| Objective: The pain has been attached importance by more and morepeople, due to its etiology is complex, high incidence rate, the cure is difficult.Pain medicine research and development has continued for a long time.Research shows that, urgent and chronic pain can cause psychological,physiological, genetic variation, This change is not only affecting the outcomeof pain, but amplifying pain responses, changing in behavior and mood. Thetheory of pain has been converted from biomedical model to bio-psycho-socialmedical mode.The pain has been identified as the result of the interaction ofbiology and psychology［1］。On the experience of pain, fear, social environmentas well as the memory of the past, work, psychological activities would be onnociceptive stimulation caused a strong reaction. The chest pain is defined asthe Intercostal percutaneous area persistent or recurring pain, lasting for atleast2months or so［2］。The patients had severe chest pain, especially in theinspiratory,it could make patients dare not to breathe hardly, a rapid shallowbreathing, hypoxia and hypercapnia, respiratory acidosis in formation。Thepain is consistented with the rib or intercostal space anatomic walking.Thenerves come from the spinal cord, divided into before root and after root,confluent originally consisting of the intercostal nerve, the pain is not a typicalintercostal neuralgia when the previous section damage generated,should becalled the segmental nerve pain, the two are very similar clinical symptoms.The majority of scholars discoveried after the research that the most importantfactors the pathophysiology of intercostals nerve pathological damagecaused by the neuropathic pain［3］。For neuropathic pain research has beencontinued for many years, definition has been modified, InternationalAssociation for the study of pain (IASP) is defined as the new to neuropathicpain:"the neuropathic pain is due to somatosensory system injury or disease caused by the pain"[4]. Neuropathic pain clinical featuresincluded:1.Spontaneous pain;2.Allodynia;3. Hyperalg esia;4. Abnormalfeeling. Neuropathic pain is mostly accompanied by long time pain, even inthe recovery of injured, allodynia is still feelling for long time existence.Neuropathic pain produced by peripheral mechanism mainly include:1.Afferent neurons occurring ectopic impulse: Noxious stimulation changed avariety of material expression on the peripheral nociceptors, afferent axons,corresponding dorsal root ganglia (DRG) neuron cell bodies, resulting inectopic discharge phenomenon. In these factors, the voltage-gated ion channelexpression change on sensory neurons is the main reason of ectopicimpulse[5]。The scholars have found through research the voltage-gated sodiumchannels increased expression in neuropathic pain states[6]。2. Non synapticconnections between the damaged fibers: Nerve fibers can occurdemyelination when the peripheral nerve damaged, electrical insulationdecreased resulted in a signal abnormal conduction.3. Sympathetic nerveinvolvement role:The sympathetic nerve can be substantial release ofnorepinephrine when peripheral nerve damaged,the norepinephrine is bindingwith the dorsal root ganglion (DRG) neurons and axons receptor,and isactivation function. Long bud phenomenon occurred in sympathetic nerveendings,it is formed of multiple synaptic contacts with impaired afferentaxons[7].4. The damaged nerve endings nociceptor excitability improves.Neuropathic pain should be abirrited early. At present, it is used ofmultimodal abirrite method On the clinical, Advocate a variety of drugs, theapplication of mixed methods,as well as the multiple mechanisms of differentanalgesic measures or multiple mechanisms of action of the differentcombination of analgesic drugs are applicated,in order to the adverse reactionsdecrease to the minimum, to achieve better analgesic effect, this represents theclinical analgesic technology latest development direction。Through multiplemode combined application,it bated of peripheral pain signals, also weakenedcentral nervous system receives the pain signals. Nerve regional anesthesia isa relatively common clinical analgesic method,and it is more often used in multimodal analgesia. Nerve block is a regional anesthesia method, alsoknown as conduction anesthesia or conduction block,as local anesthetic isinjected analytes to neural stem (plexus) side, blocking nerve conductionactivity temporaryly,coming into being analgesic effect[8]. For thoracic surgery,research focuses on the thoracic trauma and after thoracotomy chest paincaused by topical analgesic therapy. Intercostal nerve block method because ofits accurate positioning, analgesia precise, convenient operation, small sideeffects, has become one of the important measures to provide effectiveanalgesia to patients with chest pain. Research shows that the intercostal nerveblock can achieve a satisfactory analgesic effect. The principle is that localanesthetic blockade of the nerve cell membrane of sodium ion channels toopen, so that the intercostal nerve fiber conduction part or all blocked, causingpain to reduce or even