发布求助
文献互助 智能选刊 最新文献

General pharmacology最新文献

筛选
英文 中文
Effects of class I antiarrhythmic drugs on mitochondrial ATPase activity in guinea pig heart preparations. 一类抗心律失常药物对豚鼠心脏制剂中线粒体atp酶活性的影响。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90040-5
A A Almotrefi
{"title":"Effects of class I antiarrhythmic drugs on mitochondrial ATPase activity in guinea pig heart preparations.","authors":"A A Almotrefi","doi":"10.1016/0306-3623(93)90040-5","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90040-5","url":null,"abstract":"<p><p>1. The effects of three class I antiarrhythmic drugs quinidine, lidocaine and lorcainide on undamaged myocardial mitochondrial ATPase [ATP: phosphohydrolase, EC 3.6.1.3] activity were evaluated in guinea pig heart preparations. 2. All three drugs inhibited the enzyme activity in a concentration-dependent fashion. 3. Lorcainide was the most potent, exerting inhibitory effects in the range of less than 1.0 nM-2.0 mM, with IC20 and IC50 values of 9.4 +/- 0.6 nM and 87.2 +/- 5.5 microM. However, in the range of approx. 10 nM-10 microM, the enzyme response decreased only slightly with increasing lorcainide concentrations. 4. Quinidine and lidocaine, on the other hand, inhibited the enzyme activity in the range of 1.0 microM-100 mM. 5. The IC20 and IC50 values for quinidine were 0.92 +/- 0.04 mM and 4.8 +/- 0.6 mM and for lidocaine were 115 +/- 6 microM and 2.3 +/- 0.3 mM. 6. The results show that all three drugs inhibit mitochondrial ATPase activity and that lorcainide is the most potent. 7. These inhibitory effects may be related to the lipophilicity and membrane stabilizing activity of this class of antiarrhythmic drugs.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"233-7"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90040-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19465888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
Cholecystokinin-induced ventral root depolarization of neonate rat hemicord in vitro. 缩胆囊素诱导的新生儿大鼠脐带腹根去极化。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90030-2
S K Long
{"title":"Cholecystokinin-induced ventral root depolarization of neonate rat hemicord in vitro.","authors":"S K Long","doi":"10.1016/0306-3623(93)90030-2","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90030-2","url":null,"abstract":"<p><p>1. Sulphated cholecystokinin octapeptide (CCK8S, 0.03-1.00 microM), pentapeptide (CCK5) and tetrapeptide (CCK4) elicited concentration dependent depolarizations of neonate rat ventral roots in vitro. 2. CCK5 was equipotent with CCK8S although CCK4 was weaker (equipotent molar ratio 17.5). 3. CCK8S-induced depolarizations were depressed by tetrodotoxin (0.1 microM), Mg2+ ions (0.75 mM) and the NMDA receptor antagonist 2-amino-5-phosphonopentanoate (AP5, 10 microM). These results suggest that CCK8S-induced depolarizations were predominantly mediated through the release of an excitatory amino acid from interneuronal sites. 4. The selective CCKA and CCKB receptor antagonists, L-364,718 and L-365,260 both depressed CCK8S-induced depolarizations. CCK8S dose ratios in the presence of 1 microM L-364,718 or L-365,260 were 4.5 and 11.2 respectively, suggesting the response was mediated predominantly through stimulation of CCKB receptors. 5. These results suggest that the neonate rat hemicord preparation is a suitable tissue for functional CCK receptor assays.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"171-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90030-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19090863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Neuropeptide Y-induced inositol phospholipid hydrolysis in blood vessels from normotensive and spontaneously hypertensive rats. 正常和自发性高血压大鼠血管中神经肽y诱导的肌醇磷脂水解。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90043-w
E Vila, J L Reid, I M Macrae
{"title":"Neuropeptide Y-induced inositol phospholipid hydrolysis in blood vessels from normotensive and spontaneously hypertensive rats.","authors":"E Vila,&nbsp;J L Reid,&nbsp;I M Macrae","doi":"10.1016/0306-3623(93)90043-w","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90043-w","url":null,"abstract":"<p><p>1. Neuropeptide Y (NPY) increased inositol phosphate (IP) formation in the femoral artery and vein of adult Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. 2. Noradrenaline (NA, 10(-6) M) induced IP accumulation in both strains of rats. 3. Subthreshold concentrations of NPY (3 x 10(-9) M for femoral vein and 10(-8) M for femoral artery) failed to modify NA (10(-6) M)-induced IP formation in both vessels. 4. These results suggest that the direct contractile effects but not the potentiation of NA-induced contractions may be directly linked to phosphatidylinositol turnover in adult SHR and WKY rats.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"247-51"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90043-w","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19463726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 6
The effect of oral vanadyl treatment on the reactivity of tracheal smooth muscle obtained from insulin-dependent diabetic rats. 口服vanadyl对胰岛素依赖型糖尿病大鼠气管平滑肌反应性的影响。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90020-x
G Ozansoy, C Karasu, A T Ozçelikay
