O49. Nitro-fatty acid inhibition of neointima formation after endoluminal vessel injury

Nitric Oxide ◽  
2008 ◽  
Vol 19 ◽  
pp. 31
Author(s):  
Marsha P. Cole ◽  
Tanja Rudoph ◽  
Bruce A. Freeman ◽  
Philip Michael Bauer
Keyword(s):  
Fatty Acid ◽  
Acid Inhibition ◽  
Neointima Formation ◽  
Vessel Injury ◽  
Fatty Acid Inhibition

scholarly journals Nitro-Fatty Acid Inhibition of Neointima Formation After Endoluminal Vessel Injury

2009 ◽  
Vol 105 (10) ◽  
pp. 965-972 ◽  
Author(s):  
Marsha P. Cole ◽  
Tanja K. Rudolph ◽  
Nicholas K.H. Khoo ◽  
Uche N. Motanya ◽  
Franca Golin-Bisello ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Acid Inhibition ◽  
Neointima Formation ◽  
Vessel Injury ◽  
Fatty Acid Inhibition

scholarly journals Fatty Acid Inhibition of Sulfation Factor-stimulated 35SO4 Incorporation into Embryonic Chicken Cartilage

1973 ◽  
Vol 248 (6) ◽  
pp. 1901-1905
Author(s):  
Harry K. Delcher ◽  
George S. Eisenbarth ◽  
Harold E. Lebovitz
Keyword(s):  
Fatty Acid ◽  
Acid Inhibition ◽  
Embryonic Chicken ◽  
Fatty Acid Inhibition

A new strategy to recover from volatile fatty acid inhibition in anaerobic digestion by photosynthetic bacteria

2020 ◽  
Vol 311 ◽  
pp. 123501 ◽  
Author(s):  
Weixin Zhao ◽  
Jinhui Jeanne Huang ◽  
Binbin Hua ◽  
Zhiyong Huang ◽  
Ronald L. Droste ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Anaerobic Digestion ◽  
Volatile Fatty Acid ◽  
Photosynthetic Bacteria ◽  
Acid Inhibition ◽  
New Strategy ◽  
Fatty Acid Inhibition

Dichloroacetate stimulation of glucose oxidation improves recovery of ischemic rat hearts

1990 ◽  
Vol 259 (4) ◽  
pp. H1079-H1085 ◽  
Author(s):  
J. J. McVeigh ◽  
G. D. Lopaschuk
Keyword(s):  
Fatty Acid ◽  
Glucose Oxidation ◽  
Acid Inhibition ◽  
Mechanical Function ◽  
Oxidation Rates ◽  
Rat Hearts ◽  
High Concentrations ◽  
Fatty Acid Inhibition ◽  
Mechanical Recovery ◽  
Stimulation Of

We have previously shown that high concentrations of fatty acids depress reperfusion recovery of ischemic rat hearts as a result of a fatty acid inhibition of glucose oxidation. In this study, we determined whether dichloroacetate, an activator of pyruvate dehydrogenase, could overcome fatty acid inhibition of glucose oxidation and thereby improve mechanical recovery of hearts reperfused after a period of transient global ischemia. Isolated working rat hearts, perfused with 11 mM glucose, 1.2 mM palmitate, and 500 microU/ml insulin, were subjected to a 30-min period of no flow ischemia, followed by a 30-min period of reperfusion. Under these conditions, control hearts recovered 37% of preischemic function. The addition of 1 mM dichloroacetate to the perfusate at reperfusion resulted in a significant improvement in recovery of mechanical function (to 73% of preischemic function). When dichloroacetate was added before the onset of ischemia, however, this protective effect was lost, and a significant increase in myocardial lactate accumulation during ischemia was observed. The effects of dichloroacetate on glucose oxidation rates in both nonischemic and reperfused ischemic hearts was determined by perfusing hearts with 11 mM [U-14C]glucose and 1.2 mM palmitate and quantitatively collecting 14CO2 produced by the heart. In nonischemic hearts, 1 mM dichloroacetate increased steady-state glucose oxidation rates from 298 +/- 69 to 1,223 +/- 135 nmol.g dry wt-1.min-1. The addition of dichloroacetate to hearts reperfused after a 25-min period of ischemia also increased glucose oxidation rates from (112 +/- 25 to 561 +/- 83 nmol.g dry wt-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

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