谱联用（GC-MS）对其成分进行分析，用气相色谱面积归一化法测定计算了各成分的相对百分含量。结果经GC-MS分析共分离出54个峰，鉴定出38种化合物，占总峰面积的91.7％。主成分为单萜和倍半萜，占挥发油检出成分的73．6％，其中含量较大的成分有大根香叶烯（20．1％）、石竹烯（7．29％）、1，1，4，7-四甲基-八氢化-1氢-环丙基工薁（7．18％）、β-蒎烯（5．40％）、β-水芹烯（3．77％）、苎烯（3．02％）。另外还含有乙酸乙酯（7．62％）、甲酸乙酯（3．65％）、斯巴醇（3．42％）等成分。结论阿尔泰狗哇花精油中含有多种药理活性成分，有综合开发利用的价值。     

伸筋草挥发油成分的固相微萃取分析

目的：分析伸筋草中挥发油化学成分。方法：采用固相微萃取气相色谱-质谱联用法分析挥发油化学成分。结果：共分离出98个组分，鉴定了81个组分，用归一化法测定其百分含量，占总挥发油组分峰面积的97．80％。结论：主要成分是癸酸（10．63％）、β-马榄烯（6．60G）、反-石竹烯（7．29％）、白菖蒲油烯（23．77％）、旷古芸烯（3．38％）、α-姜黄烯（1．38％）、α-蛇床烯（1．67％）、δ-杜松烯（2．16％）、α-雪松醇（15．50％）等组分。     

橘叶挥发油化学成分的气相色谱-质谱分析

目的:分析橘叶挥发油的化学成分。方法:采用水蒸汽蒸馏法提取橘叶挥发油,用气相色谱-质谱(GC/MS)联用法分析鉴定其化学成分,并应用面积归一法测定各成分的相对百分含量。结果:从橘叶挥发油中分离出50种化学组分,鉴定了其中34种,占总油量的83%。结论:橘叶挥发油中主要成分为β-榄香烯(19.96%)、石竹烯(10.27%)、石竹烯氧化物(8.78%)、[1R-(1a,3aβ,4a,7β)]-1,2,3,3a,4,5,6,7-八氢-1,4-二甲基-7-(1-甲基乙烯基)-薁(6.97%)、邻伞花烃(6.27%)等。     

石菖蒲不同提取物化学成分的GC—MS分析

本文用气相色谱-质谱（GC-MS）方法分析了石草蒲不同提取物（挥发油、水提液、去油水提液）的化学成分,结果表明：石菖蒲挥发油中除β-细辛醚相对含量高外,相对含量较高的成分还有α-细辛醚,顺式甲基异丁香酚,榄香素（烯）,反式甲基异丁香酚,菖蒲二烯,石竹烯,柏木烯等,水提液中检出了石菖蒲挥发油的3个主要成分,几乎未检出α-细辛醚;去油水煎液中发现一特征成分,由于现有的谱库中未能检索到,故未能鉴定,研究结果为进一步开发石菖蒲提供依据。     

GC-MS测定白背叶中的挥发油

目的 分析白背叶挥发油的化学成分并用归一化法测定各成分的质量分数.方法 采用水蒸气蒸馏法提取白背叶中的挥发油.用GC-MS法鉴定其化学成分.结果 共鉴定了41个成分,占挥发油总成分的90%以上.结论 白背叶挥发油的主成分为橙花叔醇、1,6-辛二烯-3-醇、冰片基胺、己二酸二异辛酯和2,7-二甲基-1,6-辛二烯.     

甘肃产独活及牛尾独活挥发油成分的气-质联用分析

目的分析甘肃产独活Angelica pubescens Maxim．f.biserr-ata Shan et Yuan及牛尾独活Heraeleum moellendoffii Hance的挥发油成分。方法采用GC—MS方法分离和鉴定挥发油成分，并用面积归一化法进行定量分析。结果从独活挥发油中分离出55个化合物，占挥发油总量的94．196％；从牛尾独活挥发油中分离鉴定鉴定出47个化合物，占挥发油总量的81．657％。结论独活挥发油主要成分为α-蒎烯(20．295％)、1-甲基4-异丙基苯(15．568％)、3-甲基-壬烷(5．904％)等；牛尾独活挥发油主要成分为β-蒎烯(24．321％)、α-蒎烯(8．167％)、1-甲基4-异丙烯基-环己烯(8．061％)等。     