{"title":"The effect of oral vanadyl treatment on the reactivity of tracheal smooth muscle obtained from insulin-dependent diabetic rats.","authors":"G Ozansoy,&nbsp;C Karasu,&nbsp;A T Ozçelikay","doi":"10.1016/0306-3623(93)90020-x","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90020-x","url":null,"abstract":"<p><p>1. In this study, we investigated the contractile effects of acetylcholine (ACh) and KCl in tracheas obtained from 12-13 wk insulin-dependent (ID)-diabetic rats. 2. The maximum contractile responses to ACh and KCl were significantly increased in ID-diabetic rat tracheas compared with those from controls. But the sensitivity (pD2 values) of ID-diabetic tracheas to these agents were not significantly altered relative to controls. 3. The alterations which occurred in ID-diabetic rats were prevented with oral vanadyl treatment during a 10 wk period.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"115-9"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90020-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19464741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 13
Interaction of AZA analogs of chlorpromazine with the dopamine D2 receptor. 氯丙嗪AZA类似物与多巴胺D2受体的相互作用。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90026-t
T Farooqui, K Markovich, L Wallace, D Miller, N Uretsky
{"title":"Interaction of AZA analogs of chlorpromazine with the dopamine D2 receptor.","authors":"T Farooqui,&nbsp;K Markovich,&nbsp;L Wallace,&nbsp;D Miller,&nbsp;N Uretsky","doi":"10.1016/0306-3623(93)90026-t","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90026-t","url":null,"abstract":"<p><p>1. Permanently charged AZA analogs of chlorpromazine inhibited the binding of [3H]spiperone and antagonized the apomorphine-induced inhibition of the potassium evoked release of [3H]acetylcholine. 2. The AZA analogs were more potent in binding affinity and antagonist activity than the trimethylammonium analog of chlorpromazine but less potent than chlorpromazine. 3. These results suggest that it is possible to enhance the binding of the permanently charged trimethylammonium analog of chlorpromazine by the addition of a functional group near the quaternary nitrogen which is capable of forming a hydrogen bond with the D2 dopamine receptor. 4. However, it appears that for optimal binding, as achieved with chlorpromazine, the hydrogen-bonding proton should be on the charged nitrogen.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"147-51"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90026-t","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19465376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Hypoxia-induced coronary flow changes in the perfused rat heart: effects of high L-carnitine concentrations. 缺氧诱导的灌注大鼠心脏冠状动脉血流变化:高左旋肉碱浓度的影响。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90037-x
D Lapenna, E Porreca, A Mezzetti, S de Gioia, L Marzio, F Cuccurullo
{"title":"Hypoxia-induced coronary flow changes in the perfused rat heart: effects of high L-carnitine concentrations.","authors":"D Lapenna,&nbsp;E Porreca,&nbsp;A Mezzetti,&nbsp;S de Gioia,&nbsp;L Marzio,&nbsp;F Cuccurullo","doi":"10.1016/0306-3623(93)90037-x","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90037-x","url":null,"abstract":"<p><p>1. Hemodynamic effects of physiological (0.04 and 0.07 mM) and high (8, 15 and 25 mM) L-carnitine (LC) concentrations were tested on the normally oxygenated and hypoxic perfused rat heart. 2. No effect was detected on aerobic hearts, whereas a dose-dependent rise in coronary flow (CF) during both the hyperemic and constrictive phases was observed in hypoxic hearts with 8, 15 and 25 mM LC. This action was apparently unrelated to a resting tension (RT) improvement, which was observed only with 25 mM LC. 3. When 11 mM glucose was replaced by 11 mM mannitol in the perfusion buffer, LC effects on the hyperemic phase were abolished; however, 25 mM LC resulted in CF-values still significantly higher than those detected without the drug, though RT was similar in these glucose-free groups. 4. It may be concluded that LC is ineffective on the perfused rat heart in aerobic conditions, whereas high LC concentrations can enhance CF only during hypoxia, these effects being independent of heart function improvements and partly unrelated to glucose presence.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"211-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90037-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19465886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Positive chronotropic and inotropic responses to lysophosphatidylcholine are mediated by norepinephrine released from myocardial sympathetic nerve terminals. 心肌交感神经末梢释放的去甲肾上腺素介导对溶血磷脂酰胆碱的正性变时性和正性反应。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90041-u
H Tanaka, U Ikeda, K Shigenobu
