Neuromuscular Blocking Agents and Carotid Body Oxygen Sensing
Ventilatory depression is the leading cause behind anesthesia related postoperative morbidity and mortality worldwide (Lunnet al., 1983). Residual effects of muscle relaxants and general anesthetics are frequently associated with postoperative ventilatory failure and hypoxia. It is known that the ventilatory response to acute hypoxia is mainly mediated by afferent input from peripheral chemoreceptors of the carotid body and from the aortic arch. However, the mechanism behind oxygen sensing of the carotid bodies is not fully known. Recent studies show that hypoxia may block the leak-type potassium channel inducing a depolarisation of the cell membrane of the type I (glomus) cell. This seems to open voltage-gated calcium channels with an inward flux of calcium that result in a release of excitatory neurotransmitters. The activation of the type 1 cell chemotransmission causes an increased activity in the carotid sinus nerve (CSN) which finally gives rise to an increased ventilation.
KeywordsMuscle Relaxant Carotid Body Peripheral Chemoreceptor Hypoxic Ventilatory Response Carotid Sinus Nerve
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