추천 제품
Grade
SAJ first grade
vapor pressure
<0.0000 hPa ( 25 °C)
분석
≥97.0%
양식
solid
autoignition temp.
914 °F
재고 정보
available only in Japan
pH
9
mp
271 °C (lit.)
SMILES string
[Na+].[O-]N=O
InChI
1S/HNO2.Na/c2-1-3;/h(H,2,3);/q;+1/p-1
InChI key
LPXPTNMVRIOKMN-UHFFFAOYSA-M
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신호어
Danger
유해 및 위험 성명서
Hazard Classifications
Acute Tox. 3 Oral - Aquatic Acute 1 - Eye Irrit. 2 - Ox. Sol. 3
Storage Class Code
5.1B - Oxidizing hazardous materials
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
개인 보호 장비
Eyeshields, Faceshields, Gloves, type P3 (EN 143) respirator cartridges
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
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
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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