{"title":"Positive chronotropic and inotropic responses to lysophosphatidylcholine are mediated by norepinephrine released from myocardial sympathetic nerve terminals.","authors":"H Tanaka,&nbsp;U Ikeda,&nbsp;K Shigenobu","doi":"10.1016/0306-3623(93)90041-u","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90041-u","url":null,"abstract":"<p><p>1. The effects of beta-adrenoceptor blockade and reserpinization on the positive chronotropic and inotropic responses to lysophosphatidylcholine (LPC) were examined in isolated atrial and ventricular preparations from rat hearts. 2. The positive responses to 10(-4) M LPC were about 40-55% of those to 10(-5) M norepinephrine (NE) in each preparation. 3. The responses to LPC in the presence of propranolol or in the reserpinized preparations were significantly smaller than the corresponding values obtained in control preparations, and were about 10-25% of those to NE. 4. It was concluded that positive chronotropic and inotropic responses to LPC are at least partially mediated by release of NE from myocardial sympathetic nerve terminals.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"239-41"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90041-u","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19465889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Involvement of dopaminergic receptor subtypes in straub tail behaviour in mice. 多巴胺能受体亚型参与小鼠秸秆尾行为。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90022-p
M R Zarrindast, A Bayat, B Shafaghi
{"title":"Involvement of dopaminergic receptor subtypes in straub tail behaviour in mice.","authors":"M R Zarrindast,&nbsp;A Bayat,&nbsp;B Shafaghi","doi":"10.1016/0306-3623(93)90022-p","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90022-p","url":null,"abstract":"<p><p>1. Administration of apomorphine to mice induced straub tail behaviour dose-dependently. The response was decreased by the D1 antagonist SCH 23390, the D2 antagonist sulpiride. Reserpine plus alpha-methyl-p-tyrosine (AMPT), caused a marked increase in the response of the drug. 2. The D1 agonist SKF 38393 induced the straub tail behaviour in a dose-dependent manner, which was decreased by SCH 23390, sulpiride or reserpine + AMPT. 3. When animals were administered the D2 agonist quinpirole, a dose-dependent response was produced. This effect was decreased by sulpiride and reserpine + AMPT, but not by SCH 23390. 4. In animals pretreated with reserpine + AMPT, the combination of SKF 38393 with quinpirole produced a significant straub tail behaviour. 5. It is concluded that the concurrent D1/D2 dopamine receptor stimulation is necessary to produce straub tail behaviour in mice.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"127-30"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90022-p","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19090383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Basal and histamine-induced gastric acid secretion in alloxan diabetic rats. 四氧嘧啶糖尿病大鼠胃酸分泌的基础和组胺诱导。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90021-o
A T Ozçelikay, V M Altan, N Yildizoğlu-Ari, O Altinkurt, F Onur, Y Oztürk
{"title":"Basal and histamine-induced gastric acid secretion in alloxan diabetic rats.","authors":"A T Ozçelikay,&nbsp;V M Altan,&nbsp;N Yildizoğlu-Ari,&nbsp;O Altinkurt,&nbsp;F Onur,&nbsp;Y Oztürk","doi":"10.1016/0306-3623(93)90021-o","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90021-o","url":null,"abstract":"<p><p>1. Effects of alloxan-induced diabetes on the rat gastric acid secretion were investigated using a number of biostatistical models described earlier. 2. Histamine-induced gastric acid secretion was found to be decreased in alloxan-diabetic rats when compared with their age-matched controls. 3. Basal acid secretion was also decreased depending on experimentally-induced diabetes. 4. The above results strongly suggest that alloxan-induced diabetes depresses vagal activity and H2-receptor activity in the stomach.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"121-6"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90021-o","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19464742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 17
Josamycin concentrations in radicular cysts following a single oral administration. 单次口服后根状囊肿中乔霉素的浓度。
General pharmacology Pub Date : 1993-01-01 DOI: 10.1016/0306-3623(93)90025-s
Y Akimoto, Y Mochizuki, A Uda, H Omata, S Saito, K Kaneko, A Fujii, H Yamamoto
{"title":"Josamycin concentrations in radicular cysts following a single oral administration.","authors":"Y Akimoto,&nbsp;Y Mochizuki,&nbsp;A Uda,&nbsp;H Omata,&nbsp;S Saito,&nbsp;K Kaneko,&nbsp;A Fujii,&nbsp;H Yamamoto","doi":"10.1016/0306-3623(93)90025-s","DOIUrl":"https://doi.org/10.1016/0306-3623(93)90025-s","url":null,"abstract":"<p><p>1. Josamycin concentrations in cyst wall (wall) and cyst fluid (fluid) of radicular cyst and serum following a single oral administration of josamycin (600 mg) were assayed by a paper disk method. 2. The mean peak josamycin concentrations in wall, fluid and serum occurred at 1.5, 2 and 1.5 hr, respectively, and were 1.33 micrograms/g, 0.53 and 0.74 micrograms/ml, respectively. 3. The mean concentration ratios of wall/serum, fluid/serum and fluid/wall at the peak times (1.5, 2 and 2 hr) were 1.80, 0.64 and 0.42, respectively. 4. Josamycin concentrations in wall and fluid at the peak time exceeded MIC for 80% for clinically isolated strains of alpha-hemolytic Streptococci.</p>","PeriodicalId":12487,"journal":{"name":"General pharmacology","volume":"24 1","pages":"143-5"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0306-3623(93)90025-s","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19465375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
首页 上一页 下一页 尾页
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整，为了账户安全，请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们：info@booksci.cn Book学术提供免费学术资源搜索服务，方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号：481959085
Book学术官方微信