In the aftermath of the withdrawal of rapacuro-nium from the market, a paper addressing its effects on respiratory function has been published. In their study, which was performed while rapacuronium was still on the market in the USA, the authors observed statistically significant reductions in peak inspiratory flow rate, peak expiratory flow rate, and dynamic compliance and increases in peak inflating pressure when rapacuronium 1.5 mg/kg was given under steady-state conditions to patients who were already anesthetized, intubated, and ventilated (1C). In five of the 10 patients these changes amounted to more than 25% from baseline and were considered clinically relevant. As rapacuronium is no longer available this has no direct clinical impact. However, while discussing the mechanisms of rapacuronium-induced bronchospasm the authors speculated that differential effects of the drug on several subtypes of muscarinic acetylcholine receptors might be responsible. As raised histamine concentrations were not found in seven patients with rapacuronium-induced bronchospasm in another study (2C), they reckoned that hista-mine release was an unlikely explanation. Referring to the observation that pipecuronium, another non-steroidal muscle relaxant, blocked pilocarpine-stimulated prejunctional M2 receptors in vitro (3E), they suggested that a similar effect might result in rapacuronium-induced bronchospasm. Prejunctional M2 receptors are thought to have a role in negative feedback and inhibition of further acetylcholine release, thereby reducing smooth muscle relaxation. These aspects will need to be taken into account when new substances are considered for clinical
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.