γ-酪蛋白水解产物分离肽对不同麻醉药物处理下大鼠动脉血压的影响

L.C.A.G. Chaguri, S.A. Barreto, I. Lebrun
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引用次数: 0

摘要

从γ-酪蛋白的胰蛋白酶水解产物中分离出的肽YPVQPFTE的作用显示出缓激肽增强活性,其特征是动脉血压记录分析。采用三种常用麻醉药物:戊巴比妥钠(68 mg/kg, i.p.)麻醉,在有意识自发性高血压大鼠(SHR)和正常血压Wistar大鼠(30 μg)的慢性实验和急性实验中,静脉注射经该肽预处理的缓激肽(0.5 μg);盐酸氯胺酮(25mg /kg,口服)与盐酸噻嗪(10mg /kg,口服)和阿托品(0.05 mg/kg,口服)联合使用;水合氯醛(160mg /kg, i.p.)。该肽显示缓激肽增强活性,与血管紧张素转换酶(ACE)抑制无关。通过降压幅度(mmHg)和时间过程(min)两项参数比较血压恢复基线值。在第一个参数中,有意识SHR对动脉血压的降低幅度较大,其次是水合氯醛和戊巴比妥钠、氯胺酮-噻嗪,其降低幅度较小。在时间参数上,两种CNS抑制剂从低血压中恢复所需的时间均高于有意识SHR组,且氯胺酮-噻嗪联用效果与有意识SHR组相似。结果表明,由血管活性化合物作用引起的低血压(mmHg)的大小并没有被麻醉药物直接改变,即使是与ACE无关的化合物,但从这种低血压恢复的时间明显不同,这取决于所使用的麻醉药物的药理机制特性。这表明在这种情况下观察到的主要影响是在中枢神经系统抑制剂存在的情况下未能恢复基础平均动脉压(MAP)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of a peptide isolated from γ-casein hydrolysates on rat arterial blood pressure assay carried out under different anaesthetic drugs treatment

The action of the peptide YPVQPFTE, isolated from the tryptic hydrolysate of γ-casein, displays a bradykinin potentiating activity, characterized by the arterial blood pressure recording analysis. The intravenous injection of bradykinin (0.5 μg) pre-treated with this peptide (30 μg) was performed by chronic assay in conscious spontaneously hypertensive rats (SHR) and also by acute assay in normotensive Wistar rats, anaesthetized by three currently used anaesthetic drugs: sodium pentobarbitone (68 mg/kg, i.p.); ketamine hydrochloride (25 mg/kg, i.p.) associated with xylazine hydrochloride (10 mg/kg, i.p.) and atropine (0,05 mg/Kg, i.p.); and chloral hydrate (160 mg/kg, i.p.). The peptide displayed bradykinin potentiating activity, by means that was not related to angiotensin converting enzyme (ACE) inhibition. The hypotensive areas were compared by two parameters, namely magnitude decrease (mmHg) and time course (min) to recover the pressure baseline values. In the first parameter, conscious SHR presented a greater decrease of the arterial blood pressure, followed by chloral hydrate and sodium pentobarbitone, ketamine–xylazine, which presented a small decrease. For the time parameter, the two depressants of the CNS presented the higher time to recover from the hypotension and ketamine–xylazine association resulted similar to conscious SHR group. The results demonstrated that the magnitude of the hypotension (mmHg) caused by the action of the vasoactive compounds was not directly altered by anaesthetic drugs even with compounds not related to ACE but the time to recover from this hypotension was significantly different depending on pharmacological mechanism proprieties of the anaesthetic agent used, suggesting that the main effects observed in this case is the failure to recover basal Mean Arterial Pressure (MAP) in the presence of depressant of the central nervous system.

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