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Abstract |
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Neurogenic inflammation may participate in postoperative inflammatory pain. We evaluated, in the rat, the influence of a short and prolonged sciatic nerve block on carrageenan-induced inflammation, the time course of which may be compared to postoperative inflammation. A catheter was placed on the right sciatic nerve and injected with 0.5% bupivacaine with epinephrine (0.2 mL): one injection in the Short Block Group, and four injections performed at 90-min intervals in the Prolonged Block Group. In all groups, the two hind paws were then injected with carrageenan. The development of inflammation was evaluated in both hind paws by measurement of paw circumference (PC) before, and 1, 2, 3, 4, 6, and 24 h after carrageenan injection. Temperature of both hind paws was evaluated at the same time points. The vocalization threshold to paw pressure test (VTPP) of both hind paws was evaluated at 6, 8, 10, 12, and 24 h after carrageenan injection. The left hind paw was used for the Control Group. A Sham Group had a catheter placed on the sciatic nerve and injected with normal saline. Inflammation developed in the Control Group with a maximum increase of PC (32%) and temperature (14%) 4 h after carrageenan injection and a maximal reduction of VTPP (44%) at 6 h, reflecting mechanical allodynia. A similar evolution was observed in the Sham Group. In the Short Block Group, the nerve block did not influence the PC, the paw temperature, or the VTPP when compared with the Control Group. In the Prolonged Block Group, when compared with the Control Group, the increased PC was reduced throughout the 24 h (P < 0.0001). The maximal increase in PC at 4 h was limited to 23%, as compared with the precarrageenan value. This effect on PC did not persist at 24 h. Paw temperature was increased (P = 0.07) throughout the study in the Prolonged Block Group, as compared with the Control Group. The VTPP reduction was still limited in the Prolonged Block Group at 24 h, as compared with the Control Group (P < 0.0001). We conclude that a prolonged sciatic nerve block limits carrageenan-induced increase in PC and, subsequently, mechanical allodynia at 24 h in rats.
Implications: Our study has shown that a prolonged (6 h) but not a short sciatic nerve block (90 min) can limit edema and related pain after carrageenan-induced inflammation in rat.
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Introduction |
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Postoperative pain is mainly caused by inflammation secondary to surgical tissue trauma (1). The mechanisms of peripheral inflammation include local liberation of mediators released by the cell lysis (potassium and hydrogen ions, bradykinin, prostaglandins, leukotrienes), the inflammatory cells (histamine, serotonin), or the nerve endings (substance P [SP], calcitonin gene related peptide, neurokinin A) (1).
The vascular changes related to retrograde activation of sensory nerves indicated the concept of neurogenic inflammation (2). In animals, the direct stimulation of C-fibers induces an inflammatory response of the skin (3). However, deafferentation by peripheral nerve section reduces the early phase of inflammation induced by intraarticular kaolin and formalin injection in the rat (4,5), but increases the late phase of the inflammation 24 h after formalin injection (4). Specifically, treatment of peripheral nerve with capsaicin, destroying the C-fibers, reduced the swelling in a limb that was made arthritic in rat (6). However, other results suggest that deafferentation itself induces edema and neutrophil infiltration 10 h after denervation in the rat (7). In animals, few studies have evaluated the effect of a nerve block on peripheral inflammation. A peripheral block limits the local release of SP after heat injury of the rat paw (8). In a recent study, a prolonged sciatic and saphenous nerve block did not reduce edema induced by carrageenan in rats but prevented mechanical allodynia (9). Therefore, little evidence directly supports, in animals, the concept that a nerve block can reduce peripheral inflammation in animals.
Among the various techniques used to control postoperative pain, local anesthetics produce powerful analgesia after spinal, peripheral block, or infiltration (10). Peripheral nerve blocks may, in principle, influence the neurogenic component of inflammation. In humans, inflammation induced by capsaicin (11) or other types of stimuli (12) were not influenced by a nerve block. However, after thermal lesion in humans, a nerve block resulted in a trend toward reduced blister formation (13).
