![]() Commonly, hepatobiliary drug secretion is assumed to be the underlying mechanism (enterohepatic reabsorption, EHR), neglecting other possible mechanisms such as gastric secretion (enterogastric reabsorption, EGR). This distribution process is evidenced by multiple peaks in pharmacokinetic profiles. It is reasonable to postulate that the vagal circuit could be compromised at the NTS-DMV synapseĪfter FQ use, possibly leading to the development of permanent GI disorders in FQAD.Įnteric reabsorption occurs when a drug is secreted into the intestinal lumen and reabsorbed into the systemic circulation. Since there is sufficient evidence to suggest that GABA transmission is hindered by FQs, The context of the vagus nerve and examine how these drugs could lead to dysregulated signaling to The purpose of this review is to summarize the current knowledge on FQs in Nucleus of the Tractus Solitarius (NTS) to the Dorsal Motor Nucleus of the vagus (DMV) to tonically ![]() ![]() Nerve, involved in the control of gastrointestinal (GI) function. Preventing the binding of GABA in the central nervous system. Previous studies suggest that FQs act as selective GABAA receptor inhibitors, The FDA has proposed theĮxistence of a permanent disability (Fluoroquinolone Associated Disability FQAD), which is yet toīe formally recognized. Infections, including infections for which their use is discouraged. Fluoroquinolones (FQs) are a broad class of antibiotics typically prescribed for bacterial
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