Background and Objectives High concentrations of lidocaine have been found to cause pulmonary vasoconstriction and low concentrations (0.5-0.9 μg/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.
Methods 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 μg/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.
Results High plasma concentration of lidocaine (140 μg/mL) in the LLL inflow produced a significant increase in PAPLLL during hyperoxia, while PAPLLL did not change significantly at the 5-70-μg/mL lidocaine concentration. In LLL outflow blood, Po2 increased significantly following a 140 μg/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 μg/mL) significantly constricted the lobar vessels. In addition, lidocaine at the 140-μg/mL concentration constricted the upstream vessels (presumably the lobar arteries) more strongly than the lobar veins during hypoxia.
Conclusions Extremely high concentrations (140 μg/mL) but not low concentrations (5-70 μg/mL) of lidocaine produced pulmonary vasoconstriction and reduced shunt. Lower concentrations of lidocaine constricted the hypoxic lobar vessels.
- pulmonary circulation
- hyperoxic ventilation
- hypoxic ventilation
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Supported by a Grant-in-Aid for Scientific Research 01440066 from the Ministry of Education, Science, and Culture of Japan.