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排序方式: 共有1065条查询结果,搜索用时 203 毫秒
1.
A. Tentorio G. Ghilardi A. Pedroncelli R. Benco S. Stroppa S. Adib D. Gianola G. Pagani 《European journal of clinical pharmacology》1989,36(3):311-313
Summary The effect of nifedipine 40 mg·day–1 for 3 months on glucose tolerance, insulin and C-peptide secretion after an oral glucose tolerance test (OGTT), intra-venous glucose tolerance test (IVGTT) and glucagon stimulatory test, has been studied in 8 moderately hypertensive women suffering from non-insulin dependent diabetes mellitus (NIDDM).No significant variation in glucose metabolism was noted after nifedipine treatment, except for a slight improvement in insulin secretion after OGTT at the end of the study. There was an increase in cholesterol as a collateral effect. 相似文献
2.
本文研究硝苯吡啶对慢性肺源性心脏病血液动力学的影响,对21例临床急性发作期慢性肺源性心脏病患者作心肺阻抗微分图检查,其中治疗组9例,对照组13例。结果表明口服常规剂量硝苯吡啶1周与2周末时,患者的肺动脉压、肺血管阻力、平均动脉压及外周血管阻力与治疗前相比,明显下降,氧输送量及心指数于治疗2周末时也明显增加。本文认为常规剂量硝苯吡啶治疗缺氧性肺动脉高压有效,能降低肺动脉压、肺血管阻力,改善心脏功能,一般不会导致体循环低血压及加重低氧血症。 相似文献
3.
Richard V. Jackson A. Jane Jackson Jeffrey E. Grice Rodney D. Vella 《Clinical and experimental pharmacology & physiology》1989,16(4):257-261
1. The present study investigated the effect of prior administration of nifedipine on AVP-induced ACTH release in seven normal volunteers. Three protocols were used: 20 mg oral nifedipine; 0.14 pressor units intramuscular (i.m.) per kg bodyweight aqueous AVP; oral nifedipine plus i.m. AVP 90 min later. Plasma ACTH and cortisol were measured at intervals for 2.5 h during each test. 2. The mean peak plasma ACTH and cortisol levels and the mean peak changes from basal in these levels were significantly lower in the nifedipine/AVP test than in the AVP alone test. The integrated area under the cortisol time curve was significantly lower for the nifedipine/AVP test than that for the AVP test alone. Nifedipine alone caused no changes in ACTH or cortisol. 3. Acute administration of oral nifedipine caused an inhibition of AVP-stimulated ACTH and cortisol release in normal humans. This effect may be due to blockade of plasma membrane calcium channels normally activated during AVP stimulation of pituitary corticotrophs. 相似文献
4.
蔡道 《中国新药与临床杂志》1992,(4)
对慢性阻塞性肺气肿(简称慢阻肺)患者20例(男13例,女7例;年龄53±7a)采用硝苯啶10-15mg,tid,po×2wk,后改为5mg,tid,维持用药,总有效率95%,副作用轻微。另设24例慢阻肺患者(男17例,女7例,年龄52±6a)采用氨茶碱0.1-0.2g,tid,po,×2wk,总有效率71%,其中4例因副作用而停药。2组疗效比较无显著差别。 相似文献
5.
对老年慢性肾功能衰竭264例患者(男148例,女116例;年龄66±7a)用硝苯啶10mg联合覆醛氧化淀粉5-10mg,tid,po。另设相似88例患者(男48例,女40例;年龄66±7a)单服覆醛氧化淀粉与之对照,用法同前。2组均连服16wk。结果:前者有效216例(81.8%),后者有效49例(56%),组间比较P<0.01。2组副作用相似,均可坚持服药。 相似文献
6.
