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11.
盐酸戊乙奎醚用于全麻术前减少腺体分泌的研究 总被引:16,自引:1,他引:15
目的评价盐酸戊乙奎醚作为全麻术前用药减少腺体分泌的有效性与安全性。方法本研究采用多中心随机双盲平行对照观察。298例全麻病人随机分为三组,术前分别肌肉注射阿托品、盐酸戊乙奎醚或注射用水,测定注射后30min唾液分泌量。用视觉模拟评分(VAS)方法测定口干程度,记录不良反应。结果给药后30min,阿托品、盐酸戊乙奎醚和注射用水组唾液分泌量分别较给药前变化(-17·64±19·53)、(-22·30±21·04)和(2·71±19·46)mg。VAS阿托品、盐酸戊乙奎醚组用药后明显增加。给药后30min,阿托品、盐酸戊乙奎醚和注射用水组HR分别较给药前变化(1·65±8·82)、(-4·30±7·01)和(-0·54±6·49)次/分。观察期间无严重不良反应。结论盐酸戊乙奎醚作为全麻术前用药,可明显减少唾液分泌,无HR增快,无明显不良反应。 相似文献
12.
目的 观察异丙酚静脉全麻用于无痛人流时术前应用不同抗胆碱药对麻醉过程中某些不良事件发生的影响.方法 150例年龄18~34岁、体重42~70kg、ASA Ⅰ级拟接受无痛人流手术的病人随机分成三组,每组50例.阿托品组病人麻醉前30min肌注阿托品0.5mg,东莨菪碱组病人麻醉前30min肌注东莨菪碱0.3mg,对照组生理盐水组病人麻醉前30min肌注生理盐水1ml.每例病人麻醉时静脉注射异丙酚2.5mg/kg,手术后根据病人身体对手术刺激的反应情况必要时追加药物,每次3ml直至病人手术时安静不动.观察每例病人麻醉过程中有无流涎过多、心动过缓和苏醒期躁动等不良事件的发生.结果 阿托品组、东莨菪碱组和生理盐水组病人流涎过多发生率分别为2.0%、2.0%和16.0%;心动过缓发生率分别为4.0%、2.0%和6.0%;苏醒期躁动发生率分别为6.0%、4.0%和4.0%.阿托品组和东莨菪碱组病人流涎过多的发生都明显少于生理盐水组(P<0.05),而阿托品组和东莨菪碱组之间相比流涎过多的发生没有显著性差异(P>0.05);分别就心动过缓和苏醒期躁动的发生来说,三组中的任意两组相比都没有显著性差异(P>0.05).结论 术前肌注阿托品0.5mg或东莨菪碱0.3mg都能明显地降低异丙酚静脉全麻用于无病人流时病人流涎过多不良事件的发生,但两者都不能降低心动过缓和苏醒期躁动不良事件的发生. 相似文献
13.
The ability of the nerve agents tabun, sarin, soman, GF, VR, and VX to produce brain seizures and the effectiveness of the
anticholinergics biperiden HCl or atropine SO4 as an anticonvulsant treatment were studied in a guinea-pig model. All animals were implanted a week prior to the experiment
with cortical electrodes for electroencephalogram (EEG) recordings. On the day of exposure, the animals were pretreated with
pyridostigmine (0.026 mg/kg, i.m.) 30 min prior to challenge with a 2 × LD50 dose (s.c.) of a given agent. In separate experiments, animals were challenged with 5 × LD50 (sc) of soman. One minute after agent challenge, the animals were treated intramuscularly (i.m.) with 2 mg/kg atropine SO4 admixed with 25 mg/kg 2-PAM Cl and then observed for the onset of seizure activity. Five minutes after the start of nerve
agent-induced EEG seizures, animals were treated i.m. with different doses of biperiden HCl or atropine SO4 and observed for seizure termination. The anticonvulsant ED50 of biperiden HCl and atropine SO4 for termination of seizures induced by each nerve agent was calculated and compared. With equally toxic doses (2 × LD50) of these agents, continuous EEG seizures (status epilepticus) developed in all animals challenged with soman, tabun, or
VR, and in more than 90% of the animals challenged with GF or sarin. In contrast, only 50% of the animals developed seizures
when challenged with VX. The times to onset of seizures for soman, tabun, GF, and sarin were very similar (5–8 min) while
for VR, it was about 10 min. In the case of VX, not only was the time to seizure development longer (20.7 min), but the seizure
activity in 19% of the animals terminated spontaneously within 5 min after onset and did not return. Under these conditions,
the anticonvulsant ED50s of biperiden HCl for soman, GF, VR, tabun, sarin, and VX were 0.57, 0.51, 0.41, 0.2, 0.1, and 0.09 mg/kg, respectively,
while those of atropine SO4 for soman, VR, tabun, GF, sarin, and VX were 12.2, 11.9, 10.4, 10.3, 5.1, and 4.1 mg/kg, respectively. In separate experiments,
the anticonvulsant ED50 doses of biperiden for animals challenged with 2 or 5 × LD50 of soman were 0.48 (95% confidence limits 0.25–0.73) or 0.57 (95% CI 0.38–0.84) mg/kg, respectively, while the anticonvulsant
ED50s for atropine (12.2 mg/kg, i.m.) were identical under these same two challenge conditions. The present study demonstrates
that all nerve agents can produce status epilepticus and that the therapeutic effectiveness of atropine and biperiden roughly