气质联用分析铁筷子的挥发油成分

目的研究铁筷子挥发油的化学成分组成,为铁筷子的开发利用提供理论依据。方法水蒸气蒸馏法提取挥发油,气相色谱-质谱联用技术（GC—MS）对挥发油成分进行分离鉴定,并采用面积归一化法确定各成分的相对百分含量。结果共鉴定出30个成分,占挥发油总量的94．24％,其中相对含量较高的有桉树脑（33．67％）、龙脑（13．98％）、氧化石竹烯（10．15％）、莰烯（9．83％）。结论本法简便、快速、灵敏度高,分离度好,是分析铁筷子挥发油成分的有效手段。     

Mechanisms underlying diabetes enhancement of endothelin-1-induced contraction in rabbit basilar artery

The influence of alloxan-induced diabetes on the reactivity of rabbit basilar artery to endothelin-1 was examined. Endothelin-1 induced concentration-dependent contraction of basilar arteries that was higher in diabetic than in control rabbits. Endothelium removal produced a higher enhancement of the endothelin-1-induced contraction in control than in diabetic rabbits. N(G)-nitro-L-arginine (L-NOArg) enhanced the maximal contraction induced by endothelin-1 in control rabbits and potentiated this response in diabetic rabbits. Endothelin ETA receptor antagonist, cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123), inhibited endothelin-1-induced contraction in both rabbit groups. Endothelin ETB receptor antagonist, 2,6-Dimethylpiperidinecarbonyl-gamma-Methyl-Leu-Nin-(Methoxycarbonyl)-D-Trp-D-Nle (BQ-788), enhanced endothelin-1-induced contraction in control rabbits and decreased the potency of endothelin-1 in diabetic rabbits. Sodium nitroprusside-induced relaxation of basilar arteries was lower in diabetic than in control rabbits. These results suggest that mechanisms underlying rabbit basilar artery hyperreactivity to endothelin-1 include decreased endothelial modulation of endothelin-1-induced contraction, with impaired endothelial endothelin ETB receptor activity; decreased sensitivity to nitric oxide (NO) in vascular smooth muscle; and enhanced participation of muscular endothelin ETA and ETB receptors.     

Effects of HR780, a novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, in Watanabe heritable hyperlipidemic rabbits and cholesterol-fed rabbits

The aim of this study was to evaluate the effects of (+)-(E)-6S-(2-(4-(4-fluorophenyl)-2-(1-methylethyl)-6-phenylpyridin-3-yl)ethenyl)-4R-hydroxy-3,4,5,6-tetrahydro-2H-pyran-2-one (HR780), a novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on hypercholesterolemia in Watanabe heritable hyperlipidemic (WHHL) rabbits and rabbits fed a diet with 1% cholesterol, in comparison with the effects of simvastatin. Each drug was administered orally to WHHL rabbits for 24 weeks and to 1% cholesterol-fed rabbits for 10 weeks. In WHHL rabbits, HR780 at doses of 1, 2.5 and 5 mg/kg/day reduced the plasma total cholesterol level by 15, 24 and 20%, respectively. In contrast, simvastatin at 5 mg/kg/day lowered the level by 23%. In 1% cholesterol-fed rabbits, HR780 (1 and 2.5 mg/kg/day) was found to inhibit the increases in the plasma total cholesterol and phospholipid levels and liver cholesterol contents in a dose-dependent manner. Simvastatin (5 mg/kg/day) also inhibited their increase. Neither HR780 nor simvastatin increased the contents of cholesterol and total bile acid in the gallbladder bile. In conclusion, long-term treatment with HR780 reduced the plasma cholesterol level in WHHL rabbits and 1% cholesterol-fed rabbits, and decreased the liver cholesterol contents in 1% cholesterol-fed rabbits.     