The intraplantar injection of carrageenin is widely used to produce a model of localized inflammatory pain (14–17). Several behavioral and electrophysiological studies have shown that, after an injection of carrageenin, edema rapidly develops, followed by a period of allodynia, which peaks around 4 h after inoculation and lasts 24–96 h (14–17). This evolution can be compared to the time course of postoperative pain. We used this model of carrageenan-induced inflammation in rat: 1) to evaluate the influence of a sciatic nerve block initiated before inflammation on the evolution of edema, allodynia, and paw temperature, and (2) to test, with repeated injections using a catheter placed on the sciatic nerve, whether the duration of the block was important for the effect on inflammation.
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Methods |
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This study was conducted in concordance with the guidelines of the Ethical Standards of the International Association for the Study of Pain (18). Seventy-seven male Sprague-Dawley rats (250–300 g at the beginning of the experiments) were housed in groups of two per cage and allowed free access to food and water with a natural day/night cycle.
In the Short and Prolonged Block Groups, the sciatic nerve of the right hind paw was dissected above its trifurcation under general anesthesia. A catheter, (Vygon epidural catheter 18-gauge; Paris, France) was placed through the gluteal muscles along the sciatic nerve and tunneled under the skin toward the neck of the animal. An injection site was connected to the tip of the catheter and sutured on the back of the animal. To avoid any displacement, the catheter was passed through a piece of plastic sutured on the external face of the gluteal muscles. In all groups, the wound was closed with 3.0 silk sutures of the muscles and the skin.
Bupivacaine 0.5% with epinephrine was used as the local anesthetic, because it is the longest acting drug available in France for nerve block (Marcaine®; Astra Laboratory, Nanterre, France). The volume injected for the block (0.2 mL) was chosen according to previous studies showing that 0.1 mL of local anesthetic solution was sufficient to obtain a transcutaneous sciatic nerve block (19,20). According to a previous study (14), bupivacaine with epinephrine was injected 10 min before carrageenan to obtain anesthesia before induction of inflammation. According to our preliminary experiment on the duration of the block, reinjections were performed via the catheter every 90 min to prolong complete sensory anesthesia in the Prolonged Block Group.
The day after surgery, in the Short Block Group, bupivacaine with epinephrine (0.2 mL) was injected through the catheter and flushed with the appropriate volume of air. In the Prolonged Block Group, the same injection of 0.2 mL of bupivacaine with epinephrine was injected every 90 min for a total of four times. These injections were started 10 min before the carrageenan injection in both hind paws. During the experiment, the block was considered complete when the rat dragged the right hind paw.
In the Sham Groups used for edema, temperature, and nociceptive threshold measurements, a catheter was placed on the right sciatic nerve and injected four times with normal saline (0.2 mL every 90 min.).
Carrageenan was prepared 24 h before each experiment (0.2 mL of 1% solution of lambda carrageenan in saline) and was injected subcutaneously in the rats’ plantar hind paw. Injections were performed in nonanesthetized animals with a 25-gauge needle.
To evaluate the edema, we used a technique previously described (14,21). The paw circumference (PC) was measured by a thread, to the nearest mm, at the metatarsal level. The animals were placed in a plastic cylinder (20 x 30 cm), and the tail and the paw were pulled through a hole at the base of the cylinder; the PC was then measured.
The nociceptive threshold was evaluated with the vocalization threshold to paw pressure test (VTPP), using the Basile analgesimeter (Ugo Basile, Camerio, Italy) (14,22). The tested paw was placed under a pressure pad, the probe being applied to the dorsal part of the paw (tip diameter of the pusher: 1 mm). The weight, in grams, applied to the paw was increased at a constant rate, until an audible squeak was elicited. The choice of a cut-off value of 600 g was necessary to limit the injury of the paw (unpublished data). This cut-off value was considered sufficient to represent anesthesia of the paw.
