News and Events

Concerns about anaesthesia-related neurological injury in young children have been increasing among parents, health-care providers, and regulatory organisations. These concerns were first prompted by animal studies that showed accelerated apoptosis and neuronal death after exposure to general anaesthetic drugs.

Epidemiological studies showed that isoflurane, a general anesthetic widely used in surgery including those for the children, is associated with impairment of neurodevelopment and neurodegenerative diseases, such as Alzheimer’s disease (AD) and age-related macular degeneration (AMD), which are related to the accumulation of reactive oxygen species (ROS).

As one of the most popular anesthetics, sevoflurane is widely used in pediatric anesthesia. Unfortunately, an increasing number of studies have demonstrated that sevoflurane has potential neurotoxic effects on the developing brain and cognition, even in adolescence. Connexin 43 (Cx43) has been documented to contribute to cognitive dysfunction. The present study hypothesized that Cx43 may participate in sevoflurane-induced neuroinjury and investigated the underlying mechanisms in young Sprague Dawley (SD) rats.

Considerable evidences support the finding that the anesthesia reagent isoflurane increases neuronal cell death in young rats. Recent studies have shown that dexmedetomidine can reduce isoflurane-induced neuronal injury, but the mechanism remains unclear. We investigated whether isoflurane cause neurotoxicity to the central nervous system by regulating the N-methyl-D-aspartate receptor (NMDAR) and excitatory amino acid transporter1 (EAAT1) in young rats. Furthermore, we examined if dexmedetomidine could decrease isoflurane-induced neurotoxicity.

Inhaled anesthetic agents may be neurotoxic to the developing brain of a neonatal rodent. Isoflurane is a commonly used volatile anesthetic agent for maintenance of general anesthesia in various types of surgery. Neonatal exposure to isoflurane has been implicated in long-term neurocognitive dysfunction in children. The mechanisms of isoflurane-induced neurotoxicity have not been fully elucidated. Disruption of gut microbiota is currently attracting considerable interest as a vital pathogeny of some neurologic disorders.

Compelling evidence in animal models that, under some conditions, general anesthetics and sedatives produce changes in the brain and persistent impairments in learning, memory, and behavior. The present review summarizes recent clinical studies investigating whether the use of these agents in children causes similar neurotoxicities.