High-energy laser stimulation of creatine kinase activity in tissue cultures

1993 ◽  
Vol 116 (6) ◽  
pp. 1461-1462
Author(s):  
V. B. Matyushichev ◽  
I. N. Sokolov ◽  
T. I. Safronova
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
High Energy ◽  
Creatine Kinase Activity ◽  
Tissue Cultures ◽  
Laser Stimulation ◽  
Energy Laser ◽  
High Energy Laser ◽  
Stimulation Of

Cardiac force and high-energy phosphates under metabolic inhibition in four ectothermic vertebrates

1996 ◽  
Vol 271 (4) ◽  
pp. R946-R954 ◽  
Author(s):  
T. Hartmund ◽  
H. Gesser
Keyword(s):  
Creatine Kinase ◽  
Atpase Activity ◽  
Kinase Activity ◽  
Energy State ◽  
High Energy ◽  
Creatine Kinase Activity ◽  
The Other ◽  
Freshwater Turtle ◽  
High Energy Phosphates ◽  
Isometric Twitch

Isometric twitch tension of ventricular preparations stimulated at 0.2 Hz fell over 30 min of anoxia by a fraction decreasing in the order rainbow trout, cod, eel, and freshwater turtle. Drops in the estimated cytoplasmic energy state were related to larger tension losses for trout than for the other species, possibly due to larger changes in free phosphate. Anoxic energy degradation was slower for turtle than for the other species. Anoxia combined with glycolytic inhibition (1 mmol/l iodoacetate) enhanced the decrease in twitch tension for a drop in energy state and enlarged the increase in ADP/ATP relative to that in creatine/phosphocreatine to an extent inversely related to the creatine kinase activity. Furthermore, it increased resting tension to an extent possibly related to myosin-adenosinetriphosphatase (ATPase) activity and lowered the content of phosphorylated adenylates in trout and turtle myocardium. The results indicate that species differences in performance of the metabolically challenged myocardium depend on energy-degrading processes, e.g., myosin-ATPase activity, phosphate release, creatine kinase activity, and efflux/degradation of ADP and AMP, and that glycolysis offers protection due to its cytoplasmic localization.

Stimulation of Creatine Kinase Activity in Rat Organs by Human Growth Hormonein Vivoandin Vitro*

Endocrinology ◽  
1986 ◽  
Vol 118 (5) ◽  
pp. 1966-1970 ◽  
Author(s):  
A. GOLANDER ◽  
I. BINDERMAN ◽  
A. M. KAYE ◽  
A. NIMROD ◽  
D. SÖMJEN
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
Human Growth ◽  
Creatine Kinase Activity ◽  
Rat Organs ◽  
Stimulation Of

scholarly journals Stimulation of creatine kinase BB activity by 1α,25-dihydroxycholecalciferol and 24R,25-dihydroxycholecalciferol in rat tissues

1984 ◽  
Vol 219 (3) ◽  
pp. 1037-1041 ◽  
Author(s):  
D Sömjen ◽  
Y Weisman ◽  
I Binderman ◽  
A M Kaye
Keyword(s):  
Vitamin D ◽  
Creatine Kinase ◽  
Kinase Activity ◽  
Duodenal Mucosa ◽  
Creatine Kinase Activity ◽  
Rat Tissues ◽  
Long Bones ◽  
Vitamin D Metabolites ◽  
Creatine Kinase Bb ◽  
Stimulation Of

Vitamin D metabolites stimulate creatine kinase BB activity in organs of vitamin D-deficient rats. In epiphyses of long bones, creatine kinase BB activity increases 2.6-fold 24 h after injection of 24R,25-dihydroxycholecalciferol but not of 1 alpha,25-dihydroxycholecalciferol. Contrariwise, 1 alpha,25-dihydroxycholecalciferol, but not 24R,25-dihydroxycholecalciferol, increases creatine kinase BB activity in diaphyses and in kidney. Neither metabolite affects creatine kinase activity in duodenal mucosa.

Influence of peroxynitrite on energy metabolism and cardiac function in a rat ischemia-reperfusion model

2003 ◽  
Vol 285 (4) ◽  
pp. H1385-H1395 ◽  
Author(s):  
Warren H. Lee ◽  
John S. Gounarides ◽  
Eric S. Roos ◽  
Michael S. Wolin
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
Ischemia Reperfusion ◽  
Creatine Phosphate ◽  
High Energy ◽  
Left Ventricular ◽  
Creatine Kinase Activity ◽  
Rate Pressure Product ◽  
Partial Recovery ◽  
Developed Pressure

Ischemia-reperfusion generates peroxynitrite (ONOO–), which interacts with many of the systems altered by ischemia-reperfusion. This study examines the influence of endogenously produced ONOO– on cardiac metabolism and function. Nitro-l-arginine (an inhibitor of ONOO– biosynthesis) and urate (a scavenger of ONOO–) were utilized to investigate potential pathophysiological roles for ONOO– in a rat Langendorff heart model perfused with glucose-containing saline at constant pressure and exposed to 30 min of ischemia followed by 60 min of reperfusion. In this model, ischemia-reperfusion decreased contractile function (e.g., left ventricular developed pressure), cardiac work (rate-pressure product), efficiency of O2 utilization, membrane-bound creatine kinase activity, and NMR-detectable ATP and creatine phosphate without significantly altering the recovery of coronary flow, heart rate, lactate release, and muscle pH. Treatment with urate and nitro-l-arginine produced a substantial recovery of left ventricular developed pressure, rate-pressure product, efficiency of O2 utilization, creatine kinase activity, and NMR-detectable creatine phosphate and a partial recovery of ATP. The pattern of effects observed in this study and in previously published work with similar models suggests that ONOO– may alter key steps in the efficiency of mitochondrial high-energy phosphate generation.

Stimulation of Creatine Kinase Activity by Calcium-Regulating Hormones in Explants of Human Amnion, Decidua, and Placenta*

1986 ◽  
Vol 63 (5) ◽  
pp. 1052-1056 ◽  
Author(s):  
Y. WEISMAN ◽  
A. GOLANDER ◽  
I BINDERMAN ◽  
Z. SPIRER ◽  
A.M. KAYE ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Human Amnion ◽  
Stimulation Of

Alpha-Lamp Integration (ALI) program progressing toward integrated High Energy Laser (HEL) test

1997 ◽  
Author(s):  
David Loomis ◽  
Charles Nefzger ◽  
Ben Platt ◽  
David Loomis ◽  
Charles Nefzger ◽  
...  
Keyword(s):  
High Energy ◽  
Energy Laser ◽  
High Energy Laser
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