Background
Neurogenic inflammation caused by sevoflurane may not only limite to the nervous system, but also expand to the respiratory system. The
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.
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.