The paw temperature was evaluated with a thermocouple thermometer, as previously described (14). A stable value of the paw temperature was obtained in all cases within 10 to 15 s.
In all experiments, the carrageenan injection time was considered time zero. In all experiments, animals were evaluated for both hind paws, before carrageenan injection to obtain a precarrageenan control value of PC, paw temperature, and VTPP. In all experiments, the left hind paw was used as a control.
In preliminary experiments, we evaluated the duration of sensory anesthesia obtained with our catheter. A catheter was placed on the right sciatic nerve of the rats, as described previously (n = 6). Four hours after carrageenan injection, in both hind paws, 0.2 mL of 0.5% bupivacaine with epinephrine was injected in the catheter, and the VTPP of both hind paws was measured every 10 min after sciatic nerve block until return to control value.
These six animals used in the preliminary experiments were killed 48 h after the placement of the catheter, and the sciatic nerve was exposed on both sides. No macroscopic signs of inflammation were detected on or near the sciatic nerve.
We used nerve section of both sciatic and saphenous nerves to validate the sensitivity of our tests for evaluating edema and paw temperature. In 16 rats, the sciatic and saphenous nerves were cut before the injection of carrageenan in the right hind paw. The PC and the temperature were measured before, and 1, 2, 3, 4, 6, and 24 h after carrageenan injection.
In the main experiment, the animals were distributed in three groups: Short Block Group (n = 17), Prolonged Block Group (n = 17), and Sham Group (n = 6). The left hind paw was used for the Control Group (n = 40). The measurements of PC were performed at 1, 2, 3, 4, 6, and 24 h.
Temperature and VTPP were evaluated in another experiment (Short Block Group, n = 6; Prolonged Block Group, n = 5; Sham Group, n = 4). The left hind paw was used for the Control Group (n = 15). Temperature measurements were performed at 1, 2, 3, 4, 6, and 24 h. Because the nerve block did not allow nociceptive threshold measurement before 6 h, the VTPP was evaluated at 6, 8, 10, 12, and 24 h.
Data are expressed in millimeters (mm) for the PC, degrees Celsius for paw temperature, and grams (gr) for VTPP. All values are expressed as mean ± SEM. Comparisons among the groups throughout the study were performed with analysis of variance for repeated measures on all measurements obtained during the 24 h of the study and post hoc analysis using the Fisher’s protected least squares difference test (Fisher’s PLSD test). For differences at a particular time between groups, we used Student’s t-test with a Bonferonni correction in case of multiple comparison (
divided by the number of comparison). P < 0.05 was considered significant.
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Results |
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After one injection of bupivacaine with epinephrine in the sciatic catheter, total anesthesia (i.e., VTPP above the cut-off value of 600 g) appeared in all cases within 10 min (min.) and had a duration of 100 ± 10 min.
The nerve section significantly reduced the maximum increase in PC compared with the Control Group; a significant limitation of PC increase persisted at 24 h. The nerve section increased the VTPP to the cut-off value of 600 g and increased the temperature of the paw compared with the Control Group (data not shown).
As previously described (14,23), the PC increase in the Control Group was maximum at 4 h, stable at 6 h, and started to decrease at 24 h. Ccompared with the precarrageenan value, the maximal increase of PC in the Control Group at 4 h was 32% (37.7 ± 0.5 vs 28.5 ± 0.3 mm) (Figure 1). In the Control Group, the VTPP decreased to a minimum at 6 h then increased slightly until 24 h (Figure 2). As compared with the precarrageenan value, the maximum VTPP decrease at 6 h was 44% (162 ± 3 vs 291 ± 3 g), and at 24 h the decrease was still 36% (188 ± 4 vs 291 ± 3 g). In the Control Group, the temperature increased to a maximum at 4 h, then returned to control value at 24 h (Figure 3). Compared with the precarrageenan value, the maximal increase in temperature at 4 h was 14% (33.5 ± 0.3 vs 29.4 ± 0.4°C). No difference appeared in the Sham Group compared with the Control Group for PC, VTPP, or paw temperature throughout the study (PC: P = 0.26, VTPP: P = 0.73; temperature: P = 0.37) (Figures 1, 2, and 3).
