Acute Visceral Pain in Rats: Vagal Nerve Block Compared to Bupivacaine Administered Intramuscularly.

BACKGROUND: Visceral and parietal peritoneum layers have different sensory innervations. Most visceral peritoneum sensory information is conveyed via the vagus nerve to the nucleus of the solitary tract (NTS). We already showed in animal models that intramuscular (i.m.) injection of local anesthetics decreases acute somatic and visceral pain and general inflammation induced by aseptic peritonitis. The goal of the study was to compare the effects of parietal block, i.m. bupivacaine, and vagotomy on spinal cord and NTS stimulation induced by a chemical peritonitis. METHODS: We induced peritonitis in rats using carrageenan and measured cellular activation in spinal cord and NTS under the following conditions, that is, a parietal nerve block with bupivacaine, a chemical right vagotomy, and i.m. microspheres loaded with bupivacaine. Proto-oncogene c-Fos (c-Fos), cluster of differentiation protein 11b (CD11b), and tumor necrosis factor alpha (TNF-α) expression in cord and NTS were studied. RESULTS: c-Fos activation in the cord was inhibited by nerve block 2 hours after peritoneal insult. Vagotomy and i.m. bupivacaine similarly inhibited c-Fos activation in NTS. Forty-eight hours after peritoneal insult, the number of cells expressing CD11b significantly increased in the cord (P = .010). The median difference in the effect of peritonitis compared to control was 30 cells (CI95, 13.5-55). TNF-α colocalized with CD11b. Vagotomy inhibited this microglial activation in the NTS, but not in the cord. This activation was inhibited by i.m. bupivacaine both in cord and in NTS. The median difference in the effect of i.m. bupivacaine added to peritonitis was 29 cells (80% increase) in the cord and 18 cells (75% increase) in the NTS. Our study underlines the role of the vagus nerve in the transmission of an acute visceral pain message and confirmed that systemic bupivacaine prevents noxious stimuli by inhibiting c-Fos and microglia activation. CONCLUSIONS: In rats receiving intraperitoneal carrageenan, i.m. bupivacaine similarly inhibited c-Fos and microglial activation both in cord and in the NTS. Vagal block inhibited activation only in the NTS. Our study underlines the role of the vagus nerve in the transmission of an acute visceral pain message and confirmed that systemic bupivacaine prevents noxious stimuli. This emphasizes the effects of systemic local anesthetics on inflammation and visceral pain.

Parietal Block Using Bupivacaine in the Rat: An Anatomical, Behavioral and Histological Study.

PURPOSE: Animal models of regional anaesthesia are useful for studying the effects of blocks and improve their efficacy. The aim of our experiments was to validate a multi-site paravertebral block in the rat. MATERIAL AND METHODS: Dissection and indigo carmine dye injection were performed in five rats (3 rats were dissected and 2 were dye injected). In other groups (n=7rats/group), after inflammation inductive carrageenan injection in the abdominal wall, bupivacaine or saline was injected laterally to the spinal column at the T5, T10, L1, L4 and S1 level. The efficacy of the block on mechanical nociception was measured using von Frey hairs. In addition, we measured c-Fos immunoreactive nuclei in the cord. RESULTS: The multi-site injection showed a perinervous distribution of the injected solution without intra-thoracic, intra-abdominal or epidural diffusion. Bilateral block with a relatively small volume of bupivacaine (0.5 mL) significantly increased the threshold to mechanical pain as compared to control (p=0.007) and significantly decreased the number of c-Fos immunoreactive nuclei in the posterior horn of the spinal cord (p<0.0001). CONCLUSION: This study shows that a parietal abdominal wall block is easy to perform in the rat. This block allows investigators to explore the mechanisms of action of abdominal parietal wall blocks.

A comparison of different dosages of a continuous preperitoneal infusion and systemic administration of ropivacaine after laparotomy in rats.

INTRODUCTION: To further explain the mechanisms of action involved in the analgesic effect of a local anesthetic wound infusion, we evaluated parietal and visceral sensitivity as well as indices of inflammation after laparotomy and administration of a local anesthetic. Ropivacaine was administered at different dosages by a continuous infusion using a multiholed catheter in the preperitoneal position or systemically in rats. METHODS: Nine groups of rats received 2 injections after laparotomy or sham surgery: (1) a bolus injection (ropivacaine or saline) via a preperitoneal catheter and (2) an IM injection (IM) (ropivacaine or saline). These injections were followed by a continuous infusion (ropivacaine or saline) in the preperitoneal catheter for 24 hours and 1 IM injection every 8 hours. Mechanical and visceral thresholds after stimulation were evaluated 3 times during the 48 hours after surgery. Stimulated production of tumor necrosis factor α, and interleukin 1ß in whole-blood cultures were measured by enzyme-linked immunosorbent assay. The ropivacaine plasma concentration was measured by gas chromatography. RESULTS: Preperitoneal infusion of high doses of ropivacaine and systemic ropivacaine similarly prevented mechanical and visceral sensitivity alterations and led to a better functional recovery. The analgesic effect of systemic administration was associated with an anti-inflammatory effect. CONCLUSION: In the current study, high-dose ropivacaine administered via a preperitoneal infusion or systemic boluses had the same effect on mechanical and visceral sensitivity after laparotomy. Moreover, systemic administration was associated with an anti-inflammatory effect. The merits of the comparable benefit of systemic and high-dose preperitoneal infusion of ropivacaine need to be confirmed with further studies.