Yukioka H, Hayashi M, Tatekawa S, Fujimori M
Department of Anesthesiology and Intensive Care Medicine, Osaka City University Medical School, Japan.
Reg Anesth. 1996 Jul-Aug;21(4):327-37.
High concentrations of lidocaine have been found to cause pulmonary vasoconstriction and low concentrations (0.5-0.9 microgram/mL) to cause reversal of nitrous oxide-induced depression of hypoxic pulmonary vasoconstriction. This study was undertaken to examine the effects of high concentrations of lidocaine on pulmonary circulation during hyperoxic and hypoxic ventilation.
With use of cross-circulation consisting of ventilation and constant-flow perfusion of the left lower lobe (LLL) independently of all other lobes of the dog lung under nitrous oxide and halothane anesthesia, lidocaine was infused into the inflow system, so that plasma lidocaine concentrations in the inflow blood were maintained at either 5, 10, 20, 40, 70, or 140 micrograms/mL during ventilation with 50% oxygen or 3% oxygen. Mean arterial and venous pressures in the LLL (PAPLLL and PVPLLL), airway pressure of the LLL, and blood gas in LLL inflow and outflow were measured.
High plasma concentration of lidocaine (140 micrograms/mL) in the LLL inflow produced a significant increase in PAPLLL during hyperoxia, while PAPLLL did not change significantly at the 5-70-micrograms/mL lidocaine concentration. In LLL outflow blood, PO2 increased significantly following a 140 micrograms/mL lidocaine infusion during hyperoxia, while in LLL inflow blood, PO2 did not change. The airway pressure of LLL also did not change. During hypoxia, hypoxic pulmonary vasoconstriction did not occur, and lower plasma concentrations of lidocaine (40-70 micrograms/mL) significantly constricted the lobar vessels. In addition, lidocaine at the 140-micrograms/mL concentration constricted the upstream vessels (presumably the lobar arteries) more strongly than the lobar veins during hypoxia.
Extremely high concentrations (140 micrograms/mL) but not low concentrations (5-70 micrograms/mL) of lidocaine produced pulmonary vasoconstriction and reduced shunt. Lower concentrations of lidocaine constricted the hypoxic lobar vessels.
已发现高浓度利多卡因可引起肺血管收缩,而低浓度(0.5 - 0.9微克/毫升)可导致氧化亚氮引起的低氧性肺血管收缩抑制作用逆转。本研究旨在探讨高浓度利多卡因在高氧和低氧通气期间对肺循环的影响。
在氧化亚氮和氟烷麻醉下,利用由左下叶(LLL)通气和恒流灌注组成的交叉循环,该循环独立于犬肺的所有其他叶,将利多卡因注入流入系统,使得在50%氧气或3%氧气通气期间,流入血液中的血浆利多卡因浓度维持在5、10、20、40、70或140微克/毫升。测量LLL的平均动脉压和静脉压(PAPLLL和PVPLLL)、LLL的气道压以及LLL流入和流出的血气。
LLL流入中高血浆浓度的利多卡因(140微克/毫升)在高氧期间使PAPLLL显著升高,而在利多卡因浓度为5 - 70微克/毫升时,PAPLLL无显著变化。在高氧期间注入140微克/毫升利多卡因后,LLL流出血液中的PO2显著升高,而LLL流入血液中的PO2未改变。LLL的气道压也未改变。在低氧期间,未发生低氧性肺血管收缩,较低血浆浓度的利多卡因(40 - 70微克/毫升)显著收缩叶血管。此外,在低氧期间,140微克/毫升浓度的利多卡因对上游血管(可能是叶动脉)的收缩作用比对叶静脉更强。
极高浓度(140微克/毫升)而非低浓度(5 - 70微克/毫升)的利多卡因可引起肺血管收缩并减少分流。较低浓度的利多卡因可收缩低氧叶血管。