Pharmacokinetics of paclitaxel in rabbits with carbon tetrachloride-induced hepatic failure

The pharmacokinetic of paclitaxel (1 mg/kg, i.v.) was investigated in rabbits with carbon tetrachloride-induced hepatic failure. The area under the plasma concentration-time curve (AUC) of paclitaxel was significantly (p<0.01) increased in severe carbon tetrachloride-induced hepatic failure rabbits (1,364.54 +/- 382.07 ng/ml x hr) compared to that of normal rabbits (567.52 +/- 141.88 ng/ml x hr), but not significantly in moderate carbon tetrachloride-induced hepatic failure rabbits (803.1 +/- 208.81 ng/ml x hr). The volume of distribution (Vd) (6.25 +/- 1.56 L) and the elimination rate constant(beta) (0.09 +/- 0.025 hr(-1)) of paclitaxel in severe carbon tetrachloride-induced hepatic failure rabbits were significantly (p<0.05) decreased compared to those of normal rabbits (11.65 +/- 2.91 L, 0.12 +/- 0.030 hr(-1)), but not significantly in moderate carbon tetrachloride-induced hepatic failure rabbits (9.46 +/- 2.37 L, 0.10 +/- 0.026 hr'). Total body clearance (CLt) of paclitaxel in severe carbon tetrachloride-induced hepatic failure rabbits (0.733 +/- 0.183 L/hr/kg) was significantly (p<0.01) decreased compared to that of normal rabbits (1.762 +/- 0.440 L/hr/kg), but not significantly in moderate carbon tetrachloride-induced hepatic failure rabbits (1.245 +/- 0.311 L/hr/kg). The half-life(t 1/2) of paclitaxel in severe carbon tetrachloride-induced hepatic failure rabbits (7.71 +/- 2.16 hr) was significantly (p<0.05) increased compared to that of normal rabbits (5.75 +/- 1.44 hr), but not significantly in moderate carbon tetrachloride-induced hepatic failure rabbits (6.77 +/- 1.76 hr). This results could be due to inhibition of paclitaxel metabolism in liver disorder rabbits since paclitaxel is essentially metabolized in liver. The findings suggest that the dosage regimen of paclitaxel should be adjusted when the drug would be administered in patients with liver disorder in a clinical situation.     

Characterization of adenosine receptors involved in adenosine-induced bronchoconstriction in allergic rabbits.

1. Recent work has suggested that adenosine may be involved in asthma via the activation of A1 receptors. However, the role of the recently cloned A3 receptor in airways is largely unknown. In the present study, we have investigated the role of the A3 receptor in adenosine-induced bronchoconstriction in allergic rabbits. 2. Aerosol challenge of antigen (Ag) immunized rabbits with the adenosine precursor, adenosine 5'-monophosphate (AMP), resulted in a dose-dependent fall in dynamic compliance (Cdyn). The maximum fall in Cdyn in these rabbits was significantly greater than that in litter matched, sham immunized animals (P < 0.05). However, there was no significant difference in the maximum increase in airways resistance (Rt) between Ag and sham immunized rabbits (P > 0.05). 3. Aerosol challenge of Ag immunized rabbits with cyclopentyl-adenosine (CPA) (A1-receptor agonist) elicited a dose-dependent fall in Cdyn in Ag immunized rabbits and the maximum fall in Cdyn in these rabbits was significantly greater than that observed in sham immunized rabbits (P < 0.05). Similarly, CPA induced dose-dependent increases in R1 in Ag immunized rabbits whereas sham immunized rabbits failed to respond to CPA within the same dose range. The maximum increase in RL in Ag immunized rabbits was significantly greater than that of sham immunized rabbits (P < 0.05). 4. Aerosol challenge of either Ag or sham immunized rabbits with the A3 agonist aminophenylethyladenosine (APNEA) did not elicit dose-dependent changes in either RL or Cdyn. Moreover, there was no significant difference in the maximum response, measured by either parameter, between the two animal groups (P > 0.05). 5. These data provide further evidence for a role of the A1 receptor in the airways, but do not support a role for the A3 receptor in adenosine-induced bronchoconstriction in the allergic rabbit.     

Lack of involvement of alpha-adrenoceptors in sympathetic neural vasoconstriction in the hindquarters of the rabbit.

