Resistance to Atracurium in Thermally Injured Rats The Roles of Time, Activity, and Pharmacodynamics

Pavlin, Edward G.; Haschke, Richard H.; Marathe, Punit; Slattery, John T.; Howard, Marianne L.; Butler, Stephen

doi:10.1097/00000542-198811000-00010

Cited by 17 publications

(4 citation statements)

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“…16 In the study of Kim et a1.I6 the magnitude of the shift in the dose-response curves to d-TC, however, was lower than that seen clinically. Pavlin et al 29 demonstrated peak resistance to atracurium in rats after a 30% body surface area burn 40 days postburn. N o significant resistance was found at the 10-2 1-day period.…”

Section: Discussionmentioning

confidence: 99%

Burn injury—induced nicotinic acetylcholine receptor changes on muscle membrane

Ward

Martyn

1993

Muscle and Nerve

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Patients with thermal injury show pharmacological responses akin to those seen following denervation of motor nerve where there is an increase in the number of muscle-type acetylcholine receptors (AChR). This study in the rat, examined the effect of 20%, 30%, and 50% body surface area burn injury on gastrocnemius and diaphragm AChR number, quantitated by [125I]alpha-bungarotoxin (alpha-BGT). Pharmacodynamic responses to D-tubocurarine were evaluated in the gastrocnemius muscle. AChR from gastrocnemius muscle were significantly increased in all burn groups at 14 days after burn. After 28 days, the AChR had returned to control in the 20% and 30% burn groups, but persisted in the 50% burn group. AChR from diaphragm did not show significant changes between groups. Resistance to D-tubocurarine was not seen in burn groups compared with controls. Burn trauma causes increases of AChR at sites distant from the area of injury. Diaphragm muscle may be less sensitive than gastrocnemius to mediators which upregulate AChR.

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Section: Discussionmentioning

confidence: 99%

Burn injury—induced nicotinic acetylcholine receptor changes on muscle membrane

Ward

Martyn

1993

Muscle and Nerve

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“…Second, visual inspection showed that rats were less active only during recovery from anesthesia. And third, Pavlin et al 23 found that morning activity of rats was unaffected by a 30% BSA scald at any time up to 4 weeks after injury. Sepsis is also unlikely to be present at 72 h because at this time the eschar had not begun to separate and expose the underlying granulating area and thus still protected the wound from infection.…”

Section: Discussionmentioning

confidence: 97%

“…10,11,29,30 Although one study describes a correlation between dTC resistance and nAChR upregulation after thermal injury in the rat, 10 other investigations have failed to demonstrate such a relationship. 14,23,29 Consequently, the precise contribution of nAChR upregulation to NDNB resistance remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Marathe et al 14 reported no detectable change in nAChR number in rat diaphragm following a 30% BSA scald at 40 days after injury, a time at which their rats had previously exhibited maximal resistance to NDNB. 23 In contrast, Ward and Martyn 29 found that despite a significant increase in nAChR levels in rat gastrocnemius following 30% and 50% BSA scald, the same muscles were not resistant to the effects of dTC in vivo and, in fact, tended to be more sensitive to dTC than were controls. Many other factors could play a role in NDNB resistance after burn, including altered pharmacokinetics and plasma protein binding of dTC, altered affinity of nAChR for dTC, 19 and a decrease in acetylcholinesterase activity.…”

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confidence: 96%

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Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat

et al. 1999

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Atracurium Resistance in a Critically Ill Patient

Tschida,

Hoey,

Nahum

et al. 1995

Pharmacotherapy

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A previously healthy 25‐year‐old man with metastatic testicular teratocarcinoma became resistant to atracurium‐induced neuromuscular blockade as evidenced by train‐of‐four (TOF) monitoring combined with clinical assessment. Subsequently he had an adequate response with a standard dosage of pancuronium. During the first 10 days of neuromuscular blockade, the atracurium requirements escalated from 0.31 to 1.7 mg/kg/hour, guided by TOF monitoring, movement, and spontaneous respirations. The infusion was discontinued but later reinstituted. Despite a total atracurium loading dose of 1.4 mg/kg followed by an infusion rate titrated to 1.7 mg/kg/hour, inadequate paralysis persisted. Atracurium was terminated and an intravenous infusion of pancuronium 0.10 mg/kg/hour was started. Over the next 3 days the pancuronium infusion was titrated down to a range of 0.04‐0.06 mg/kg/hour, followed by a maintenance infusion of 0.01‐0.05 mg/kg/hour for 5 days. A pharmacokinetic alteration, such as increased metabolism or elimination, may have caused the atracurium resistance.

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Resistance to Atracurium in Thermally Injured Rats The Roles of Time, Activity, and Pharmacodynamics

Cited by 17 publications

References 0 publications

Burn injury—induced nicotinic acetylcholine receptor changes on muscle membrane

Burn injury—induced nicotinic acetylcholine receptor changes on muscle membrane

Increased quantal release of acetylcholine at the neuromuscular junction following scald injury in the rat

Atracurium Resistance in a Critically Ill Patient

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