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Abstract
The introduction of muscle relaxants into clinical anesthesia 60 years ago has revolutionized our specialty, for reasons that were not entirely obvious at the time. Although the need for drugs that provide unconsciousness and analgesia seems obvious, there is no intuitive reason why an agent causing paralysis of skeletal muscle would be such a great advance. The subsequent popularity of the drugs known as muscle relaxants, more accurately called neuromuscular blocking agents, indicates that anesthesiologists were impressed by their advantages in the clinical setting. Thanks to neuromuscular blocking agents, the dosage of concomitant drugs, and their cardiovascular effects, could be limited, immobility could be guaranteed during difficult surgical procedures, mechanical ventilation could be performed more efficiently, and sicker patients could get the benefit of surgery.
The neuromuscular junction contains three types of nicotinic receptors: two on the muscle surface, one junctional and the other extrajunctional, and a presynaptic receptor on the parasympathetic-nerve ending. On the arrival of a nerve impulse, a burst of molecules of the neurotransmitter acetylcholine is released from the presynaptic nerve ending. Acetylcholine crosses the junctional cleft and stimulates the postsynaptic junctional receptors, allowing ions to flow through them and depolarize the end plate. Acetylcholine is then rapidly broken down by the enzyme acetylcholinesterase, which is present in the junctional cleft.