The hypothesis that sympathetic nerves in arterial blood vessels activate excitatory receptors distinct from alpha-adrenoceptors was investigated in vivo in the rabbit. In anaesthetized, ganglion-blocked rabbits, graded stimulation of the lumbar sympathetic nerve chains caused graded hind limb vasoconstriction. The responses to single pulses and short trains of stimuli were unaffected by benextramine (10 mg kg-1) and the longer trains were enhanced. Phenoxybenzamine (5 mg kg-1) slightly reduced the responses to short trains of stimuli and did not affect the responses to long trains. The dose-response curve to intra-arterial noradrenaline (after beta-adrenoceptor blockade) was shifted rightwards about ten fold by benextramine (10 mg kg-1) and by phenoxybenzamine (5 mg kg-1). In conscious rabbits the vasoconstriction caused by the nasopharyngeal reflex initiated by smoke inhalation was unaffected by benextramine (10 mg kg-1). Small mesenteric arteries (less than 250 microns) taken from untreated rabbits responded to noradrenaline with a threshold concentration of about 1 microM. Similar tissues from benextramine (10 mg kg-1)-treated rabbits were unresponsive to noradrenaline at concentrations up to 300 microM. However, these tissues were able to respond to potassium and angiotensin II. Aortic ring segments taken from the same rabbits were only about ten fold less sensitive to noradrenaline than segments from control rabbits. These results are in accord with the hypothesis that sympathetic nerves activate non-alpha-receptors in the vasculature of the rabbit.     

The vasoconstrictor effects of L-NAME, a nitric oxide synthase inhibitor, in pregnant rabbits.

1. We have used anaesthetized, acutely instrumented non-pregnant (NP) and late pregnant (P) New Zealand white rabbits to examine the possible role of nitric oxide (NO) in the pregnancy-induced fall of vascular tone and arterial pressure. Systemic, renal and pulmonary vascular resistance, as well as plasma concentrations of cyclic GMP (PcGMP) were compared before and after the inhibition of NO synthesis by N(G)-nitro-L-arginine methyl ester (L-NAME). 2. P rabbits had lower baseline total peripheral resistance (TPR), mean arterial pressure (MAP) and higher PcGMP than NP controls (all P < 0.05 or less). L-NAME (1, 10, 50 mg kg1, i.v.) resulted in dose-dependent elevation of TPR in both groups. However, the absolute, as well as percentage increases in TPR were greater (P < 0.05) in NP than in P rabbits. 3. Cardiac output (CO) was reduced more (P < 0.01) by NO inhibition in NP than P rabbits. Therefore, despite the smaller increase in TPR, the elevation of MAP was greater (P < 0.001) in P than NP rabbits. After L-NAME, NP rabbits developed more severe bradycardia and a greater increase of pulmonary vascular resistance which might have contributed to the more pronounced reduction of CO. 4. PcGMP increased in both groups following L-NAME, but more (P < 0.01) in NP than P rabbits. 5. Infusion of acetylcholine (ACh, 0.02 micromol l-1 kg-1) reduced MAP and TPR more (both P < 0.05) in NP than P rabbits and L-NAME reduced the ACh-induced depressor response only in NP rabbits. 6. These results suggest that the low vascular tone and arterial pressure in pregnant rabbits is not mediated by NO.     

Pharmacokinetics of tolbutamide after oral administration to rabbits with folate-lnduced renal failure

The pharmacokinetic of tolbutamide was studied after the oral administration to normal rabbits or rabbits with mild to medium folate-induced renal failure. The plasma concentrations of tolbutamide were significantly elevated (p<0.05) during 9 to 24 h in rabbits with mild or medium folate-induced renal failure. Consequently, the area under the plasma concentration-time curves (AUC) was significantly higher in mild (p<0.05) and medium (p<0.01) folate-induced renal failure rabbits (i.e., 2906 microg/mL x h for mild renal failure and 4074 microg/mL x h for moderate renal failure) than that in normal rabbits (i.e., 2295 microg/mL x h). The cumulative urinary excretion of tolbutamide was significantly depressed (p<0.05) in medium folate-induced renal failure rabbits (i.e., 3.3 mg) compared with that in normal rabbits (i.e., 5.9 mg). The elimination rate constant (Kel) of tolbutamide was significantly decreased in medium renal failure rabbits (i.e., 0.027 h(-1)) than that in normal rabbits (i.e., 0.044 h(-1)); As a result, the terminal half-life of tolbutamide in medium folate-induced renal failure rabbits (i.e., 25.5 h) was significantly longer (p<0.01) than that in normal rabbits (i.e., 15.7 h). The change in pharmacokinetic parameters is consistent with the hypothesis that the alteration is mediated by the depressed metabolic elimination of the drug by the induction of renal failure. Therefore, these observations indicated that the dosage adjustment may be necessary for tolbutamide in patients with renal insufficiency.     

