Halothane
(Synonyms: 氟烷) 目录号 : GC63001
Halothane (Narcotane) is a general inhalation anesthetic used for induction and maintenance of general anesthesia.
Cas No.:151-67-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Halothane (Narcotane) is a general inhalation anesthetic used for induction and maintenance of general anesthesia.
| Cas No. | 151-67-7 | SDF | |
| 别名 | 氟烷 | ||
| 分子式 | C2HBrClF3 | 分子量 | 197.38 |
| 溶解度 | : ≥ 50 mg/mL (253.32 mM) | 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 | 5.0664 mL | 25.3318 mL | 50.6637 mL |
| 5 mM | 1.0133 mL | 5.0664 mL | 10.1327 mL |
| 10 mM | 0.5066 mL | 2.5332 mL | 5.0664 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。
Mechanisms of Halothane toxicity: novel insights
Pharmacol Ther 1993;58(2):133-55.PMID:8415876DOI:10.1016/0163-7258(93)90047-h.
Exposure of individuals to Halothane causes, in 20% of patients, a mild form of hepatotoxicity. In contrast, a very small subset of individuals only develops Halothane hepatitis, which is thought to have an immunological basis. Sera of Halothane hepatitis patients contain antibodies directed against some discrete liver trifluoroacetyl (TFA)-protein adducts, which arise upon oxidative biotransformation of Halothane and include protein disulfide isomerase, microsomal carboxylesterase, calreticulin, ERp72, GRP 78 and ERp99. No immune response occurs in the majority of human individuals, although evidence suggests that TFA-protein adducts arise in all halothane-exposed individuals. The lack of immunological responsiveness of individuals might be due to tolerance, induced by a presumed repertoire of self-peptides that molecularly mimic TFA-protein adducts. Thus, constitutively expressed proteins of 52 and 64 kDa have been identified that confer molecular mimicry of TFA-protein adducts. The 64 kDa protein corresponds to the E2 subunit of the mitochondrial pyruvate dehydrogenase complex. Lipoic acid, the prosthetic group of the E2 subunit, is involved in the molecular mimicry process. A fraction of Halothane hepatitis patients exhibit irregularities in the expression levels of the 52 kDa protein and the E2 subunit protein. Molecular mimicry of TFA-protein adducts by the 52 kDa protein and the E2 subunit protein might play a role in the susceptibility of individuals to development of Halothane hepatitis.
Absorption, biotransformation, and storage of Halothane
Environ Health Perspect 1977 Dec;21:165-9.PMID:348455DOI:10.1289/ehp.7721165.
Current knowledge of the quantitative aspects of biotransformation of Halothane and the fate of its metabolites are reviewed. Absorbed quantities of the inhalation anesthetic average 12.7 and 18 g during 1 and 2 hr, respectively, of anesthesia. Reported fractions of Halothane recovered as urinary metabolites range from 10 to 25%. An analysis of reports of bromide ion accumulation in plasma during and following anesthesia suggests that metabolism of Halothane continues for 20-40 hr after exposure and that 22-24% of absorbed Halothane is metabolized following 8 hr of anesthesia. Half-times for excretion of trifluoroacetic acid (TFA), a principal urinary metabolite of Halothane, tend to confirm that biotransformation proceeds for 2 to 3 days following exposure. Other urinary metabolites which occur in small amounts include a dehydrofluorinated metabolite of Halothane conjugated with L-cysteine and N-trifluoroacetyl-n-ethanolamine, both of which are evidence of the occurrence of reactive intermediates during the metabolism of Halothane. Support for free radical formation has come from in vivo and in vitro demonstrations of stimulation of lipoperoxidation of polyenoic fatty acids by Halothane. Irreversible binding of Halothane metabolites to microsomal proteins and phospholipids has been shown to depend on the microsomal P-450 cytochrome system. Irreversible binding is increased by microsomal enzyme induction and by anaerobic conditions. Hypoxia increases irreversible binding to phospholipids, augments the release of inorganic fluoride and is followed by centrilobular hepatic necrosis. It is concluded that one-fourth to one-half of Halothane undergoes biotransformation in man. One fraction is excreted as trifluoroacetic acid, chloride and bromide. A second fraction is irreversibly bound to hepatic proteins and lipids. Under anaerobic conditions fluoride is released, binding to phospholipids is increased, and hepatic necrosis may occur.
[Is Halothane obsolete? An illustration of measurement with two standards]
Anaesthesist 1987 Jul;36(7):315-20.PMID:3310723doi
In 1986 the discussion on the further use of Halothane broke out anew, especially after the Bristol symposium and the European Congress of Anesthesiology in Vienna. Everywhere there is great uncertainty on whether or not Halothane should continue to be used. A critical analysis of the literature shows that there are two standards applied to Halothane. When judged by the same stringent criteria as Halothane other anesthetic techniques are also dubious, e.g. neuroleptanesthesia or epidural block. Finally, experience with isoflurane, the strongest rival of Halothane, is not adequate to warrant abandoning Halothane, especially as long as the question of coronary steal is still open. At present there is no solid scientific basis for vanishing Halothane.
Current concept of Halothane hepatitis (review)
In Vivo 1987 May-Jun;1(3):163-6.PMID:2979781doi
Clinically, Halothane is still a useful volatile anesthetic, but since many cases of liver disorders considered attributable to Halothane have been reported up to date, a number of studies have been made on the etiology and mechanism of Halothane hepatitis. There are at least two possible mechanisms of Halothane hepatitis; the first is the direct toxic reaction associated with free radical that is related to reductive pathway enhanced by hypoxia, and the other is the immune--mediated reaction in which the antigen is associated with the oxidative and/or reductive route. However, the etiology and mechanism of Halothane hepatitis have yet to be elucidated, and clinically there is no obvious evidence that Halothane can induce hepatic disorders. We have concluded at present that the use of Halothane should be avoided in patients with liver disorders, in patients under long-term administration of drugs that may induce enzymes involved in Halothane metabolism, in patients with high allergic sensitivity, and in patients undergoing operations in which liver circulation is reduced.
Measurement of Halothane by ultraviolet spectroscopy
Anesth Analg 1980 Jul;59(7):481-3.PMID:7190783doi
Halothane absorbs strongly in the ultraviolet region of the spectrum. This property has been employed to measure the concentration of Halothane in samples in which the effect of Halothane on enzyme kinetics was being studied. Halothane can be completely extracted into heptane, displays a concentration-dependent linear increase in absorbance over a broad concentration range, and has a molar extinction coefficient of 447 M cm-1 at 208 nm. The procedure described for the measurement of Halothane will enable other investigators who do not have a gas chromatograph to measure the concentration of Halothane.