English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Elevated intracellular calcium ( i Ca 2+ ) plays an important role in the pathophysiology of ischemic brain damage. The mechanisms by which  i Ca 2+  increases are uncertain. Recent evidence implicates the voltage-dependent calcium channel (VDCC) as a likely site for the alteration in Ca 2+  homeostasis during ischemia. The purpose of this study was to determine whether VDCCs are altered by global ischemia and reperfusion in a canine cardiac arrest, resuscitation model. We employed the radioligand, [ 3 H]PN200-110, to quantitate the equilibrium binding characteristics of the VDCCs in the cerebral cortex. Twenty-five adult beagles were separated into four experimental groups: (a) nonischemic controls, (b) those undergoing 10-min ventricular fibrillation and apnea, (c) those undergoing 10-min ventricular fibrillation and apnea followed by spontaneous circulation and controlled respiration for 2 and (d) 24 h. Brain cortex samples were taken prior to killing of the animal, frozen immediately in liquid nitrogen, and crude synaptosomal membranes isolated by differential centrifugation/filtration. After 10 min of ischemia the maximal binding (B max ) of [ 3 H]PN200-110 increased to &gt;250% of control values (control B max  11.16 ± 0.98; ischemic 28.35 ± 2.78 fmol/mg protein; p &lt; 0.05). B max  returned to near control values after 2 h of reperfusion but remained significantly greater than the control at 24 h. Although the affinity constant (K d ) (control = 0.12 ± 0.03 n M) appeared to increase with ischemia and normalize with reperfusion, the changes were not statistically significant. We conclude that the binding of [ 3 H]PN200-110 to L-type VDCCs is increased after 10 min of global ischemia/anoxia produced by ventricular fibrillation and apnea in the dog. This change is only partially reversible after 24 h of reperfusion. This study supports the hypothesis that ischemia increases the number of VDCCs in the cell membrane which may allow increased entry of Ca 2+  into the cell during ischemia and early reperfusion.

Alteration of Voltage-Dependent Calcium Channels in Canine Brain during Global Ischemia and Reperfusion