scholarly journals High Energy Phosphate Compounds in the Myocardium during Experimental Congestive Heart Failure. Purine and Pyrimidine Nucleotides, Creatine, and Creatine Phosphate in Normal and in Failing Hearts*

1965 ◽  
Vol 44 (2) ◽  
pp. 202-218 ◽  
Author(s):  
Arthur C. Fox ◽  
Norman S. Wikler ◽  
George E. Reed
1966 ◽  
Vol 44 (7) ◽  
pp. 1015-1033 ◽  
Author(s):  
Doris I. Fraser ◽  
W. J. Dyer ◽  
H. M. Weinstein ◽  
J. R. Dingle ◽  
J. A. Hines

Muscular activity just before death critically affected the levels of glycolytic metabolites in the skeletal muscle of feeding, aquarium-held cod. Relaxed cod could be obtained by slow anesthetization without visible excitation; these contained very little lactate in the white muscle (7–28 mg/100 g), and exhibited high, uniformly distributed levels of high-energy phosphate compounds (about 17 μmoles acid-labile P/g plus equal or higher amounts of creatine phosphate). A trend to lower glycogen levels in the anterior portion of the fillet was indicated. Unexercised fish caught and killed with negligible struggling appeared to have undergone some antemortem activity. Compared with relaxed cod, they showed higher lactate levels (about 100 mg/100 g), much lower levels of creatine phosphate and other high-energy phosphate compounds, together with some ammonia. Again, glycogen was lower in the anterior than in the posterior portion. Exhaustion uniformly depleted energy reserves to low levels in the white muscle; in the red muscle, however, high glycogen levels were maintained, although the content of other glycolytic metabolites indicated partial activation of the glycolytic processes during the antemortem struggle. In all fish examined, levels of inorganic and total acid-soluble phosphorus were lower in the red than in the white muscle.


1977 ◽  
Vol 29 (6) ◽  
pp. 959-977 ◽  
Author(s):  
O. H. Lowry ◽  
S. J. Berger ◽  
M. M.-Y. Chi ◽  
J. G. Carter ◽  
A. Blackshaw ◽  
...  

1978 ◽  
Vol 235 (5) ◽  
pp. H475-H481 ◽  
Author(s):  
J. M. Jarmakani ◽  
T. Nagatomo ◽  
M. Nakazawa ◽  
G. A. Langer

The effect of hypoxia on myocardial high-energy phosphate content in the newborn, 2-wk-old, and adult rabbit was determined and compared with mechanical function. Studies were done on the ventricular septum arterially perfused with Krebs-Henseleit bicarbonate buffer solution equilibrated with 95% O2 and 5% CO2 (control) or 95% N2 and 5% CO2 (hypoxia) at 60 beats/min and 27 degrees C. In the adult, ATP concentration decreased to 68%, 56%, and 39% of control after 2, 30, and 60 min of hypoxia, respectively. After 30 min of hypoxia, ATP concentration was not different from control in the newborn but decreased to 82% of control in the 2-wk-old. After 2 min of hypoxia, creatine phosphate concentration decreased to 55% and 10% of control in the newborn and adult rabbit, respectively. Lactate production increased significantly during hypoxia and was greater in the newborn than in the adult. The data indicate that the newborn rabbit is capable of maintaining glycolysis and normal levels of myocardial ATP during hypoxia, which ensures normal myocardial mechanical function for longer periods than in the adult.


1985 ◽  
Vol 248 (4) ◽  
pp. E457-E462 ◽  
Author(s):  
P. A. Low ◽  
K. Ward ◽  
J. D. Schmelzer ◽  
S. Brimijoin

We examined the effect of ischemia on nerve conduction in experimental diabetic neuropathy (EDN) and related electrophysiological changes to nerve adenosine triphosphate (ATP), creatine phosphate (CP), and lactate under anoxic conditions. Rats rendered diabetic with streptozotocin had a resistance to ischemic conduction block (RICB). Caudal nerve action potential (NAP) was well maintained for 10 min in controls and for 15 min in EDN, after which time NAP declined in both groups but more rapidly in normal rats. Time to 50% reduction in nerve ATP and CP was 10 and 3 min, respectively, in controls and delayed to 20 and 8 min in EDN. Rate of utilization of high-energy phosphate (approximately P) was linear for 5 min in controls to be followed by a progressive decline. In EDN rate of utilization of approximately P was linear to 15 min to be followed by a more gradual decline than in normal nerves. These findings suggest that the maintenance of nerve transmission in anoxic-ischemic states depends on anaerobic metabolism and that RICB in EDN is due in part to the ability of diabetic nerves to maintain a higher level of anaerobic glycolysis and for a longer time than normal nerves.


Surgery ◽  
1996 ◽  
Vol 120 (3) ◽  
pp. 534-541 ◽  
Author(s):  
Steven N. Hochwald ◽  
Lawrence E. Harrison ◽  
Jeffrey L. Port ◽  
David Blumberg ◽  
Murray F. Brennan ◽  
...  

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