Pancuronium mechanism

Furthermore, these allosteric effects were shown to be truly subtype specific, depending on the nature of the allosteric modulating compound. Thus, alcuronium exerts positive copperativity with [3H]NMS at the M2 and M4 but not at the Mi and M3 receptors [26,27], while other neuromuscular junction blockers such as stercuronium, pancuronium, and d-tubocurarine have been shown to exhibit their effects via an allosteric mechanism specifically on the M2 receptors [28-30]. 

Avoid imnecessary stimulation, which may induce rigidity and spasms. The primary treatment for spasms and rigidity is sedation with a benzodiazepine, such as midazolam or diazepam. Additional sedation may be provided with propofol or a phenothiazine, usually chlorpromazine. In severe disease prolonged spasms and respiratory dys-fimction will necessitate tracheal intubation and mechanical ventilation will be required. If the patient has been intubated and sedation alone is inadequate to control spasms, a neuromuscular blocking drug, e.g., intermittent doses of pancuronium or a continuous infusion of atracurium, will be required. 

Cardiovascular adverse effects are minimal with pancuronium. Ganglion blockade does not occur. Shght dose-dependent rises in heart rate, blood pressure, and cardiac output are common (5), but are often masked by the actions of other co-administered agents, such as fentanyl or halothane, which cause bradycardia or hypotension. These adverse effects of pancuronium are thus often beneficial and can be deliberately harnessed. Several mechanisms contribute vagal blockade via selective blockade of cardiac muscarinic receptors (6), release of noradrenaline from adrenergic nerve endings (7), increased blood catecholamine concentrations (8), inhibition of neuronal catecholamine reuptake (9-11), and direct effects on myocardial contractility (12). These have been reviewed (13-15). 

Saxena PR, Bonta IL. Mechanism of selective cardiac vagolytic action of pancuronium bromide. Specific blockade of cardiac muscarinic receptors. Eur J Pharmacol 1970 ... 

In liver disease, increased amounts of D-tubocurarine may be reqnired. In the past it has been suggested that this could be due to reduced synthesis of acetylcholinesterase, or to increased concentrations of gammaglobulins binding the relaxant (14), although this is disputed (15). Similar kinetic mechanisms to those suggested for pancuronium may be involved, but there are no studies on D-tubocurarine. In primary liver cancer in children, resistance to D-tubocurarine (and alcuronium) has been reported (SEDA-13,104) (16). 

As indicated, the principal use of pancuronium bromide is as an adjunct to anesthesia, to induce relaxation of skeletal muscle, but it is al.so used to facilitate the management of patients undergoing mechanical ventilation. Only experienced clinicians equipped with facilities for applying artificial re.spiration should admini.stcr it. and the dosage should be adjusted and controlled carefully. 

Pipecurium Bromide. Pipecurium bromide. 4.4 -(.3a. 17 ihydroxy-5o-androstan-2. l6/5-ylene)bis( 1.1- dimeth-ylpiperazinium)dibromide diacctatc (Arduan). is a nondepolarizing muscle relaxant similar, both chemically and clinically, to pancuronium bromide. It is a long-acting drug indicated as an adjunct to anesthesia and in patients undergoing mechanical ventilation. 

Gut and liver catechol-O-methyltransferase Postganglionic sympathetic nerve terminals Preganglionic S3Tnpathetic nerve terminals Vascular smooth muscle cell receptors A semiconscious patient in the intensive care unit is being artificially ventilated. Random spontaneous respiratory movements are rendering the mechanical ventilation ineffective. A useful dmg to reduce the patient s ineffective spontaneous respiratory activity is (A) Baclofen Dantrolene Pancuronium Pyridostigmine Succinylcholine... 

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