Histamine H1 receptor; Histamine H2 receptor

体外活性：组胺 (10 μM) 在牛肾上腺嗜铬细胞中产生更大的肌醇单磷酸积累。组胺 (10 μM) 会刺激牛肾上腺嗜铬细胞中含有 InsP3 的组分的放射性水平。组胺 (100 μM) 刺激掺入含有 InsP3 的洗出液的程度低于血管紧张素 I1 和缓激肽。

磷酸组胺 (0.025 mg/kg) 可使狗的基底血流量平均增加 145% 的对照组。当静脉注射并用电磁流量传感器测量时，磷酸组胺会显着增加狗的基底血流量并降低股动脉血压。磷酸组胺 (4 μg/kg) 导致未麻醉绵羊的淋巴流量从 6.0 增加到 27.0 (SEM) ml/h。磷酸组胺 (4 μg/kg) 还会导致未麻醉羊的肺水、肺血管阻力、动脉 PCO2、pH 和血细胞比容增加，以及心输出量和动脉 PO2 减少。磷酸组胺（8.3 mg/kg/min）不会导致麻醉开胸犬的肺淋巴流量（QL）或蛋白质浓度（CL）发生显着变化，但四氧嘧啶后两者均有所增加。磷酸组胺 (8.3 mg/kg/min) 也不会导致麻醉开胸犬的肺毛细血管膜滤过系数 (Kf) 和最大毛细血管压力 (PCritic) 发生显着变化。磷酸组胺（50 mg/kg）使未麻醉的完整大鼠的酸分泌显着增加，但胃蛋白酶的输出保持不变。磷酸组胺 (50 mg/kg) 可最大程度地刺激胃酸分泌，并且对未麻醉的完整大鼠无毒性作用。

组胺、缓激肽和血管紧张素II刺激肾上腺髓质释放儿茶酚胺。在这里，我们使用培养的牛肾上腺嗜铬细胞表明，这些激动剂以及卡巴胆碱（含六甲铵）刺激肌醇磷酸盐的产生。组胺反应对美吡拉敏敏感，暗示H1受体，而缓激肽的EC50低于Met-Lys缓激肽，[Des-Arg9]-缓激肽相对无活性，暗示BK-2受体。测量了锂存在下形成的总肌醇磷酸盐，组胺的反应最大。评估了嗜铬细胞和非嗜铬细胞在反应中的相对贡献。在每种情况下，发现嗜铬细胞对激动剂有反应；在组胺的情况下，反应仅发生在嗜铬细胞上。当在Dowex阴离子交换柱上分离不含锂的情况下积累超过2或5分钟的肌醇磷酸盐时，缓激肽对肌醇三磷酸部分的刺激最大，而组胺则积累了更大的肌醇一磷酸。刺激2分钟后，刺激肌醇三磷酸异构体分解，每种情况下存在的主要异构体都是肌醇1,3,4-三磷酸。讨论了组胺和缓激肽不同反应的两个假设[1]。

An intermandibular-transclival approach to the posterior cranial fossa has been developed which allows exposure of the basilar artery for attachment of a small electromagnetic blood flow transducer. The results of single intravenous injections of betahistine hydrochloride indicated a mean increase in basilar artery blood flow of 54% and a simultaneous decrease in systemic arterial blood pressure of a duration of action of approximately one minute. Histamine phosphate yielded results similar to betahistine hydrochloride, while nicotinic acid produced only slight increases in blood flow in the basilar artery.[2]

