Pre-emptive lidocaine inhibits arterial vasoconstriction but not vasopressin release induced by a carbon dioxide pneumoperitoneum in pigs

Background. We assessed the preventive effects of i.v. or i.p.lidocaine administration on increases in vascular resistanceproduced by carbon dioxide pneumoperitoneum and related thisto vasopressin release. Methods. Carbon dioxide pneumoperitoneum (14 mm Hg intra-abdominalpressure) was performed in 32 anaesthetized young pigs and monitoredusing a pulmonary artery catheter. Animals received lidocaine0.5% (0.5 mg kg^–1) i.v. (n=9) or 2 ml kg^–1 i.p.(n=9) or saline (n=5) 15 min before the pneumoperitoneum andwere compared with a control group (n=9). Results. I.V. and i.p. lidocaine inhibited increases in meansystemic vascular resistance induced by the pneumoperitoneum[2109 (SD 935) and 2282 (895), respectively, vs 3013 (1067)dyne s^–1 cm^–5 in the control group]. Cardiac outputwas increased. Plasma lidocaine concentrations were threefoldhigher after i.p. administration than after i.v. administration.After pneumoperitoneum insufflation, plasma lysine-vasopressinconcentrations increased in all groups (control 74%, saline65%, i.p. lidocaine 57%, i.v. lidocaine 74%). Conclusions. I.V. and i.p. lidocaine blunted systemic vascularresponses to carbon dioxide pneumoperitoneum in pigs, but withoutinfluencing vasopressin release. Br J Anaesth 2003; 90: 343–8