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 segments of ileum externalized in situ. Plasma epinephrine and norepinephrine levels were measured in animals receiving epidural blockade (0.4 ml/kg lidocaine 1.5%, n = 5) and in control animals given intramuscular lidocaine 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 norepinephrine release from sympathetic nerves in the mesenteric veins was determined by using topical tetrodotoxin (n = 8) and by assessing the effect of topical lidocaine (10 and 100 micrograms/ml, n = 5) administered in the solution bathing the mesentery. RESULTS: Epidural injectate extended from T2 to L5. Plasma epinephrine decreased 68.3 +/- 4.4% (mean +/- SEM) with epidural anesthesia, and norepinephrine was lower after epidural 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 prevented venodilatation by subsequent epidural lidocaine. Topical lidocaine 10 micrograms/kg produced no change in vein diameter, but lidocaine 100 micrograms/ml increased it 3.5 +/- 1.3%. CONCLUSIONS: Splanchnic venodilatation during epidural anesthesia is an active process: a decrease in intravenous pressure concurrent with dilatation indicates that vein wall tension diminished. Significant dilatation with tetrodotoxin and lack of dilatation with subsequent epidural block point to a minor role for changes in circulating catecholamines. A direct effect of lidocaine does not contribute to splanchnic venodilatation except when circulating lidocaine concentrations reach very high levels.
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 segments of ileum externalized in situ. Plasma epinephrine and norepinephrine levels were measured in animals receiving epidural blockade (0.4 ml/kg lidocaine 1.5%, n = 5) and in control animals given intramuscular lidocaine 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 norepinephrine release from sympathetic nerves in the mesenteric veins was determined by using topical tetrodotoxin (n = 8) and by assessing the effect of topical lidocaine (10 and 100 micrograms/ml, n = 5) administered in the solution bathing the mesentery. RESULTS: Epidural injectate extended from T2 to L5. Plasma epinephrine decreased 68.3 +/- 4.4% (mean +/- SEM) with epidural anesthesia, and norepinephrine was lower after epidural 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 prevented venodilatation by subsequent epidural lidocaine. Topical lidocaine 10 micrograms/kg produced no change in vein diameter, but lidocaine 100 micrograms/ml increased it 3.5 +/- 1.3%. CONCLUSIONS: Splanchnic venodilatation during epidural anesthesia is an active process: a decrease in intravenous pressure concurrent with dilatation indicates that vein wall tension diminished. Significant dilatation with tetrodotoxin and lack of dilatation with subsequent epidural block point to a minor role for changes in circulating catecholamines. A direct effect of lidocaine does not contribute to splanchnic venodilatation except when circulating lidocaine concentrations reach very high levels.
Authors: Seung Mo Lim; Mee Ran Shin; Kyung Ho Kang; Hyun Kang; Francis Sahngun Nahm; Baek Hui Kim; Hwa Yong Shin; Young Jin Lim; Sang Chul Lee Journal: Korean J Pain Date: 2012-10-04