推荐产品
等級
SAJ first grade
蒸汽壓力
<0.0000 hPa ( 25 °C)
化驗
≥97.0%
形狀
solid
自燃溫度
914 °F
存貨情形
available only in Japan
pH值
9
mp
271 °C (lit.)
SMILES 字串
[Na+].[O-]N=O
InChI
1S/HNO2.Na/c2-1-3;/h(H,2,3);/q;+1/p-1
InChI 密鑰
LPXPTNMVRIOKMN-UHFFFAOYSA-M
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訊號詞
Danger
危險分類
Acute Tox. 3 Oral - Aquatic Acute 1 - Eye Irrit. 2 - Ox. Sol. 3
儲存類別代碼
5.1B - Oxidizing hazardous materials
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
個人防護裝備
Eyeshields, Faceshields, Gloves, type P3 (EN 143) respirator cartridges
Lucas C Pinheiro et al.
Free radical biology & medicine, 53(4), 701-709 (2012-06-23)
The new pathway nitrate-nitrite-nitric oxide (NO) has emerged as a physiological alternative to the classical enzymatic pathway for NO formation from l-arginine. Nitrate is converted to nitrite by commensal bacteria in the oral cavity and the nitrite formed is then
Peter J Rix et al.
Clinical pharmacokinetics, 54(3), 261-272 (2014-11-26)
The efficacy of nebulized sodium nitrite (AIR001) has been demonstrated in animal models of pulmonary arterial hypertension (PAH), but it was not known if inhaled nitrite would be well tolerated in human subjects at exposure levels associated with efficacy in
Rustem F Dautov et al.
Nitric oxide : biology and chemistry, 40, 36-44 (2014-05-27)
Previous studies in non-human blood vessels and in platelets have demonstrated that under hypoxic conditions release of NO from nitrite (NO2(-)) is potentiated by deoxyhaemoglobin. In the current study, we characterized hypoxic potentiation of NO2(-) effects in human vasculature and
Edward H Oldfield et al.
Journal of neurosurgery, 119(3), 634-641 (2013-05-28)
Intravenous sodium nitrite has been shown to prevent and reverse cerebral vasospasm in a primate model of subarachnoid hemorrhage (SAH). The present Phase IIA dose-escalation study of sodium nitrite was conducted to determine the compound's safety in humans with aneurysmal
Borja Ibáñez et al.
Journal of the American College of Cardiology, 65(14), 1454-1471 (2015-04-11)
The damage inflicted on the myocardium during acute myocardial infarction is the result of 2 processes: ischemia and subsequent reperfusion (ischemia/reperfusion injury). During the last 3 decades, therapies to reduce ischemic injury (mainly reperfusion strategies) have been widely incorporated into
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