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

Abstract

Background. We assessed the preventive effects of i.v. or i.p. lidocaine administration on increases in vascular resistance produced by carbon dioxide pneumoperitoneum and related this to vasopressin release. Methods. Carbon dioxide pneumoperitoneum (14 mm Hg intra-abdominal pressure) was performed in 32 anaesthetized young pigs and monitored using a pulmonary artery catheter. Animals received lidocaine 0.5% (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 and were compared with a control group (n=9). Results. I.V. and i.p. lidocaine inhibited increases in mean systemic 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 output was increased. Plasma lidocaine concentrations were threefold higher after i.p. administration than after i.v. administration. After pneumoperitoneum insufflation, plasma lysine-vasopressin concentrations increased in all groups (control 74%, saline 65%, i.p. lidocaine 57%, i.v. lidocaine 74%). Conclusions. I.V. and i.p. lidocaine blunted systemic vascular responses to carbon dioxide pneumoperitoneum in pigs, but without influencing vasopressin release.