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Merck

487031

Sigma-Aldrich

重碳酸钠-12C

99.9 atom % 12C

别名:

碳酸氢钠-12C

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About This Item

线性分子式:
NaH12CO3
CAS号:
分子量:
84.00
EC號碼:
MDL號碼:
分類程式碼代碼:
12352302
PubChem物質ID:

描述

13C-depleted

同位素純度

99.9 atom % 12C

形狀

solid

mp

>300 °C (lit.)

質量偏移

depleted

SMILES 字串

[Na+].O[12C]([O-])=O

InChI

1S/CH2O3.Na/c2-1(3)4;/h(H2,2,3,4);/q;+1/p-1/i1+0;

InChI 密鑰

UIIMBOGNXHQVGW-XUGDXVOUSA-M

包裝

This product may be available from bulk stock and can be packaged on demand. For information on pricing, availability and packaging, please contact Stable Isotopes Customer Service.

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

Eyeshields, Gloves, type N95 (US)


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分析证书(COA)

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Shay P McGuinness et al.
Critical care medicine, 41(7), 1599-1607 (2013-05-21)
Cardiac surgery-associated acute kidney injury occurs in up to 50% of patients and is associated with increased mortality and morbidity. This study aimed to discover if perioperative urinary alkalinization with sodium bicarbonate infusion reduces the prevalence of cardiac surgery-associated acute
Eric A J Hoste et al.
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 25(3), 747-758 (2009-08-26)
There have been conflicting reports on the use of intravenous administration of sodium bicarbonate for prevention of contrast-induced acute kidney injury (CI-AKI). The aim of this study was to evaluate the use of sodium bicarbonate for prevention of CI-AKI. This
Sophia Zoungas et al.
Annals of internal medicine, 151(9), 631-638 (2009-11-04)
Intravenous sodium bicarbonate has been proposed to reduce the risk for contrast-induced nephropathy (CIN). To determine the effect of sodium bicarbonate on the risk for CIN. MEDLINE, PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials from 1950 to
Joshua C Tremblay et al.
The Journal of physiology, 593(3), 723-737 (2014-11-25)
Blood flow through intrapulmonary arteriovenous anastomoses (IPAVA) is increased by acute hypoxia during rest by unknown mechanisms. Oral administration of acetazolamide blunts the pulmonary vascular pressure response to acute hypoxia, thus permitting the observation of IPAVA blood flow with minimal
Roberto J Diaz et al.
American journal of physiology. Cell physiology, 306(12), C1191-C1199 (2014-04-25)
We have previously shown that ischemic preconditioning (IPC) protection against necrosis in whole hearts and in both fresh and cultured cardiomyocytes, as well as the improved regulatory volume decrease to hypoosmotic swelling in cardiomyocytes, is abrogated through Cl(-) channel blockade

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