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In the Short Block Group, the course of PC and VTPP throughout the 24 h of the study was not different compared with the Control Group (P = 0.18 and P = 0.83, respectively, Figures 1 and 2). The maximal increase of PC in the Short Block Group at 4 h was 33% compared with the precarrageenan value (37.8 ± 0.6 vs 28.4 ± 0.4 mm) (Figure 1). In the Short Block Group, the maximal decrease of VTPP at 6 h was 43% compared with the precarrageenan value (168 ± 9 vs 295 ± 7 g). This reduction of the VTPP was still 38% at 24 h (183 ± 6 vs 295 ± 7 g). In the Short Block Group, after the initial increase at 1 h, the temperature was stable at 2 h and similar to that in the Control Group. It increased again to a maximal increase at 3 h of 14% compared with the precarrageenan value (33.8 ± 0.4 vs 29.1 ± 0.7°C) and returned to precarrageenan value at 24 h. Throughout the study, the increase in paw temperature was not different in the Short Block and the Control Groups (P = 0.34).
In the Prolonged Block Group, the PC increase was limited throughout the study compared with the Control and the Short Block Groups (P < 0.0001 and P = 0.004, respectively) (Figure 1). The first significant difference between the Prolonged Block and Control Groups appeared at 3 h (P = 0.0013). The maximal increase of PC in the Prolonged Block Group at 4 h was 23% when compared with the precarrageenan value (35 ± 0.6 vs 28.4 ± 0.3 mm) (Figure 1). At 24 h, the PC was similar to that in the Control Group (P = 0.20).
In the Prolonged Block Group, after the initial increase of the VTPP at 6 h caused by the persistent effect of the block, the VTPP decreased progressively with a maximal reduction of 21% at 24 h compared with the precarrageenan value. Throughout the study, the decrease of the VTPP was less important in the Prolonged Block Group than in the Control and Short Block Groups (P < 0.0001 for both Groups). At 24 h, the VTPP was still higher in the Prolonged Block Group compared with the Control and Short Block Groups (231 ± 8 vs 188 ± 4 and 183 ± 6 g; P < 0.0001 for both Groups) (Figure 2).
In the Prolonged Block Group, after the rapid increase of temperature at 1 h, the temperature continued to increase with a maximal increase at 3 h of 13% compared with the precarrageenan value (33.8 ± 0.4 vs 29.1 ± 0.7°C) and a return to precarrageenan value at 24 h. Throughout the study, increase in temperature was similar in the Prolonged Block and in the Control Group (P = 0.07)
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study describes a significant limitation of carrageenan-induced edema in rats, related to a peripheral nerve block when this block is prolonged. This antiinflammatory effect is associated with a persistent analgesic effect of the prolonged block.
