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Ischemia-reperfusion (I / R) is a complex hemodynamic process that can cause tissue damage through oxidative stress, mitochondrial dysfunction, and inflammatory reactions. It is an important factor leading to poor prognosis in patients, and the exploration of effective prevention and treatment measures is of significant clinical significance. As an endogenous hormone with strong antioxidant and anti-inflammatory properties, Melatonin plays an important role in reducing cell death and improving tissue I / R injury. Therefore, this article reviews the relationship between Melatonin and organ I/R injury in order to provide a theoretical basis for the clinical application of melatonin to alleviate organ I/R injury.
RESUMO
Objective To evaluate the role of GABAA receptors in sevoflurane-induced inhibition of the discharge activities of inspiratory neurons in the medullary respiratory center of neonatal rats.Methods The medulla oblongnta slices of neonatal rats (aged 0-4 days) including the medial region of the nucleus retrofacialis with the hypoglossal nerve rootlets retained were prepared.The slices were perfused with artificial cerebrospinal fluid (ACSF),and the activity of the inspiratory neurons in the medial region of the nucleus retrofacialis and the respiratory rhythmical discharge activity of the hypoglossal nerve rootlets were simultaneously recorded using microelectrodes and suction electrodes,respectively.The ACSF,5％ sevoflurane,GABAA receptor blocker bicuculline 10 μmol/L and combination of 5％ sevoflurane and 10 μmol/L bicuculline were added to the perfusion liquid after the discharge activity was stable.The respiratory cycle (RC),inspiratory time (TI),integral amplitude (IA) and changes in peak frequency (PFn) of the inspiratory neurons were recorded.Results Compared with that after giving ACSF,RC was significantly prolonged,TI was shortened,and IA and PFn were decreased after giving sevoflurane,and RC was significantly shortened,IA and PFn were increased (P＜0.05),and no significant change was found in TI after giving bicuculline (P＞ 0.05).Compared with that after giving sevoflurane,RC was significantly shortened,TI was prolonged,and IA and PFn were increased after giving sevoflurane and bicuculline (P＜ 0.05).Conclusion Sevoflurane inhibits the discharge activities of inspiratory neurons through GABAA receptors in the medullary respiratory center of neonatal rats.
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Objective To investigate the effect of doxapram on inhibition of medullary respiratory center excitability by sevoflurane in rats.Methods Neonatal Sprague-Dawley rats of both sexes,aged 1-4 days,were used in this study.Isolated medulla oblongata-spinal cord specimens were made according to the method described by Suzue and perfused with the artificial cerebrospinal fluid saturated with 95％O2-5％CO2.The specimens were randomly divided into 3 groups ( n =9 each):control group (group C),sevoflurane group (group S) and sevoflurane + doxapram group (group S + D).Respiratory rhythmical discharge activity of the hypoglossal nerve rootlets was recorded using suction electrode.After 10 min of equilibration,the specimens were perfused with the artificial cerebrospinal fluid,5％ sevoflurane and the mixture of 5％ sevoflurane and 5 μmol/L doxapram for 10 min in groups C,S,and S + D respectively.The respiratory cycle,inspiratory time and integral amplitude of inspiratory discharge were recorded.Results Compared with group C,the respiratory cycle was significantly prolonged,the inspiratory time was significantly shortened,and the integral amplitude of inspiratory discharge was significantly decreased in group S (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group S + D (P ＞ 0.05).Compared with group S,the respiratory cycle was significantly shortened,the inspiratory time was significantly prolonged,the integral amplitude of inspiratory discharge was significantly increased in group S + D ( P ＜ 0.05).Conclusion Doxapram antagonizes sevoflurane-induced inhibition of excitability of medullary respiratory center in rats.