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首页> 外文期刊>Ciencia Rural >Hemodynamic and hemogasometric in the atropine administration in dogs anesthetized with chlorpromazine and dexmedetomidine and isoflurane
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Hemodynamic and hemogasometric in the atropine administration in dogs anesthetized with chlorpromazine and dexmedetomidine and isoflurane

机译:阿托品给药氯丙嗪,右美托咪定和异氟烷麻醉的狗的血流动力学和血压测定

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> face="Verdana, Arial, Helvetica, sans-serif" size="2">Six dogs weighing 17.9 ±3.9 kg were anesthetized on two occasions, at least 7 days apart, in randomized blinded manner. Anesthesia was induced and maintained with isoflurane in mechanical ventilation. After instrumentation, the end-tidal isoflurane was maintained at 1,3%V throughout the study. After a 30 minutes stabilization period (M -15), baseline hemodynamic parameters and arterial blood gases were recorded and atropine (atropine group) or 0.9% NaCl (saline group) were administered. Fifteen minutes later, data were recorded again (M0) and a chlorpromazine- dexmedetomidine (Chlor-Dex) combination was administered. Variables were measured for an additional 65 minutes after Chlor-Dex. A one-way ANOVA-Student-Newman-Keuls was used for comparisons within groups, while a paired t test was used for comparisons between groups (P face="Symbol">£0,05). Heart rate was higher in atropine group after Chlor-Dex administration. Cardiac index (CI) was reduced from baseline after Chlor-Dex in both treatments. Although mean CI values tended to be higher in atropine group, CI did not differ between groups. Chlor-Dex administration caused increased arterial blood pressure in dogs treated with atropine. Mean arterial pressure (MAP) was significantly higher in the atropine group from 5 to 65 min after Chlor-Dex. The systemic vascular resistance index (SVRI) increased from baseline in both groups after Chlor-Dex administration. No significant differences were observed for arterial blood gases. Atropine administration prior to Chlor-Dex resulted in increased arterial blood pressure. Bradycardia induced by the administration of these drugs was prevented by the anticholinergic given, however decrease in cardiac output was not prevented.
机译:> face =“ Verdana,Arial,Helvetica,sans-serif” size =“ 2”>对六只重17.9±3.9千克的狗进行两次麻醉,间隔至少7天,以随机盲法进行。在机械通气中用异氟烷诱导并维持麻醉。仪器安装后,整个研究过程中,潮汐末异氟烷保持在1,3%V。经过30分钟的稳定期(M -15),记录了基线血液动力学参数和动脉血气,并服用了阿托品(阿托品组)或0.9%氯化钠(盐水组)。 15分钟后,再次记录数据(M0),并给予氯丙嗪-右美托咪定(Chlor-Dex)组合。 Chlor-Dex处理后再测量变量65分钟。组间比较使用单向方差分析-学生-纽曼-基尔(Atuman-Student-Newman-Keuls),组间比较使用配对t检验(P face =“ Symbol”>£ 0.05)。服用Chlor-Dex后,阿托品组的心率较高。在两种疗法中,Chlor-Dex治疗后的心脏指数(CI)均较基线降低。尽管阿托品组的平均CI值趋于升高,但两组之间的CI没有差异。氯霉素的给药导致用阿托品治疗的狗的动脉血压升高。 Chlor-Dex治疗后5至65分钟,阿托品组的平均动脉压(MAP)显着升高。服用Chlor-Dex后,两组的全身血管阻力指数(SVRI)均较基线升高。没有观察到动脉血气的显着差异。在Chlor-Dex之前服用阿托品会导致动脉血压升高。给予抗胆碱能可预防这些药物引起的心动过缓,但不能防止心输出量的减少。

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