Pancuronium (bromide hydrate)
(Synonyms: NSC 293162) 目录号 : GC47869
An antagonist of muscle-type nAChRs
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Pancuronium is an aminosteroid antagonist of muscle-type nicotinic acetylcholine receptors (nAChRs) with an IC50 value of 14.8 nM using patch clamp electrophysiology in BOSC23 cells expressing mouse nAChRs.1 It acts as a non-depolarizing neuromuscular blocking agent.2 Pancuronium enhances anesthesia induced by isoflurane , reducing immobilization with an ED50 value of 1.62 µg/kg.3
1.Liu, M., and Dilger, J.P.Site selectivity of competitive antagonists for the mouse adult muscle nicotinic acetylcholine receptorMol. Pharmacol.75(1)166-173(2009) 2.Buckett, W.R., Marjoribanks, C.E., Marwick, F.A., et al.The pharmacology of pancuronium bromide (Org.NA97), a new potent steroidal neuromuscular blocking agentBr. J. Pharmacol. Chemother.32(3)671-682(1968) 3.Miyazaki, Y., Sunaga, H., Hobo, S., et al.Pancuronium enhances isoflurane anesthesia in rats via inhibition of cerebral nicotinic acetylcholine receptorsJ. Anesth.30(4)671-676(2016)
| Cas No. | N/A | SDF | |
| 别名 | NSC 293162 | ||
| Canonical SMILES | O=C(C)O[C@H]1[C@@H]([N+]2(C)CCCCC2)C[C@@]3([H])[C@]4([H])CC[C@@]5([H])C[C@H](OC(C)=O)[C@@H]([N+]6(C)CCCCC6)C[C@]5(C)[C@@]4([H])CC[C@@]31C.[Br-].[Br-].O | ||
| 分子式 | C35H60N2O4.2Br [XH2O] | 分子量 | 732.7 |
| 溶解度 | DMF: 5 mg/ml,DMSO: 5 mg/ml,Ethanol: 10 mg/ml,PBS (pH 7.2): 1 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.3648 mL | 6.8241 mL | 13.6482 mL |
| 5 mM | 0.273 mL | 1.3648 mL | 2.7296 mL |
| 10 mM | 0.1365 mL | 0.6824 mL | 1.3648 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Medication Use in the Neonatal Intensive Care Unit and Changes from 2010 to 2018
J Pediatr 2022 Jan;240:66-71.e4.PMID:34481808DOI:10.1016/j.jpeds.2021.08.075.
Objective: To provide up-to-date medication prescribing patterns in US neonatal intensive care units (NICUs) and to examine trends in prescribing patterns over time. Study design: We performed a cohort study of 799 016 infants treated in NICUs managed by the Pediatrix Medical Group from 2010 to 2018. We used 3 different methods to report counts of medication: exposure, courses, and days of use. We defined the change in frequency of medication administration by absolute change and relative change. We examined the Food and Drug Administration (FDA) package insert for each medication to determine whether a medication was labeled for use in infants and used PubMed to search for pharmacokinetics (PK) studies. Results: The most frequently prescribed medications included ampicillin, gentamicin, caffeine citrate, poractant alfa, morphine, vancomycin, furosemide, fentanyl, midazolam, and acetaminophen. Of the top 50 medications used in infants with extremely low birth weight, only 20 (40%) are FDA-labeled for use in infants; of the 30 that are not labeled for use in infants, 13 (43%) had at least 2 published PK studies. The medications with the greatest relative increase in use from 2010 to 2018 included dexmedetomidine, clonidine, rocuronium, levetiracetam, atropine, and diazoxide. The medications with the greatest relative decrease in use included tromethamine acetate, Pancuronium, chloral hydrate, imipenem + cilastatin, and amikacin. Conclusion: Trends of medication use in the NICU change substantially over time. It is imperative to identify changes in medication use in the NICU to better inform further prospective studies.
Chloral hydrate toxicity in a preterm infant
Pediatr Pharmacol (New York) 1984;4(3):161-5.PMID:6493839doi
Ventilator care in premature infants with hyaline membrane disease (HMD) may be complicated by episodes of irritability and "fighting" the respirator, resulting in significant hypoxemia. Neuromuscular blockade with pharmacologic agents such as Pancuronium bromide is frequently used to manage this problem [Crone and Favorito, 1980]. This therapy results in the loss of important clinical signs, such as alterations in muscle tone and spontaneous movements, which are important in monitoring the critically ill newborn. As a result of these considerations, we occasionally have utilized the sedative-hypnotic effects of chloral hydrate to achieve adequate ventilation and oxygenation in these infants. We report, however, a case of a preterm infant who developed severe chloral hydrate toxicity after its administration as an adjunct to the treatment of HMD.
[Intracranial hypertension during status asthmaticus]
Ann Fr Anesth Reanim 1987;6(1):38-41.PMID:3578944DOI:10.1016/s0750-7658(87)80008-4.
