MECHANISM OF MESENTERIC VENODILATATION AFTER EPIDURAL LIDOCAINE IN RABBITS

Citation
Qh. Hogan et al., MECHANISM OF MESENTERIC VENODILATATION AFTER EPIDURAL LIDOCAINE IN RABBITS, Anesthesiology, 81(4), 1994, pp. 939-945
Citations number
27
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
81
Issue
4
Year of publication
1994
Pages
939 - 945
Database
ISI
SICI code
0003-3022(1994)81:4<939:MOMVAE>2.0.ZU;2-6
Abstract
Background: Increased splanchnic venous capacitance has been observed during extensive thoracolumbar epidural anesthesia in rabbits, but the mechanism is not clear. The present study examines the contributions of intravascular pressure changes, catecholamine levels, neural input, and direct effects of lidocaine to mesenteric venodilatation. Methods : Epidural catheters were inserted in rabbits anesthetized with alpha- chloralose. Vein diameter was measured by videomicrography from segmen ts of ileum externalized in situ. Plasma epinephrine and norepinephrin e levels were measured in animals receiving epidural blockade (0.4 ml/ kg lidocaine 1.5%, n = 5) and in control animals given intramuscular l idocaine 15 mg/kg (n = 5). Intraluminal pressure was monitored during the onset of epidural anesthesia (0.4 ml/kg lidocaine 1.0%, n = 9) by a servo-null micropressure technique. The effect of inhibiting norepin ephrine release from sympathetic nerves in the mesenteric veins was de termined by using topical tetrodotoxin (n = 8) and by assessing the ef fect of topical lidocaine (10 and 100 mu g/ml, n = 5) administered in the solution bathing the mesentery. Results: Epidural injectate extend ed from T2 to L5. Plasma epinephrine decreased 68.3 +/- 4.4% (mean +/- SEM) with epidural anesthesia, and norepinephrine was lower after epi dural block than after intramuscular lidocaine (1,868 +/- 290 pg/ml vs . 3,049 +/- 712 pg/ml). Mesenteric vein pressure decreased 35.3 +/- 3. 5% and vein diameter increased 10.2 +/- 3.3% during epidural blockade. Tetrodotoxin caused mesenteric venodilatation (7.6 +/- 2.0%) and prev ented venodilatation by subsequent epidural lidocaine. Topical lidocai ne 10 mu g/kg produced no change in vein diameter, but lidocaine 100 m u g/ml increased it 3.5 +/- 1.3%. Conclusions: Splanchnic venodilatati on during epidural anesthesia is an active process: a decrease in intr avenous pressure concurrent with dilatation indicates that vein wall t ension diminished. Significant dilatation with tetrodotoxin and lack o f dilatation with subsequent epidural block point to a minor role for changes in circulating catecholamines. A direct effect of lidocaine do es not contribute to splanchnic venodilatation except when circulating lidocaine concentrations reach very high levels.