Disease relevance of Pipecurium

• Effects of respiratory and metabolic alkalosis and acidosis on pipecuronium neuromuscular block [1].
• The duration of neuromuscular block following six successive doses of pipecuronium was prolonged 1.4-fold during long-lasting metabolic alkalosis while this parameter was shortened to half of that in control cats during acidosis [1].
• In contrast, (+)tubocurarine and pipecuronium, neuromuscular blocking agents that do not cause tachycardia, did not affect release of NE [2].
• Pharmacokinetics and pharmacodynamics of pipecuronium in patients with cirrhosis [3].
• Electrocardiographic abnormalities were observed in two pipecuronium patients: ST segment depression in one and premature ventricular contractions in another [4].

High impact information on Pipecurium

• Its clearance (0.27 L/h/kg) is intermediate between those of pipecuronium and rapacuronium, but its elimination half-life is long (83 minutes) [5].
• Only pancuronium and pipecuronium potentiated vagally induced bronchoconstriction [6].
• 2. Atropine enhanced, and non-depolarizing muscle relaxants [+)-tubocurarine, pancuronium and pipecuronium) reduced, the release of [3H]-ACh evoked by high frequency trains of stimulation (50 Hz, 40 shocks) of the phrenic nerve [7].
• The pharmacokinetics of pipecuronium bromide have been studied in anesthetized beagle dogs with and without ligated renal pedicles [8].
• Since the total recovery of unaltered pipecuronium approximated 85% of the administered dose in the intact animals, biotransformation seems to play an insignificant role in disposition of this new neuromuscular blocking drug.(ABSTRACT TRUNCATED AT 250 WORDS)[8]

Biological context of Pipecurium

• CONCLUSIONS: Although pipecuronium is an M2 receptor antagonist with no M3 receptor antagonist properties, potentiation of reflex-induced bronchoconstriction is unlikely, because this effect occurred only at doses greater than those used clinically [6].
• There were no changes in cardiac rhythm, heart rate, or blood pressure attributable to pipecuronium during this study [9].
• Heart rate, systolic and diastolic blood pressures, and cardiac output were non-invasively measured during the onset of the neuromuscular blockade and compared to a saline control group to separate the effect of anesthesia from those of pipecuronium [10].
• Clinical pharmacology of pipecuronium bromide [10].
• To test the hypothesis that acetylcholine "spillover" from motor nerves contributes significantly to skeletal muscle vasodilation during exercise, we measured the forearm blood flow responses during attempted handgripping after local paralysis of the forearm with the neuromuscular-blocking drug pipecuronium [11].

Anatomical context of Pipecurium

• Cardiovascular effects of pipecuronium and pancuronium in patients undergoing coronary artery bypass grafting [12].
• The neuromuscular blocking effect of pipecuronium was evaluated by recording of the mechanical twitch of the adductor pollicis muscle in response to stimulation of the ulnar nerve at the wrist [10].
• Under ultrasound guidance, pancuronium or pipecuronium 0.2 mg.kg-1 was injected into the fetal gluteal region [13].
• Pancuronium or pipecuronium were used in a randomised study to temporarily arrest movement in 16 fetuses undergoing intra-uterine procedures [13].
• The effects of pipecuronium bromide (Pi.) and pancuronium bromide (Pa.) on the contractile response of rat-phrenic nerve diaphragm and frog's musculus rectus abdominis preparation were studied [14].

Associations of Pipecurium with other chemical compounds

• Pharmacokinetics and pharmacodynamics of pipecuronium bromide (Arduan) in elderly surgical patients [15].
• Our recovery data also demonstrate that residual neuromuscular blockade due to pipecuronium can easily be antagonized with neostigmine as long as spontaneous recovery of T1- at the time of reversal administration is greater than 13% [16].
• Clinical pharmacology of pipecuronium in infants and children during halothane anesthesia [9].
• For example, the ratio of the fourth to first twitch (T4/T1) of the TOF at 10 and 15 min after reversal was significantly less with doxacurium (59 +/- 14% and 61 +/- 16%, respectively) than with either pancuronium (75 +/- 6% and 75 +/- 10%) or pipecuronium (76 +/- 9% for both).(ABSTRACT TRUNCATED AT 250 WORDS)[17]
• Edrophonium priming alters the course of neuromuscular recovery from a pipecuronium neuromuscular blockade [18].

Gene context of Pipecurium

• Pulmonary function and head lift during spontaneous recovery from pipecuronium neuromuscular block [19].

Analytical, diagnostic and therapeutic context of Pipecurium

• Long-lasting neuromuscular blockade from pipecuronium [20].
• Following an iv bolus injection of 0.1 mg/kg, pipecuronium disappeared from the plasma exponentially with distribution half-lives of 3.9 +/- 1.1 min and 12.7 +/- 9.5 min (mean +/- SD), and elimination half-lives of 44.8 +/- 2.6 min and 196.7 +/- 102.0 min in animals with and without renal pedicle ligation, respectively [8].
• Dose requirements and plasma concentrations of pipecuronium during bilateral renal exclusion and orthotopic liver transplantation in pigs [21].
• Plasma concentrations of pipecuronium were determined by high-pressure liquid chromatography [3].
• Similarly, pipecuronium dosage requirements calculated on the basis of body surface area were significantly less in infants 3-12 mo of age than in children 1-6 yr of age [9].

References