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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

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 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.[1]

References

  1. Pre-emptive lidocaine inhibits arterial vasoconstriction but not vasopressin release induced by a carbon dioxide pneumoperitoneum in pigs. Boccara, G., Eliet, J., Pouzeratte, Y., Mann, C., Colson, P. British journal of anaesthesia. (2003) [Pubmed]
 
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