复方辛夷滴鼻液的研制与临床应用

目的：对复方辛夷滴鼻液的工艺和质控标准进行了研究。方法：通过改进工艺,采用提取挥发油和煎煮相结合的方法。结果：该法工艺合理、质量可靠,所制滴鼻液对治疗鼻炎疗效高,有效率达８６．３％。结论：可用该法制备复方辛夷滴鼻液,并应用于临床。     

血液分离胶的制备研究

目的 :对血液分离胶的制备进行研究。方法 :用天然橡胶和特效触变剂等原料制备具有触变性的凝胶 ,研究该凝胶分离血清的较优组成。结果 :血液分离胶的较优组成是天然橡胶 12 .8%、特效触变剂 2 8.0 %和溶剂汽油 5 8.2 %。结论 :所制备的血液分离胶具有制备容易、分离效果好和成本较低等优点。     

升丹制剂对小鼠机械性创面微循环影响的实验研究

目的 通过不同浓度的升压制剂对创面微循环影响来控制其对创面愈合的作用机制。方法 应用彩色病理图文分析系统,分析创面微血管增生数、扩张度及微血栓数。结果 在造模后３天、７天,实验且数值均显著高于对照组。结论 升丹制课题可以和改善创面微循环,减少微血栓,增加创面营养和血供,有利创面愈合。     

黄芪、水蛭、地龙不同配伍治疗缺血性中风实验研究

提出气虚血瘀络阻为缺血性中风的基本病机,而益气活血通络则为基本治法。通过黄芪水蛭地龙、黄芪水蛭、黄芪地龙、水蛭地龙四个配伍组比较,以观察其对急性脑缺血大鼠血浆一氧化氮(NO)、丙二醛(MDA)、血小板聚集性及大鼠在体血栓形成时间的影响。结果表明,黄芪水蛭地龙配伍组在以上诸方面的作用明显优于其他组。     

茯苓多糖颗粒剂的研制及质量检测

以提取的茯苓多糖为主要原料,制成颗粒剂保健品,并拟定质检项目其进行定性、定量检测。工艺简单易行,具有较好的治疗、保健功效。     

钙增敏剂MCI-154对内毒素休克大鼠左心室肌原纤维ATP酶活性的影响

目的　研究钙增敏剂MCI 15 4对内毒素休克大鼠左心室肌原纤维ATP酶活性的影响。方法　利用心室肌原纤维制备 ,测定其在不同钙浓度的激活液中的ATP酶活性。结果　内毒素休克组心肌肌原纤维在不同pCa(-log[Ca2 +] )溶液中的ATP酶活性及最大ATP酶活性均明显低于假休克组 ,ATP酶 pCa曲线向右移位约 0 .35个pCa单位 ,曲线的中位值pCa50 (产生 5 0 %最大ATP酶活性所对应的pCa)明显降低。 5×10 -5mol/L甲腈吡酮对上述异常无明显的纠正作用。内毒素休克大鼠心室肌原纤维经含 1× 10 -5mol/L的MCI 15 4的激活液处理后 ,各pCa点ATP酶活性及最大ATP酶活性均明显增加 ,显著高于内毒素休克组和甲腈吡酮组 ;ATP酶 pCa曲线向左移位约 0 .4个pCa单位 ,pCa50 值增加 ,显著高于内毒素休克组和甲腈吡酮组值 ,与假休克组值无明显差别。结论　内毒素休克后 ,心肌肌原纤维活力下降 ,ATP酶活性降低 ;钙增敏剂MCI 15 4可通过增加心肌收缩蛋白对钙的敏感性而提高心肌肌原纤维活力 ,增加ATP酶活性     

黄参方剂诱导胃癌癌前病变细胞凋亡和影响BCL—2蛋白表达的研究

目的：探讨黄参方剂对胃癌癌前病变细胞凋亡及相关基因表达的影响。方法：将７２例胃癌癌前变患者随机分为２组,治疗组３７例,口服黄参方剂６０ｍｌ／ｄ;对照组３５例,口服维酶素片１２片／天,疗程２月。治疗后胃镜同一部位取材,检测治疗前后细胞凋亡指数和ＢＣＬ－２蛋白的表达。采用原位末端标记法（ＴＵＮＥＬ）检测细胞凋亡,采用免疫组化检测ＢＣＬ－２蛋白的表达。结果：黄参方剂组服药前后细胞凋亡指数分别为（１９．８     

