EFFECTS OF LIDOCAINE ON PULMONARY CIRCULATION DURING HYPEROXIA AND HYPOXIA IN THE DOG

Citation
H. Yukioka et al., EFFECTS OF LIDOCAINE ON PULMONARY CIRCULATION DURING HYPEROXIA AND HYPOXIA IN THE DOG, Regional anesthesia, 21(4), 1996, pp. 327-337
Citations number
37
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
0146521X
Volume
21
Issue
4
Year of publication
1996
Pages
327 - 337
Database
ISI
SICI code
0146-521X(1996)21:4<327:EOLOPC>2.0.ZU;2-Z
Abstract
Background and Objectives. High concentrations of lidocaine have been found to cause pulmonary vasoconstriction and low concentrations (0.5- 0.9 mu g/mL) to cause reversal of nitrous oxide-induced depression of hypoxic pulmonary vasoconstriction. This study was undertaken to exami ne the effects of high concentrations of lidocaine on pulmonary circul ation during hyperoxic and hypoxic ventilation. Methods. With use of c ross-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 i nfused into the inflow system, so that plasma lidocaine concentrations in the inflow blood were maintained at either 5, 10, 20, 40, 70, or 1 40 mu g/mL during ventilation with 50% oxygen or 3% oxygen. Mean arter ial and venous pressures in the LLL (PAP(LLL) and PVPLLL), airway pres sure of the LLL, and blood gas in LLL inflow and outflow were measured . Results. High plasma concentration of lidocaine (140 mu g/mL) in the LLL inflow produced a significant increase in PAP(LLL) during hyperox ia, while PAP(LLL) did not change significantly at the 5-70-mu g/mL li docaine concentration. In LLL outflow blood, PO2 increased significant ly following a 140 mu g/mL lidocaine infusion during hyperoxia, while in LLL inflow blood, PO2 did not change. The airway pressure of LLL al so did not change. During hypoxia, hypoxic pulmonary vasoconstriction did not occur, and lower plasma concentrations of lidocaine (40-70 mu g/mL) significantly constricted the lobar vessels. In addition, lidoca ine al the 140-mu g/mL concentration constricted the upstream vessels (presumably the lobar arteries) more strongly than the lobar veins dur ing hypoxia. Conclusions. Extremely high concentrations (140 mu g/mL) but not low concentrations (5-70 mu g/mL) of lidocaine produced pulmon ary vasoconstriction and reduced shunt. Lower concentrations of lidoca ine constricted the hypoxic lobar vessels.