ABSTRACT
The nerve block technique guided by ultrasound has been able to accurately block tiny nerves throughout the body in recent years. It has been increasingly used to treat multisystem diseases or analgesia in surgical patients, but the latter accounted for the vast majority of cases. The nonanalgesic effect of nerve blocks is also in wide demand. After searching ultrasound-guided nerve block works on the PubMed database, we systematically summarized the current clinical application of the nerve block technique and the unique role and related mechanism of nerve block in the prevention and treatment of multi-system diseases or symptoms, including disorders of the circulatory and respiratory systems, postoperative cognitive dysfunction, immune function, posttraumatic stress disorder, and postoperative digestive system, to put forward the potential prospective application in future and serve as a reference for future research of nerve block therapy in these diseases mentioned.
ABSTRACT
Background: Neurogenic inflammation caused by sevoflurane may not only limite to the nervous system, but also expand to the respiratory system. The purpose of this study was to investigate the expression changes of transient receptor potential vanilloid 1 (TRPV1), neurokinin A (NKA), neurokinin B (NKB), calcitonin gene related peptide (CGRP) and substance P (SP) in 14, 21 and 42-day-old rats after inhaling 0.4% sevoflurane, in order to evaluate whether the residual sevoflurane be harmful to the respiratory system through neurogenic inflammation. Methods: The anesthetic inhalation device was designed to allow 14, 21 and 42-day-old rats inhale 0.4% sevoflurane, while rats in the control group inhaled 40% O2 for 1h. Rats in the antagonist group inhaled 0.4% sevoflurane or 40% O2 for 1 h after Capsazepine (CPZ) pretreatment. The expression of TRPV1 in lung tissue was detected by western blot, and the expression of NKA, NKB, CGRP and SP in trachea was detected by immunohistochemistry. Results: After inhaling 0.4% sevoflurane, the expression of TRPV1 in lung tissue of 14 and 21-day-old rats was significantly higher than that of the control group, as well as increased the expression of CGRP and SP in the trachea of 14-day-old rats and NKA, NKB, CGRP and SP in the trachea of 21-day-old rats. CPZ pretreatment could antagonize these effects. Conclusion: Residual sevoflurane during resuscitation of inhalation anesthesia could induce neurogenic inflammation by activating TRPV1, which damaged to the developing respiratory system, but has no significant effect on the respiratory system in adulthood.