丹参对耳蜗辐射防护作用的实验研究

为探讨内耳辐射损伤的防治,采用丹参作为保护药物,用相同剂量的６０Ｃｏ γ射线照射丹参防护组和单纯放射组豚鼠耳颞部,２ 周后作形态与机能检查。结果发现：丹参防护组耳蜗机能与结构损害较轻,而单纯放射组耳蜗机能明显受损,血管纹和柯替氏器病变严重;复合动作电位（ＣＡＰ） 反应阈和毛细胞损伤率两组比较差异有显著性（ Ｐ ＜ ０ ．０１） 。表明丹参对内耳辐射损伤有保护作用。     

Ischaemia induced alternans of action potential duration in the intact-heart: dependence on coronary flow, preload and cycle length

Clinical and experimental evidence relate action potential duration(APD) alternans to ischaemic heart disease and ventricular arrhythmias.The present investigation was performed to study the quantitativerelationship between APD alternans and the degree ofischaemia,loading conditions and cycle length (CL) in an intact heart. Monophasic action potentials (MAP) were simultaneously recordedby contact electrodes from two left (LV) undone right ventricular(RV) sites in 20 Langendorff-perfused rabbit hearts. The preparationswere subjected to global ischaemia at flow rates ranging from40% of normal flow to complete cessation of flow. Pacing wasperformed at either constant or regularly changing CL. The magnitudeof APD alternans was expressed as beat-to-beat differences inaction potential duration of two consecutive MAPs. During normalper fusion, neither very fast pacing at a CL of 200 ms nor periodicalrate switches resulted in persistent APD alternans. Pacing ata constant CL of 800 ms did not induce A PD alternans at completecessation of flow for 6 min. However, alternans developed progressivelyat a constant CL of 400 ms after 2.8±0.3 min of completeischaemia at the pre-loaded LV, andafter 4.6±0.4 minat the unloaded RV (P<0.01). The reduction of preload atthe LV from 15 to 5 mmftg end-diastolic pressure delayed developmentof APD alternans from 2.8±0.3 min to 4.3±0.4 min(P < 0.05) at 400 ms CL. Following graded under per fusionof 40%, 20% and 10% of initial flow, persistent APD alternansdeveloped in relation to the degree of flow reduction and increasedprogressively with duration ofischaemia. APD alternans at theLV always preceded the onset of APD alternans at the RV. Inexperiments with identical flow rates the shortest CL of 200ms resulted in the greatest and earliest initiation of APD alternanscompared to the longer CL (P<0.01, P<0.001). An increasein CL from 400 to 800 ms immediately abolished APD alternans,generated by the shorter CL, at any time during the 6 min periodof complete ischaemia. Similarly, increasing the cycle lengthfrom 200 or 400 to 600 ms eliminated APD alternans up to 6 minof ischaemia and significantly reduced its magnitude between7 and 10 min within a few beats. We conclude that persistent APD alternans is a characteristicfinding in the rabbit heart during global ischaemia. It is asensitive parameter of the severity of ischaemia and dependson the degree and duration of ischaemia as well as on the preload.The CL appears to have an independent effect on the generationof APD alternans, which is functionally separate from the effectof CL on the ischaemic burden. An eventual impact of these observationscould be the application of APD alternans as a diagnostic toolin electrophysiological examinations of myocardial ischaemiain experimental and clinical settings.     

Effects of adenosine on electrical activity of isolated guinea pig hearts

Summary Negative chronotropic and dromotropic effects of adenosine seem to be responsible for its antiarrhythmic action on supraventricular tachyarrhythmias. To further characterize the effects of adenosine on supraventricular arrhythmias heart rate, conduction, refractoriness, the time to steady-state of AV-nodal conduction slowing and of sinus rate reduction were evaluated.Changes of heart rate, conduction intervals and effective refractory periods were determined by the use of a high-resolution ECG recording technique in isolated guinea pig hearts perfused by the method of Langendorff.Adenosine in concentrations of 3 and 10 M reduced sinus rate and prolonged AV-nodal conduction significantly, while intraventricular and His bundle conduction were not altered. The maximal effect of adenosine on the sinus node and AV nodal conduction occurred after 636±109 and 111±35 (mean±SE) beats, respectively.During programmed stimulation at a cycle length of 250 ms, adenosine reduced atrial ERP in a dose-dependent manner. At cycle lengths of 170 and 200 ms, adenosine increased the atrial ERP at 3 M, and then progressively shortened the ERP at higher doses. At all adenosine concentrations used, the usual rate-dependent adaption in ERP was suppressed.These observations explain the efficacy of adenosine against supraventricular tachyarrhythmias where the AV-node forms a part of a reentrant circuit. Adenosine shortened the atrial ERP, but at high pacing rates also led to a relative prolongation of the atrial ERP as the rate-dependent adaption was suppressed. These opposite effects of adenosine may explain earlier contradictory findings of its action on atrial arrhythmias.