disappear[9], so that patients can effectively breathingand coughing, early functional exercise, avoid the occurrence of pneumonia,atelectasis, thrombosis of the lower limbs and a series of complications.the compound lidocaine hydrochloride, because of the role offast, wide dispersion, penetrating power, no obvious dilation of bloodvessels characteristics have been increasingly used in clinical. Compoundlidocaine hydrochloride for chest pain on analgesic effect of intercostal nerveblock and whether the normal neural tissue effects still need further research.This experiment selects the internationally recognized pain research fieldclassic chronic constriction injury of the sciatic nerve model (CCI). Throughthe comparison of compound lidocaine hydrochloride, bupivacaine, lidocainehydrochloride injection in rat sciatic nerve chronic constriction injury (chronicconstriction injury CCI) model mechanical and thermal pain threshold and theeffect of pain behavior in the therapeutic effect of compound lidocainehydrochloride and effect of the normal nerve tissue, intercostal nerve blockanalgesia clinical application.Methods: Healthy adult male Wister rats preparation of animal model ofCCI were successful20cases, CCI group were randomly divided into A: thephysiological saline group (n=5), B: compound lidocaine hydrochloride group (n=5), C: bupivacaine hydrochloride group (n=5), D: lidocaine hydrochloridegroup (n=5), CCI group all groups were in the sciatic nerve by injection ofsaline(0.6ml), compound lidocaine hydrochloride(0.7ml), bupivacainehydrochloride (0.5%bupivacaine hydrochloride0.4ml), lidocainehydrochloride(1%lidocaine hydrochloride0.5ml), respectively in the prior toadministration after administration of1H,1H,8h,12h,24h,48h,72h,120h,192h,240h rat paw withdrawal reflex threshold to mechanicalstimula-tion (mechanical withdrawal threshold, MWT) and the thermalshrinkage leg reflex latency (thermal withdraw latency, TWL) and motorfunction, motor function was graded and adverse reactions were recorded.After the administration of tenth days,it put the rats to death, acquisition ofrats with lateral sciatic nerve specimens, HE staining, use Estebe scoringmethods for sciatic nerve histological grading score.Result: Sciatic nerve by injection of compound lidocaine hydrochloridesciatic nerve block effect is better than that of bupivacaine hydrochloride andlidocaine hydrochloride:1. MWT and TWL results show: Compound lidocainehydrochloride, bupivacaine, lidocaine hydrochloride injection by sciaticnerve, MWT and TWL value in the1h after injection were significantlyprolonged (P <0.05), comparing with saline group,and no significantdifference between the three groups (P>0.05). Effect of compound lidocainehydrochloride group significantly extend block, comparing with bupivacainehydrochloride group and lidocaine hydrochloride group. MWT weresignificantly prolonged (P <0.05) after administration to120h,comparingwith saline group, TWL was significantly prolonged (p <0.05)afteradministration to192h comparing with saline group；and the block effect oflidocaine hydrochloride is reduced after the administration of12h block,it hadno significant difference to the24h compared with saline group(p>0.05)；Bupivacaine hydrochloride group declined after administration of24h,it hadno significant difference to48h compared with saline group(p>0.05).2.Animal movement function evaluation results show that compound lidocainehydrochloride, bupivacaine, lidocaine hydrochloride group show different degrees of motor dysfunction, the motor scores has significant differences,compound lidocaine hydrochloride group in192h, bupivacaine hydrochloridegroup in12h, lidocaine hydrochloride group within the8h,compared withsaline group and befort the injection(P <0.05),but the three groups of ratsmotor function can be completely restored.3. Nerve tissue pathologyevaluation results show, that four groups of rats are not obvious pathologicalchanges of the sciatic nerve, nerve histological grading score between twogroups shows no significant difference (P>0.05),and it clues to that the threedrugs were not caused by organic damage to nerve tissue.Conclusion: the comparison of sciatic nerve block by Sciatic nerveinjection:it can play a role of nerve blocks,that compound lidocainehydrochloride, bupivacaine, lidocaine hydrochloride injected by sciatic nerve,comparing with three kinds of anesthetics, three kinds of drugs acting atessentially the same time, but the compound lidocaine hydrochloride than theother two kinds of drugs at block time is significantly longer (up to192h-240h), bupivacaine hydrochloride lidocaine block time secondly,lidocaine hydrochloride has the shortest time. The three drugs can producenerve block resulted and result in motor dysfunction, but may be recovered.The three drugs showed no obvious pathological changes of the sciatic nerve.So the compound lidocaine hydrochloride is a rapid onset of action, longacting time, safe and effective anesthetic drugs, can be used for chest pain ofintercostal nerve block analgesia therapy. |
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