Time course of changes in aryl sulfatase activity in the initial period of acute experimental focal myocardial ischemia

1988 ◽  
Vol 105 (3) ◽  
pp. 318-321
Author(s):  
V. A. Frolov ◽  
�. A. Badrieva ◽  
T. A. Kazanskaya
2016 ◽  
Vol 67 (13) ◽  
pp. 591
Author(s):  
Aleksandra Binek ◽  
Rodrigo Fernandez-Jimenez ◽  
Inmaculada Jorge ◽  
Emilio Camafeita ◽  
Juan Antonio Lopez ◽  
...  

1991 ◽  
Vol 65 (4) ◽  
pp. 891-898 ◽  
Author(s):  
D. S. Barth ◽  
S. Di

1. Laminar field potentials produced by paired electrocortical stimuli were recorded with a linear microelectrode array inserted perpendicular to the surface of rat somatosensory cortex. Current source-density (CSD) distributions of the direct cortical response (DCR) were computed from the potential profiles. Principal component analysis (PCA) was used to estimate the time course of evoked transmembrane currents of putative pyramidal cell populations in the supragranular and infragranular layers. 2. Both supra- and infragranular cells displayed an initial period after the conditioning stimulus in which test stimuli produced subnormal evoked response amplitudes. This was followed in both layers by a long period of supernormal then subnormal responses and a second period of supernormal responses. 3. The main laminar difference encountered was a general shortening of all phases of the excitability cycle in the supragranular cells. 4. Excitability cycles in the supra- and infragranular layers closely followed the morphology of average evoked responses to the conditioning stimulus alone. These results and physiological support to the validity of lamina-specific evoked response waveforms derived from combined CSD and PCA analysis of extracellular potential measurements. 5. The relationship between evoked potential amplitude changes and cortical excitability is discussed.


2018 ◽  
Vol 243 (9) ◽  
pp. 780-785 ◽  
Author(s):  
Kui Li ◽  
Chen Li ◽  
Ying Xiao ◽  
Tao Wang ◽  
Y James Kang

The distribution of copper (Cu) in the biological system is regulated by Cu transporters and chaperones. It has been known for a long time that myocardial ischemia is accompanied by the loss of Cu from the heart, but the mechanism by which this occurs remains unknown. The present study was undertaken to understand the relationship between Cu loss and alterations in Cu transporters during the pathogenesis of myocardial ischemia. Male mice (C57 BL/6J) were subjected to left anterior descending (LAD) coronary artery ligation to induce myocardial ischemia. Changes in Cu concentrations in serum and hearts were determined from blood and tissue samples harvested at different time points for a total of 28 days after the operation. Cu concentrations in the ischemic myocardium were continuously decreased starting at the fourth day after LAD artery ligation, gradually depleted by more than 80% of the normal level at the 10th day, and remained at the lowest level (about 20% of normal levels) thereafter. Serum Cu concentrations were correspondingly increased starting at the fourth day, reached to the highest level between day 7 and 10, and gradually recovered to the normal level until 21st day after the operation. Along with the same time course, the intracellular Cu exporter copper metabolism MURR domain 1 (COMMD1) was significantly and sustainably increased, but ATP7A and ATP7B were not significantly changed in the ischemic myocardium. These results suggest that during the pathogenesis of myocardial ischemia, COMMD1 would play a critical role in exporting Cu from the ischemic myocardium to the blood. Impact statement In this work, we found that copper efflux from the ischemic heart leads to the elevation of serum copper concentrations, addressing a long-term question related to serum copper elevation in myocardial ischemia patients. The efflux of copper from the ischemic heart results at least in part from the upregulation of copper metabolism MURR domain 1 (COMMD1) in the heart upon ischemic insult. This work provides a novel insight into copper homeostasis and alteration in cardiovascular system.


1980 ◽  
Vol 28 (02) ◽  
pp. 141-149 ◽  
Author(s):  
Th. Stegmann ◽  
W. Daniel ◽  
L. Bellmann ◽  
G. Trenkler ◽  
H. Oelert ◽  
...  

1971 ◽  
Vol 142 (2) ◽  
pp. 623-632 ◽  
Author(s):  
Walter A. Scott ◽  
Kenneth D. Munkres ◽  
Robert L. Metzenberg

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