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Effect of PaCO2 and PaO2 on Lidocaine and Articaine Toxicity

机译:PaCO2和PaO2对利多卡因和青蒿素毒性的影响

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Alterations in arterial PaCO2 can influence local anesthetic toxicity.The objectivenof this study was to evaluate the effect of stress-induced changes in PaCO2 andnPaO2 on the seizure threshold of lidocaine and articaine. Lidocaine (2% withn1 : 100,000 epinephrine) or articaine (4% with 1 : 100,000 epinephrine) was ad-nministered intravenously under rest or stress conditions to 36 rats separated inton4 groups. Propranolol and prazosin were administered preoperatively to mini-nmize cardiovascular effects of epinephrine. Mean arterial pressure (MAP), heartnrate (HR), and arterial pH, PaCO2,andPaO2 were measured. Results showednno differences in MAP, HR, or pH. Stress significantly increased the latency peri-nod for the first tonic-clonic seizure induced by a toxic dose of both lidocaine andnarticaine (P ,.05).Seizureswerebroughtonmorerapidlybyarticaine.Nosignif-nicant difference between toxic doses of lidocaine and articaine was noted.Stressnraised the seizure threshold dose for both drugs and significantly (P , .01) in-ncreased arterial PaO2 from 94.0 6 1.90 mm Hg to 113.0 6 2.20 mm Hg, andnreduced PaCO2 from 36.0 6 0.77 mm Hg to 27.0 6 0.98 mm Hg. In conclusion,nreduction in PaCO2 and/or increase in PaO2 raised the seizure threshold of lido-ncaine and articaine. This study also confirmed that lidocaine and articaine havenequipotent central nervous system toxicity
机译:动脉PaCO2的改变可影响局麻药的毒性。本研究的目的是评估压力引起的PaCO2和nPaO2的变化对利多卡因和青蒿素癫痫发作阈值的影响。在静息或应激条件下,分别对36只inton4组的大鼠静脉注射利多卡因(1%:100,000肾上腺素占2%)或青蒿素(1:100,000肾上腺素占4%)。术前给予普萘洛尔和哌唑嗪以最小化肾上腺素的心血管作用。测量平均动脉压(MAP),心率(HR)和动脉pH,PaCO2和PaO2。结果显示MAP,HR或pH值无差异。应激显着增加了有毒剂量利多卡因和纳替卡因引起的第一次强直性阵挛性癫痫发作的潜伏期潜伏期(P,.05)。两种药物的阈值剂量以及显着(P,.01)的动脉PaO2从94.0 6 1.90 mm Hg升高到113.0 6 2.20 mm Hg,并且PaCO2从36.0 6 0.77 mm Hg降低到27.0 6 0.98 mm Hg。总之,PaCO2的减少和/或PaO2的增加提高了利多卡因和青蒿素的癫痫发作阈值。这项研究还证实了利多卡因和青蒿素对中枢神经系统具有中等毒性

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