目的 :探讨钙拮抗剂硝苯地平控释片 (商品名 :拜新同 )对原发性高血压 (EH)患者血管内皮功能的影响。方法 :观察34例EH(EH组 )患者用硝苯地平控释片治疗前后的抗氧化能力、白细胞黏附血管壁功能及血管内皮舒张功能等方面的变化 ,并与 2 1例正常对照组对比分析。结果 :硝苯地平控释片治疗前 ,EH组血清可溶性细胞间黏附分子 1(SICAM 1)、丙二醛(MDA)的含量均明显高于对照组 (P <0 .0 1) ;血清超氧化物歧化酶 (SOD)活性、一氧化氮 (NO)及血浆C 型利钠肽 (CNP)的含量均明显降低 (P <0 .0 1) ;硝地平控释片治疗 4周后 ,EH组SICAM 1、MDA的含量均较治疗前明显降低 (P <0 .0 1) ,SOD活性及CNP含量均较治疗前明显升高 (P <0 .0 1) ;硝苯地平控释片降压总有效率 82 .35 %。结论 :硝苯地平控释片在有效降压的同时 ,不仅能抑制白细胞在血管内皮细胞的黏附、增加机体抗氧化能力 ,而且可改善内皮功能障碍 ,因而对EH患者的靶器官具有保护作用。 相似文献
7.
The bioavailability of nifedipine in man is highly variable. This may be partly due to its poor aqueous solubility (5–6 µg/ml over pH 2.2–10.0, as determined in this laboratory). We initiated this study to examine the enhancement of aqueous nifedipine solubility via complexation. A series of substituted aromatic ligands was studied to identify those structural features important for complexation with nifedipine. The studies were performed at 25°C employing the solubility technique, using pH 2.2 or 7.0 buffers at an ionic strength of 0.25 M. The apparent equilibrium complexation constants for the 1:1 and/or 1:2 complexes were determined, where appropriate. A linear free-energy approach was used to relate K
1:1 with Hammett's sigma () and fractional partition coefficient () parameters. The following correlation was obtained: log (K
l:l/K
o = 0.31 + 0.l0 + 0.36 (r
2 = 0.86, P < 0.003, N = 9), where K
o is the complexation constant for phenol. Statistical analyses showed that was more important than in affecting nifedipine complexation. The exact location of this interaction on the nifedipine molecule is undefined at present. 相似文献
8.
9.
TORE K. USKI KARL-ERIK ANDERSSON LENNART BRANDT BENGT LJUNGGREN 《Acta physiologica (Oxford, England)》1984,121(4):369-378
The contractile and relaxant effects of various prostanoids were studied on isolated human pial arteries. Contractions were elicited with the following order of potency: U46619?U44069>PGB2>PGF2a>PGE2?PGD2>PGF1a≥TXB2, indicating that prostanoid-induced contractions probably are mediated by a thromboxane-sensitive receptor. Relaxation of PGF2a-contracted arteries was induced with the order of potency: PGE2> PGE1>PGD2?PGD1. Vessels contrated by K+ were relaxed only by PGE,. Since PGI2 was previously found to be more potent than all the prostanoids tested in the present study, relaxant responses are probably mediated via a PGI2-sensitive receptor. The roles of free extracellular and cellularly bound calcium for the contractile effects of PGF2a and K+ were estimated by incubating the arteries for various times in calcium-free medium containing 10-5 M EGTA. Incubation for 5–10 min abolished K+-induced contractions, whereas after 40 min of incubation PGF2a still induced contractions that reached 70% of control. The PGF2a-induced contraction was biphasic in 8 out of 10 preparations. The second phase could be eliminated by increasing the EGTA-concentration to 10-4 M, as well as by nifedipine pretreatment. In calcium-free, high K+ medium calcium-induced contractions were elicited at lower concentrations in the presence of PGF2a. The results suggest that PGF2a-induced contractions in human pial arteries are relatively independent of free extracellular calcium. PGF2a may promote trans-membrane influx of calcium, as well as release calcium from seemingly superficially located cellular stores. 相似文献
10.
M. B. Murphy M. A. Orchard E. L. Conway S. E. Barrow 《European journal of clinical pharmacology》1985,29(4):413-416
Summary Pre-incubation of human platelets with nifedipine in vitro or treatment of normal volunteers with nifedipine, 30 mg daily for one week, did not alter ADP induced aggregation measured by whole blood aggregometry. 6-oxo-Prostaglandin F1 remained undetectable in plasma following oral administration of nifedipine to normal volunteers. The hypotensive response to intravenous nifedipine administration was similar in spontaneously hypertensive rats pretreated with indomethacin or placebo. These results conflict with previous reports that nifedipine alters platelet aggregation and prostaglandin metabolism. 相似文献