首页> 美国卫生研究院文献>Brazilian Journal of Medical and Biological Research >Evidence for the involvement of peripheralβ-adrenoceptors in delayed liquid gastric emptying induced by dipyrone4-aminoantipyrine and antipyrine in rats
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Evidence for the involvement of peripheralβ-adrenoceptors in delayed liquid gastric emptying induced by dipyrone4-aminoantipyrine and antipyrine in rats

机译:周围器官受累的证据β-肾上腺素在双嘧啶引起的延迟性液体胃排空中的作用大鼠体内的4-氨基安替比林和安替比林

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摘要

Dipyrone (Dp), 4-aminoantipyrine (AA), and antipyrine (At) delay liquid gastric emptying (GE) in rats. We evaluated adrenergic participation in this phenomenon in a study in male Wistar rats (250-300 g) pretreated subcutaneously with guanethidine (GUA), 100 mg·kg−1·day−1, or vehicle (V) for 2 days before experimental treatments. Other groups of animals were pretreated intravenously (iv) 15 min before treatment with V, prazosin (PRA; 1 mg/kg), yohimbine (YOH; 3 mg/kg), or propranolol (PRO; 4 mg/kg), or with intracerebroventricular (icv) administration of 25 µg PRO or V. The groups were treated iv with saline or with 240 µmol/kg Dp, AA, or At. GE was determined 10 min later by measuring the percentage of gastric retention (%GR) of saline labeled with phenol red 10 min after gavage. %GR (mean±SE, n=8) indicated that GUA abolished the effect of Dp (GUA vs V=31.7±1.6 vs 47.1±2.3%) and of At (33.2±2.3 vs 54.7±3.6%) on GE and significantly reduced the effect of AA (48.1±3.2 vs 67.2±3.1%). PRA and YOH did not modify the effect of the drugs. %GR (mean±SE, n=8) indicated that iv, but not icv, PRO abolished the effectof Dp (PRO vs V=29.1±1.7 vs 46.9±2.7%) and At(30.5±1.7 vs 49±3.2%) and significantly reduced the effect ofAA (48.4±2.6 vs 59.5±3.1%). These data suggest activation ofperipheral β-adrenoceptors in the delayed GE induced by phenylpyrazolonederivatives.
机译:敌敌畏(Dp),4-氨基安替比林(AA)和安替比林(At)会延迟大鼠的液体胃排空(GE)。我们在雄性Wistar大鼠(250-300 g)的皮下注射胍乙啶(GUA)100 mg·kg -1 ·day -1 或媒介物(V)进行实验治疗前2天。其他组的动物在接受V,哌唑嗪(PRA; 1 mg / kg),育亨宾(YOH; 3 mg / kg)或普萘洛尔(PRO; 4 mg / kg)或静脉内治疗前15分钟进行静脉内预处理(iv)脑室内(icv)注射25 µg PRO或V。用生理盐水或240 µmol / kg Dp,AA或At静脉内治疗各组。 10分钟后,通过在管饲10分钟后测量用酚红标记的盐水的胃滞留率(%GR)来确定GE。 %GR(平均值±SE,n = 8)表明,GUA消除了Dp(GUA vs V = 31.7±1.6 vs 47.1±2.3%)和At(33.2±2.3 vs 54.7±3.6%)对GE的影响,且显着降低了AA的效果(48.1±3.2比67.2±3.1%)。 PRA和YOH不会改变药物的作用。 %GR(平均值±SE,n = 8)表示iv(但不是icv)PRO取消了该作用Dp(PRO vs V = 29.1±1.7 vs 46.9±2.7%)和(30.5±1.7 vs 49±3.2%),显着降低了AA(48.4±2.6比59.5±3.1%)。这些数据表明激活了苯并吡唑啉酮诱导的延迟GE诱导的外周β-肾上腺素受体衍生品。

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