Synthesis of a Sodium–Hydrogen Exchange Type 1 Inhibitor: An Efficient Cu-Catalyzed Conjugated Addition of a Grignard Reagent to an Acetyl Pyridinium Salt

2013 ◽  
Vol 17 (3) ◽  
pp. 382-389 ◽  
Author(s):  
Wenjun Tang ◽  
Nitinchandra D. Patel ◽  
Xudong Wei ◽  
Denis Byrne ◽  
Ashish Chitroda ◽  
...  
Keyword(s):  
Grignard Reagent ◽  
Hydrogen Exchange ◽  
Pyridinium Salt ◽  
Sodium Hydrogen

A RARE CASE MORTALITY OF DIABETIC KETOACIDOSIS- CEREBRAL EDEMA WITH TONSILLAR HERNIATION- A CONTRADICTORY OPINION.IS SODIUM BICARBONATE A REAL CULPRIT?

2021 ◽  
pp. 8-10
Author(s):  
Sruthi P ◽  
Manzoor Sharieff M ◽  
Prasanth Kumar P ◽  
Vishnu priya V ◽  
Nagarajan N ◽  
...  
Keyword(s):  
Diabetic Ketoacidosis ◽  
Cerebral Edema ◽  
Hydrogen Exchange ◽  
Ketone Bodies ◽  
Acetoacetic Acid ◽  
Tonsillar Herniation ◽  
Sodium Hydrogen ◽  
Uncontrolled Diabetes ◽  
Case Mortality

Diabetic ketoacidosis (DKA) is the most common complication seen in uncontrolled diabetes mellitus. DKA is most commonly seen with patients of type 1 diabetes. Depletion of Insulin leads to high blood sugars which in turn leads osmotic diuresis, production of ketone bodies i.e, βhydroxybutyric acid and acetoacetic acid, dysregulation of sodium hydrogen exchange mechanism[2]. As a consequence to the above stated mechanisms, cerebral edema has been documented as a fatal complication in DKA. Mortality documented due to cerebral edema is 21-25%[4].

scholarly journals Sodium, Hydrogen exchange type 1 and bile ductular secretory activity in the guinea pig

Hepatology ◽  
2000 ◽  
Vol 31 (3) ◽  
pp. 562-571 ◽  
Author(s):  
Christian Hübner ◽  
Wolfgang Stremmel ◽  
Christoph Elsing
Keyword(s):  
Guinea Pig ◽  
Hydrogen Exchange ◽  
Secretory Activity ◽  
Sodium Hydrogen

scholarly journals A unique sodium-hydrogen exchange isoform (NHE-4) of the inner medulla of the rat kidney is induced by hyperosmolarity.

1994 ◽  
Vol 269 (47) ◽  
pp. 29704-29709
Author(s):  
C Bookstein ◽  
M W Musch ◽  
A DePaoli ◽  
Y Xie ◽  
M Villereal ◽  
...  
Keyword(s):  
Hydrogen Exchange ◽  
Rat Kidney ◽  
Sodium Hydrogen

scholarly journals Simulated diabetic ketoacidosis therapy in vitro elicits brain cell swelling via sodium-hydrogen exchange and anion transport

2015 ◽  
Vol 309 (4) ◽  
pp. E370-E379 ◽  
Author(s):  
Keeley L. Rose ◽  
Andrew J. Watson ◽  
Thomas A. Drysdale ◽  
Gediminas Cepinskas ◽  
Melissa Chan ◽  
...  
Keyword(s):  
Diabetic Ketoacidosis ◽  
Hydrogen Exchange ◽  
Brain Slices ◽  
Anion Transport ◽  
Brain Cell ◽  
Cell Swelling ◽  
Sodium Hydrogen ◽  
Disulphonic Acid

A common complication of type 1 diabetes mellitus is diabetic ketoacidosis (DKA), a state of severe insulin deficiency. A potentially harmful consequence of DKA therapy in children is cerebral edema (DKA-CE); however, the mechanisms of therapy-induced DKA-CE are unknown. Our aims were to identify the DKA treatment factors and membrane mechanisms that might contribute specifically to brain cell swelling. To this end, DKA was induced in juvenile mice with the administration of the pancreatic toxins streptozocin and alloxan. Brain slices were prepared and exposed to DKA-like conditions in vitro. Cell volume changes were imaged in response to simulated DKA therapy. Our experiments showed that cell swelling was elicited with isolated DKA treatment components, including alkalinization, insulin/alkalinization, and rapid reductions in osmolality. Methyl-isobutyl-amiloride, a nonselective inhibitor of sodium-hydrogen exchangers (NHEs), reduced cell swelling in brain slices elicited with simulated DKA therapy (in vitro) and decreased brain water content in juvenile DKA mice administered insulin and rehydration therapy (in vivo). Specific pharmacological inhibition of the NHE1 isoform with cariporide also inhibited cell swelling, but only in the presence of the anion transport (AT) inhibitor 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid. DKA did not alter brain NHE1 isoform expression, suggesting that the cell swelling attributed to the NHE1 was activity dependent. In conclusion, our data raise the possibility that brain cell swelling can be elicited by DKA treatment factors and that it is mediated by NHEs and/or coactivation of NHE1 and AT.

scholarly journals Mineralocorticoid Action and Sodium-Hydrogen Exchange: Studies in Experimental Cardiac Fibrosis

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3848-3851 ◽  
Author(s):  
Morag Young ◽  
John Funder
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Hydrogen Exchange ◽  
Cardiac Fibrosis ◽  
Inflammatory Cell ◽  
Mineralocorticoid Receptor Antagonist ◽  
Sodium Hydrogen ◽  
Sodium Hydrogen Exchanger ◽  
Coronary Vasculitis ◽  
Potassium Canrenoate

Abstract There is increasing evidence that the trigger for cardiac fibrosis in response to mineralocorticoid/salt administration is coronary vasculitis and that effects can be seen within days of deoxycorticosterone acetate (DOCA) administration. Furthermore, rapid, nongenomic mineralocorticoid effects on the sodium-hydrogen exchanger (NHE-1) in vascular smooth muscle cells have recently been described. That this mechanism may act as an inflammatory or profibrotic signal was tested by comparing the specific NHE-1 antagonist cariporide and the mineralocorticoid receptor antagonist K canrenoate in the rat model of mineralocorticoid/salt perivascular fibrosis over 8 d of DOCA/salt administration. Interstitial collagen, inflammatory cell infiltration, and inflammatory markers were determined. DOCA elevated blood pressure above control, cariporide +DOCA, or K canrenoate +DOCA rats, without cardiac hypertrophy. At 8 d interstitial collagen was significantly elevated in the DOCA-alone group, with levels in cariporide- and K canrenoate-treated rats not different from control. Expression of osteopontin, cyclooxygenase-2, and ED-1 were elevated by DOCA treatment, blocked by potassium canrenoate, and (for ED-1 and osteopontin) partially reduced by cariporide. These results suggest mineralocorticoid/salt-induced cardiac fibrosis may involve coronary vascular smooth muscle cell NHE-1 activity as a possible contributor to the cascade of transcriptional events that produce the characteristic coronary vasculitis seen with excess mineralocorticoid and salt.

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