In three consecutive patients suffering from life-threatening asthma in a comatose state (mean age: 37 +/- 4 yr; Glasgow coma score: 3; bilateral mydriasis), intracranial pressure was monitored with an extradural transducer set-up a mean of 2 h after the onset of the coma. The aims were to detect intracranial hypertension and to improve its therapy. Basal therapy associated: 1) mechanical ventilation; 2) theophylline 1.5 g X 24 h-1, salbutamol 30 mg X 24 h-1, hydrocortisone 2 g X 24 h-1, Pancuronium 0.5 mg X kg-1 X 24 h-1; 3) pentobarbitone 35 mg X kg-1 X 24 h-1, normal hydration, normothermia and 30 degrees head-up tilt. If the intracranial pressure rose above 15 mmHg, an i.v. bolus of pentobarbitone (5 mg X kg-1) was given if the barbiturate blood level was equal or below 100 micrograms X l-1. In case of failure, a dose of mannitol (20 mg) completed the therapy if blood therapy was equal or below 320 mosm X l-1. All patients developed intracranial hypertension (21, 53 and 23 mmHg, respectively). The intracranial hypertension followed the bronchospasm and disappeared with it. Hypoxaemia, hypercapnia and high peak airway pressures could explain the intracranial hypertension. All patients recovered without sequelae. This data should make us use with great care all treatments likely to increase the intracranial pressure during life-threatening asthma.
Nitric oxide (NO): in vivo electrochemical monitoring in the dorsal horn of the spinal cord of the rat
Brain Res 1997 Oct 31;773(1-2):66-75.PMID:9409706DOI:10.1016/s0006-8993(97)00898-6.
NO synthase (NOS) is largely distributed in the superficial and deep laminae of the dorsal horn as well as in dorsal root ganglion cells. It has been proposed that nitric oxide (NO) participates in the transmission of sustained, and possibly brief, nociceptive, inputs at the spinal level. The aim of this study was to check the ability of in vivo electrochemical monitoring of NO within the dorsal horn of the lumbar spinal cord (L3-L4 level) of chloral hydrate anesthetized or decerebrated spinalized rats. 30 microm diameter and 450 microm length treated carbon fiber electrodes coated with nickel(II) tetrakis (3-methoxy-4-hydroxy-phenyl) porphyrine and NafionR, and associated with differential normal pulse voltammetry, gave a peak of oxidation current around 650 mV (vs. Ag-AgCl) in vitro in NO solutions between 0.125 and 1.25 microM. In vivo, a 650 mV peak appeared which was stable (recording interval 2 min) for up to 3 h (+/-6%). Comparison between in vitro calibration and in vivo voltammograms gave an estimated in vivo extracellular concentration of 0.50 microM. In vivo, peaks decreased by 95% at 90 min and for up to 3 h after an i.p. injection of 100 mg/kg of the NOS inhibitor (NOSI) L-arginine-p-nitroanilide (L-ANA). At the same dose i.p., N(G)-nitro-L-arginine methyl ester (L-NAME) was almost ineffective after 90 min in animals paralyzed with Pancuronium bromate or gallamine trethiodide. However, in non-curarized decerebrated spinalized animals, L-NAME depressed the voltammograms by 36% at 90 min. S-Ethylthiourea (80 mg/kg i.p.), also decreased the voltammograms by 45% at 140 min, and finally, 7-nitroindazole (7-NI, 90 mg/kg i.p), induced a important decrease of the 650 mV peak (23% of control) at 120 min. These results are in agreement with biochemical data showing the decrease of NOS activity within the lumbar spinal cord by L-NAME (45% of control at 90 min) and 7-NI (20% of control at 90 min). The NO donor hydroxylamine (30 mg/kg i.p.) significantly increased the peaks (140% at 90 min), and sodium nitroprusside (SNP, 20 mM) when directly superfused upon the spinal cord (200-300 microl min(-1)) induced a large increase in the peak (300% at 90 min). Moreover, SNP 60 min after L-ANA, or 90 min after L-NAME, rapidly restored the 650 mV peak up to control values. These results demonstrate the validity of electrochemical monitoring of NO within the dorsal horn of the spinal cord. The in vivo electrochemical detection of NO is in progress to study the implication of this messenger in the transmission of nociceptive messages at the spinal level.
[The malignant neuroleptic syndrome and malignant hyperthermia]
Anaesthesist 1989 Apr;38(4):210-3.PMID:2729540doi
We report on a patient with neuroleptic malignant syndrome (NMS) caused by a therapy for endogenous depression. The symptoms were hyperpyrexia (39.2 degrees C), rigidity, elevated creatine kinase (CK: 594 U/l) and coma. After transfer from an outside hospital, he was treated, at first without effect with dantrolene p.o. (80 mg q.i.d.) and i.v. (1 mg/kg-1/h-1). Clinical improvement and temperature reduction were noted when the levels of neuroleptic drugs fell during unspecific intensive care with mechanical ventilation, sedation (flunitrazepam, barbiturates), relaxation (Pancuronium), and hydration. After uncomplicated weaning from the ventilator the patient became more cooperative and was returned to the psychiatric ward. Further treatment took the form of combined drug therapy with biperiden and flunitrazepam and in addition a series of 12 electroconvulsive therapies (ECT). The elevated CK levels initially decreased, serum potassium levels were found to be within normal limits, and myoglobinuria was not detected during the further course. Trigger agents for NMS are antipsychotic drugs such as thioxanthenes, phenothiazines and butyrophenones. Because the signs and symptoms are so similar to those of malignant hyperthermia (MH), it has been suggested that NMS and MH are related diseases. The postulated mechanisms of NMS become apparent in the CNS, whereas those of MH affect the muscle cell itself. An abnormal in vitro contraction test after NMS should suggest to triggering of MH crisis after succinylcholine administration in anaesthesia for ECT.(ABSTRACT TRUNCATED AT 250 WORDS)