paralleled the seizurogenic potential of these agents.
Received: 16 November 1999 / Accepted: 9 February 2000 相似文献
14.
Penequine hydrochloride (Ⅰ) is a new potent anticholinergic drug, the degradation mechanism of Ⅰ in aqueous solutions is reported in this paper. Ⅰ is an ethereal compound, stable in neutral and alkaline solutions, but it decomposes in strong acidic solutions. Its main degradation products have been separated and identified by means of TLC, MS, GC/MS and GC/FTIR. With reference to the general degradation rule of ethereal compound and the structure of the degradation products, we deduced that the ether linkage of Ⅰ splits in acidic solutions by the catalysis of hydrogen ion, producing 3- quinuclidinol (DP1) and 1-phenyl- 1-cyclopentyl glycol. The latter turns into 1-phenyl-l-cyclopentyl acetaldehyde through dehydration and rearrangement. In addition, small amounts of other degradation compounds, e. g. benzaldehyde, acetophenone, phenylcyclopentyl ketone, etc. have also been found, but the mechanism remains to be further studied. 相似文献
15.
16.
Hiroko Uemura Yukio Hara Masayuki Endou Katsumi Mori Haruaki Nakaya 《Naunyn-Schmiedeberg's archives of pharmacology》1995,353(1):73-79
We have recently reported that class III antiarrhythmic drugs inhibit the muscarinic acetylcholine (ACh) receptor-operated K+ current (I
K, ACh) in guinea-pig atrial cells by different molecular mechanisms. The data obtained from the patch-clamp study suggest that d,l-sotalol inhibits I
K, ACh by blocking the muscarinic receptors, whereas MS-551 inhibits the K+ current by blocking the muscarinic receptors and depressing the function of the K+ channel itself and/or the guanine nucleotide-binding protein (G protein). This study was undertaken to determine whether the class III antiarrhythmic drugs d,l-sotalol and MS-551 interact with the muscarinic receptors of cardiac and peripheral tissues. Both drugs inhibited concentration dependently the specific [3H]N-methylscopolamine ([3H]-NMS) binding to membrane preparations obtained from guinea-pig atria and submandibular glands. The competition curves of these drugs for [3H]-NMS binding to glandular membranes were monophasic, suggesting competition with [3H]-NMS at a single site. Although the competition curve of d,l-sotalol for [3H]-NMS binding to atrial membranes was monophasic, that of MS-551 was biphasic and showed high- and low-affinity states of binding. d,l-Sotalol showed slightly, but significantly, higher affinity for cardiac-type muscarinic receptors (M2) than for glandular-type muscarinic receptors (M3). The inhibition constant (K
i) for MS-551 in glandular membranes was also slightly greater than the high-affinity K
i value for the drug in atrial membranes. In guinea-pig left atria and ilea, d,l-sotalol shifted the concentration-response curves for the negative inotropic effect and the contracting effect of carbachol in a parallel manner. The slopes of Schild plot were not significantly different from unity, suggesting competitive antagonism, and the pA2 for d,l-sotalol in left atria was slightly greater than that in ilea. MS-551 also shifted the concentration response curve for the negative inotropic effect of carbachol in atrial preparations to a greater extent than that for the contracting effect in ileal preparations, although MS-551 failed to show a pure competitive antagonism. These results suggest that both d,l-sotalol and MS-551 interact with cardiac M2 and peripheral M3 receptors, and that at high concentrations they exert anticholinergic activity in cardiac and peripheral tissues. 相似文献
17.