The first result of our study is the duration-dependent antiinflammatory effect of a nerve block on carrageenan-induced edema. We observed that a short nerve block does not influence the development of edema, although the same nerve block prolonged for at least six hours can reduce edema. Few studies have evaluated the effect of a nerve block on the development of peripheral inflammation. In a study using thermal injury to the rat paw, a nerve block reduced the peripheral liberation of SP (8). In a recent study using tonicaine, a transcutaneous sciatic and saphenous nerve block (duration 11.2 ± 1.2 h), did not influence edema but abolished hyperalgesia induced by carrageenan (9). In this study (9), the nerve block was performed with another technique (transcutaneous approach versus our catheter technique), used another local anesthetic (bupivacaine with epinephrine versus tonicaine) and the number of animals per group was less than in the present study. Interestingly in this recent report (9), the PC value (mean ± SD) at three and five hours postcarrageenan was 35.4 ± 1.6 and 38.6 ± 1.3 mm, respectively, in the nerve block group compared with 39.1 ± 2.1 and 41.0 ± 1.6 mm, respectively, in the control group. Although not significantly different, these results may represent a trend toward reduction in edema in the nerve block group, which did not appear as a result of the small number of animals per group. Therefore, our study is the first one to suggest an antiinflammatory effect of a peripheral nerve block in animals. In humans, a nerve block was ineffective in limiting the development of inflammation after capsaicin injection (11) or thermal lesion (13). However, a trend toward reduced blister formation induced by thermal lesioning was observed after nerve block (13).
Our study design can exclude the bias of the systemic effect of local anesthetic, because the control value was obtained on the contralateral paw of the animal. The direct antiinflammatory effect of bupivacaine can be reasonably excluded, because the site of injection was far from the inflamed distal hind paw. The nonspecific effect of the catheter and the injection on the evolution of inflammation is also excluded by the Sham Groups. Therefore, the observed antiinflammatory effect may be caused by the direct effect of bupivacaine with epinephrine on neuronal efferent and/or afferent activity responsible of neurogenic inflammation. We cannot define which type of nerve fibers should be blocked to obtained this antiinflammatory effect.
The effect on paw temperature suggests that the prolonged block is responsible for a vasodilation by a sympatholytic effect. A trend toward increased temperature throughout the study in the Prolonged Block Group appeared when compared with the Control Group. Therefore, it seems that the nerve block is responsible for a sympatholytic effect, which may participate in the effect observed on peripheral edema, as previously suggested in other animal model (24).
According to our results, the duration of the block seems important to successfully induce this antiinflammatory effect. We cannot be certain that six hours of nerve block is the critical duration necessary to limit peripheral inflammation, but we observed that a short block (i.e., 100 minutes of sensory anesthesia) did not limit the peripheral inflammation. The limited contribution of neurogenic mechanisms to the development of peripheral inflammation probably requires a prolonged interruption of neuronal efferent activity to obtain a detectable effect. Alternatively, one can hypothesize that the observed effect on edema may involve more complicated mechanisms, involving afferent nociceptor activity and subsequent spinally mediated effects (25).
We observed our second result, the persistent analgesia, 24 hours after carrageenan injection in the Prolonged Block Group. Because we evaluated the pain threshold for 18 hours after the end of the prolonged block, this analgesia is not totally related to a persistent local anesthetic effect, but rather to other peripheral and/or central mechanisms. The antiinflammatory effect observed for the first six hours may persist beyond the end of the block and reduce nociceptive inputs. However, we did not evaluate the edema from 6 to 24 hours, and the edema may be comparable during this period to that observed in the Control Group. Edema can be dissociated from nociception, because at 24 hours, when significant analgesia is still present in the Prolonged Block Group, there was no persistent reduction of edema. Spinally mediated mechanisms may therefore participate in both the antiinflammatory and persistent analgesic effects observed after the prolonged block. It was recently observed that a prolonged block (12–16 hours) may abolish long-lasting mechanical allodynia but have no detectable effect on edema (9). We did not observe a total prevention of allodynia, because our block was probably not long enough to cover the period of intense nociceptive input responsible for central hypersensitivity (25). However, our study suggests that the limitation of allodynia by a prolonged block may be a result of both the antiinflammatory effect and the limitation of central sensitization.
This experiment suggests that when a peripheral nerve block in the rat is prolonged for at least 6 hours, the development of peripheral inflammation and subsequent mechanical allodynia may be decreased.
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Footnotes |
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Presented in part at the congress of the European Society of Anesthesiology Lausanne, 1997, and the Congress of the Société Francaise d’Anesthésie Réanimation, Paris, France, 1997.
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