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To see whether antihistamines could prevent and reverse histamine-induced pulmonary edema and increased lung vascular permeability, we compared the effects of a 4-h intravenous infusion of 4 mug/kg per min histamine phosphate on pulmonary hemodynamics, lung lymph flow, lymph and plasma protein content, arterial blood gases, hematocrit, and lung water with the effects of an identical histamine infusion given during an infusion of diphenhydramine or metiamide on the same variables in unanesthetized sheep. Histamine caused lymph flow to increase from 6.0+/-0.5 to 27.0+/-5.5 (SEM) ml/h (P less than 0.05), lymph; plasma globulin concentration ratio to increase from 0.62+/-0.01 to 0.67+/-0.02 (P less than 0.05), left atrial pressure to fall from 1+/-1 to -3+/-1 cm H2O (P less than 0.05), and lung lymph clearance of eight protein fractions ranging from 36 to 96 A molecular radius to increase significantly. Histamine also caused increases in lung water, pulmonary vascular resistance, arterial PCO2, pH, and hematocrit, and decreases in cardiac output and arterial PO2. Diphenhydramine (3 mg/kg before histamine followed by 1.5 mg/kg per h intravenous infusion) completely prevented the histamine effect on hematocrit, lung lymph flow, lymph protein clearance, and lung water content, and reduced histamine effects on arterial blood gases and pH. 6 mg/kg diphenhydramine given at the peak histamine response caused lymph flow and lymph: plasma protein concentration ratios to fall. Metiamide (10 mg/kg per h) did not affect the histamine lymph response. We conclude that diphenhydramine can prevent histamine-induced pulmonary edema and can prevent and reverse increased lung vascular permeability caused by histamine, and that histamine effects on lung vascular permeability are H1 actions.[3]

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We estimated the pulmonary capillary membrane filtration coefficient (Kf) and the maximum capillary pressure (PCcritical) at which the lung could maintain a constant weight in 1) 5 control experiments in anesthetized open-chested dogs, 2) 7 experiments in which the dogs were given 3.6-8.3 microgram . kg-1 . min-1 of histamine phosphate, and 3) in 6 experiments after 75-100 mg/kg of alloxan. In additional experiments, pulmonary lymph flow (QL) and protein concentration (CL) were measured during the infusion of histamine and alloxan. After histamine, Kf averaged 0.045 +/- 0,008 ml . min-1mmHg-1 (SE) and PCcritical was 22.1 +/- 1.1 mmHg. These values were not significantly different from the control Kf and PCcritical (0.036 +/- 0.006 and 22.5 +/- 2.3, respectively). After alloxan, Kf (1.43 +/- 0.69) was larger and PCcritical (12.4 +/- 1.3) was significantly less than control (P less than 0.05). Histamine caused no significant change in QL or CL; however, both were increased after alloxan. These results show that Kf, PCcritical, QL, and CL are all changed by an increase in capillary membrane permeability caused by alloxan. Because none of these factors as significantly affected by histamine, dog lung capillary membrane permeability may not be affected by histamine.[4]

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8.3 mg/kg

Rat

[1]. J Neurochem . 1988 Aug;51(2):634-41.

[2]. Stroke . 1971 Jul-Aug;2(4):409-15.

[3]. J Clin Invest . 1976 Aug;58(2):391-8.

[4]. Am J Physiol . 1980 Jul;239(1):H96-100.

[5]. Gut . 1961 Mar;2(1):32-6.

Histamine phosphate is a phosphate salt that is the diphosphate salt of histamine. It has a role as a histamine agonist. It contains a histamine.
See also: Histamine (has active moiety).

C5H15N3O8P2

307.14

307.03

C, 19.55; H, 4.92; N, 13.68; O, 41.67; P, 20.17

51-74-1

Histamine dihydrochloride; 56-92-8; Histamine; 51-45-6

65513

White to off-white solid powder

887.3ºC at 760 mmHg

128-132 °C

490.4ºC

142.27

8

10

2

18

115

0

NCCC1=CNC=N1.O=P(O)(O)O.O=P(O)(O)O

ZHIBQGJKHVBLJJ-UHFFFAOYSA-N

InChI=1S/C5H9N3.2H3O4P/c6-2-1-5-3-7-4-8-5;2*1-5(2,3)4/h3-4H,1-2,6H2,(H,7,8);2*(H3,1,2,3,4)

2-(1H-imidazol-5-yl)ethanamine;phosphoric acid

Histamine acid phosphate; Histamine diphosphate; Histamine phosphate; Histamine biphosphate; Histamine dihydrogen phosphate; Histamine diphosphate; 51-74-1; Histamine acid phosphate; Histamine biphosphate; 2-(1H-imidazol-4-yl)ethanamine bis(phosphate); Histamine phosphate (1:2); Histamine dihydrogen phosphate;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: 50 mg/mL (162.79 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。