Mechanisms underlying the antispasmodic and bronchodilatory properties of Terminalia bellerica fruit
AIM OF THE STUDY: The present investigation was carried out to provide the pharmacological basis for the medicinal use of Terminalia bellerica in hyperactive gastrointestinal and respiratory disorders. MATERIALS AND METHODS: Crude extract of Terminalia bellerica fruit (Tb.Cr) was studied in in vitro and in vivo. RESULTS: Tb.Cr caused relaxation of spontaneous contractions in isolated rabbit jejunum at 0.1-3.0mg/mL. Tb.Cr inhibited the carbachol (CCh, 1microM) and K(+) (80mM)-induced contractions in a pattern similar to that of dicyclomine, but different from nifedipine and atropine. Tb.Cr shifted the Ca(++) concentration-response curves to right, like nifedipine and dicyclomine. In guinea-pig ileum, Tb.Cr produced rightward parallel shift of acetylcholine-curves, followed by non-parallel shift at higher concentration with the suppression of maximum response, similar to dicyclomine, but different from nifedipine and atropine. Tb.Cr exhibited protective effect against castor oil-induced diarrhea and carbachol-mediated bronchoconstriction in rodents. In guinea-pig trachea, Tb.Cr relaxed the CCh-induced contractions, shifted CCh-curves to right and inhibited the contractions of K(+). Anticholinergic effect was distributed both in organic and aqueous fractions, while CCB was present in the aqueous fraction. CONCLUSIONS: These results indicate that Terminalia bellerica fruit possess a combination of anticholinergic and Ca(++) antagonist effects, which explain its folkloric use in the colic, diarrhea and asthma. 相似文献
18.
Paul R. Sanberg Kristanne H. Russell Starr H. Hagenmeyer-Houser Magda Giordano Eve M. Zubrycki 《Psychopharmacology》1989,99(1):60-63
Most investigators have found adecrease in emotional defecation in rats given neuroleptics in novel environments, supporting their action as a major tranquilizer. We have found, however, that in rats a profoundincrease in emotional defecation can result from neuroleptic administration in well habituated environments, such as the homecage. Anticholinergics are known to be effective in treating the side effects associated with neuroleptic administration in humans. Therefore the present study determined the effects of anticholinergic treatment in this animal model. In male rats, defecation was measured for a 1-h test period in their homecage following various doses of the central and peripheral anticholinergics, scopolamine, andn-methylscopolamine, respectively. A decrease in fecal excretions and an attenuation of haloperidol-induced defecation was found following administration of scopolamine.n-Methylscopolamine reduced defecation at all doses. Whenn-methylscopolamine was combined with haloperidol, both fecal mass and number decreased significantly. Since both anticholinergic agents reduced haloperidol-induced defecation it is suggested that their effectiveness is mediated through peripheral mechanisms. 相似文献
19.
Scholz EP Konrad FM Weiss DL Zitron E Kiesecker C Bloehs R Kulzer M Thomas D Kathöfer S Bauer A Maurer MH Seemann G Katus HA Karle CA 《Naunyn-Schmiedeberg's archives of pharmacology》2007,376(4):275-284
The anticholinergic antiparkinson drug orphenadrine is an antagonist at central and peripheral muscarinic receptors. Orphenadrine
intake has recently been linked to QT prolongation and Torsade-de-Pointes tachycardia. So far, inhibitory effects on I
Kr or cloned HERG channels have not been examined. HERG channels were heterologously expressed in a HEK 293 cell line and in
Xenopus oocytes and HERG current was measured using the whole cell patch clamp and the double electrode voltage clamp technique.
