Acid-base behavior of sulfoxides. Measurement of pKa values by ultraviolet and nuclear magnetic resonance techniques

1969 ◽  
Vol 91 (24) ◽  
pp. 6703-6707 ◽  
Author(s):  
D. Landini ◽  
Giorgio Modena ◽  
Gianfranco Scorrano ◽  
Ferdinando Taddei
1957 ◽  
Vol 27 (3) ◽  
pp. 641-642 ◽  
Author(s):  
Ernest Grunwald ◽  
A. Loewenstein ◽  
S. Meiboom

1999 ◽  
Vol 77 (11) ◽  
pp. 1941-1945 ◽  
Author(s):  
Eugene P. Mazzola ◽  
Sandra J. Bell ◽  
Saleh A. Turujman ◽  
Julie N. Barrows ◽  
John E. Bailey, Jr. ◽  
...  

1990 ◽  
Vol 258 (1) ◽  
pp. F34-F40
Author(s):  
S. Adler ◽  
V. Simplaceanu ◽  
C. Ho

It is well known that brain pH changes rapidly in acute hypercapnia or hypocapnia. The effect of acute isocapnic metabolic acid-base change on brain pH is less certain. To study this problem, acute isocapnic metabolic acidosis was induced by HCl or lactic acid infusions in rats, and recovery from acidosis was accomplished by NaHCO3 infusion. Brain pH was measured by 31P-nuclear magnetic resonance. Despite decreases in blood pH of 0.34 and 0.36 units, respectively, in less than 1 h of acid infusion and rapid recovery during bicarbonate infusion, brain pH was unaffected (ranging between 7.08 and 7.11) and was uncorrelated with blood pH. The blood pH minus brain pH gradient was eliminated by the acidosis. By contrast, hypoxia-induced endogenous lactic acidosis lowered blood and brain pH equivalently, but the fall in brain pH preceded that in blood. During normoxic recovery, brain pH overshot and became alkaline when blood pH was still significantly reduced and blood lactate levels were markedly elevated. Presumably, this is due to stimulated active H+ transport. The results demonstrate that brain pH is affected differently in metabolic, respiratory, and endogenous acid-base disturbances. Thus brain pH cannot be predicted solely from blood pH values.


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