同义名 :	乙基异硫脲氢溴酸盐 ;S-Ethylisothiourea hydrobromide; S-ethyl Isothiourea (hydrobromide); WR 539; SEIT (HBr); 2-Ethyl-2-thiopseudourea hydrobromide; Ethiron bromide
	CAS号 :	1071-37-0
	货号 :	A793027
	分子式 :	C3H9BrN2S
	纯度 :	98%
	分子量 :	185.09
	MDL号 :	MFCD00012585
	存储条件：	Pure form Sealed in dry,2-8°C In solvent -20°C:3-6个月-80°C:12个月
	溶解度 :	-
	动物实验配方：

生物活性

描述

EIT (S-ethylisothiourea) Hydrobromide is a selective inhibitor of type II NOS. EIT elicited a dose-dependent and > 95% inhibition of the LPS-induced increase in plasma [NOx]. The ED50 values for EIT was 0.4 mg/kg. Pretreatment with L-arginine (but not D-arginine) prevented the mortality, while not affecting the type II NOS-dependent NO production, suggesting the toxicity may be due to inhibition of one of the other NOS isoforms (endothelial or neuronal)[1]. Selective NOS II antagonists attenuate but do not block shear stress-induced vasodilation in the fetal lung. Stimulation of NOS II activity, perhaps from smooth muscle cells, contributes in part to the NO-mediated fall in PVR (pulmonary vascular resistance) during shear stress-induced pulmonary vasodilation[2]. Spleen cells stimulated with alloantigens in the presence of AMT or S-ethylisothiourea (EIT), an another selective iNOS inhibitor, produced considerably more interleukin (IL)-4 and IL-10 than the cells stimulated in the absence of iNOS inhibitors. The production of Th1 cytokines IL-2 and interferon (IFN)-gamma was not enhanced by the inhibition of NO synthesis[3]. Acute administration of EIT (380 nmol/h), another inducible nitric oxide synthase selective inhibitor, also attenuated pregnancy-induced increases in glomerular filtration rate and effective renal plasma flow[4].

实验方案
	1mg	5mg	10mg
1 mM 5 mM 10 mM	5.40mL 1.08mL 0.54mL	27.01mL 5.40mL 2.70mL	54.03mL 10.81mL 5.40mL

参考文献

[1]Tracey WR, Nakane M, Basha F, Carter G. In vivo pharmacological evaluation of two novel type II (inducible) nitric oxide synthase inhibitors. Can J Physiol Pharmacol. 1995 May;73(5):665-9 [2]Rairigh RL, Storme L, Parker TA, le Cras TD, Kinsella JP, Jakkula M, Abman SH. Inducible NO synthase inhibition attenuates shear stress-induced pulmonary vasodilation in the ovine fetus. Am J Physiol. 1999 Mar;276(3):L513-21 [3]Holán V, Krulová M, Zajícová A, Pindjáková J. Nitric oxide as a regulatory and effector molecule in the immune system. Mol Immunol. 2002 May;38(12-13):989-95 [4]Alexander BT, Cockrell K, Cline FD, Granger JP. Inducible nitric oxide synthase inhibition attenuates renal hemodynamics during pregnancy. Hypertension. 2002 Feb;39(2 Pt 2):586-90