乙醇对家兔抗利尿激素分泌的影响

目的观察乙醇对家兔抗利尿激素(antidiuretic hormone,ADH)和尿量的影响。方法将20只雄性家兔随机分为乙醇组和生理盐水组,经耳缘静脉注射50%乙醇(1.0 ml.kg-1)和等量的生理盐水,每隔20 min注射1次,直至家兔死亡。经心脏采取第1次给药20 min后两组家兔的血清,ELISA法测定ADH的含量;记录随乙醇累积浓度增加时的尿量变化,并计算静脉注射乙醇对家兔的致死剂量。结果与生理盐水组相比,乙醇1.0 ml.kg-1可明显减少血清ADH含量并增加尿量(P<0.05);当乙醇累积浓度为3.0 ml.kg-1时尿量明显减少甚至无尿(P<0.05);经静脉注射乙醇对家兔的致死剂量为(8.77±1.02)ml.kg-1。结论乙醇浓度为1.0 ml.kg-1时可抑制家兔ADH的分泌,使尿量增加;但随乙醇累积浓度增加后尿量减少甚至无尿。     

Contribution of endothelin receptors and cyclooxygenase-derivatives to the altered response of the rabbit renal artery to endothelin-1 in diabetes

The influence of diabetes on regulatory mechanisms and specific receptors implicated in the response of isolated rabbit renal artery to endothelin-1 was examined. Endothelin-1 induced a concentration-dependent contraction that was less potent in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal or N(G)-nitro-L-arginine (L-NOARG) enhanced contractions to endothelin-1 either in control and diabetic arteries. Indomethacin inhibited endothelin-1-induced response in control arteries, but enhanced it in diabetic arteries. In contrast to that observed in rubbed and in L-NOARG treated arteries, in the presence of indomethacin the contractile action of endothelin-1 was higher in diabetic arteries than in control arteries. Nimesulide enhanced endothelin-1 contractions both in control and diabetic arteries. Cyclo-(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123, endothelin ET(A) receptor antagonist), attenuated endothelin-1 vasoconstriction in control rabbits, while vasoconstriction resulted increased in diabetic rabbits. 2,6-Dimethylpiperidinecarbonyl-gamma-Methyl-Leu-N(in)-(Methoxycarbonyl)-D-Trp-D-Nle (BQ-788, endothelin ET(B) receptor antagonist), enhanced the contractile response in control rabbit arteries without modifying this response in diabetic rabbits. In summary, diabetes decreases the sensitivity of the rabbit renal artery to endothelin-1 by decreasing the ratio between vasoconstrictor and vasodilator prostanoids released after activation of endothelin ET(A) receptors.     

气道滴入肺表面活性物质和吸入一氧化氮治疗经气道肺泡灌洗诱发 …

目的：比较单独或联合应用气道滴入肺表面活性物质（Ｓｕｒｆ）和吸入一氧化氮（ｉＮＯ）对急性呼吸窘迫综合征的疗效。方法：成年兔反复气道生理盐水灌洗,去除内源Ｓｕｒｆ,经机械通气诱发急性肺损伤和呼吸衰竭,随机分组给予：ｉＮＯ０．８μｍｏｌ．Ｌ＾－１;Ｓｕｒｆ磷脂１００ｍｇ．ｋｇ＾－１;联合应用ｉＮＯ和Ｓｕｒｆ;或不约药对通气８小时生存率以联合治疗组为最高,Ｓｕｒｆ组及联合治疗组的氧合指数（ＯＩ）、肺顺应