Orphenadrine inhibits cloned HERG channels in a concentration dependent manner, yielding an IC50 of 0.85 μM in HEK cells. Onset of block is fast and reversible upon washout. Orphenadrine does not alter the half-maximal
activation voltage of HERG channels. There is no shift of the half-maximal steady-state-inactivation voltage. Time constants
of direct channel inactivation are not altered significantly and there is no use-dependence of block. HERG blockade is attenuated
significantly in mutant channels lacking either of the aromatic pore residues Y652 and F656. In conclusion, we show that the
anticholinergic agent orphenadrine is an antagonist at HERG channels. These results provide a novel molecular basis for the
reported proarrhythmic side effects of orphenadrine. 相似文献
20.
《Clinical toxicology (Philadelphia, Pa.)》2013,51(2):104-110
Introduction.?Datura species, especially Datura stramonium (e.g., jimsonweed), are the focus of scores of case reports that chronicle the toxidrome of anticholinergic toxicity.?Mechanisms of toxicity.?Toxicity occurs because of the presence of up to 28 belladonna alkaloids, predominated by atropine and scopolamine. There are significant interspecies differences in the ratio of the belladonna alkaloids, atropine to scopolamine, and the presence of at least 26 other related alkaloids will vary, even between and among specimens of the same species. The differences may account for unexpected dose–response effects that are observed in some patients and even different profiles of toxicity. All parts of the Datura species contain belladonna alkaloids; in decreasing order, the belladonna alkaloid content is generally the greatest in the petioles (flowers), stem, fruit (seeds), leaves, and roots.?Features.?The most prominent symptoms are due to the blockade of peripheral muscarinic receptors that innervate exocrine glands, smooth muscle, and cardiac tissue. Therefore, the primary toxic manifestations include mydriasis, which is due to the blockade of papillary sphincter muscle and iris muscle; dry mouth, secondary to parasympathetic blockade of salivary secretion; tachycardia, caused by competition at muscarinic receptors in postganglionic parasympathetic neurons and blockade of receptors in the SA node; and fever and erythema, because of vasodilation and inhibition of sweating.?Direct ocular exposure.?Well known to produce mydriasis after ingestion, Datura is also notorious for producing maladies such as “gardeners eye” and “cornpickers eye,” which is a testament to the high concentrations of belladonna alkaloids in the entire plant. When the sap or dried plant material from a member of the Datura species enters the eye directly, the papillary sphincter and ciliary muscles are affected resulting in mydriasis and cycloplegia. Pupil dilation is sudden in onset and often profound. In a dose–response fashion, the mydriasis and its persistence will be dependent on the alkaloidal content and quantity of the sap. The mydriasis can be bilateral, but most commonly it is unilateral, which is frightening to the victim and to the clinician and suggestive of significant cerebral pathology.?Management.?As with any toxic exposure, the foundation of patient management is supportive care and patient reassurance. Because of the central nervous system effects of the belladonna alkaloids, the patient may be agitated, combative, confused, and disoriented. Initial intervention focuses on addressing those issues that protect the patient and their caregivers. In severe cases, physostigmine, a cholinesterase inhibitor, should be used to reverse anticholinergic toxicity. Physostigmine should be given intravenously to an adult in a dose of 0.5–2.0 mg at a rate of no more than 1 mg/min; a second dose may be administered if necessary. Children should receive 0.02 mg/kg intravenously and the rate should not exceed 0.5 mg/min. Extracorporeal elimination and forced diuresis of the belladonna alkaloids are not viable options.?Conclusions.?Members of the Datura species contain abundant amounts of belladonna alkaloids that can produce both local and systemic anticholinergic toxicity. Fatalities because of Datura species exposure are rare, but adverse effects are very common. Treatment is supportive with the use of physostigmine in more severe cases of poisoning. 相似文献