Cytokines, neuropeptides, and reperfusion injury during magnesium deficiency.
In summary, hypomagnesemia enhances reperfusion injury. We postulate that neurogenic inflammation, which occurs very early during hypomagnesemia, predisposes the myocardium to reperfusion injury by depleting endogenous antioxidants and recruiting inflammatory cells, which can participate in enhanced free radical production during postischemic reperfusion. Vitamin E supplements can prevent the occurrence of this enhanced injury possibly through the restoration of endogenous antioxidant defenses.
Weglicki
W B
WB
Department of Physiology, George Washington University Medical Center, Washington, D.C. 20037.
Phillips
T M
TM
Mak
I T
IT
Cassidy
M M
MM
Dickens
B F
BF
Stafford
R
R
Kramer
J H
JH
D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000097:blood; D009202:Cardiomyopathies / Q000209:etiology*; D006224:Cricetinae; D016207:Cytokines / Q000378:metabolism*; D007249:Inflammation / Q000150:complications; D008275:Magnesium Deficiency / Q000150:complications* / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000209:etiology; D009479:Neuropeptides / Q000378:metabolism*; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013373:Substance P / Q000097:blood; D013997:Time Factors; D014810:Vitamin E / Q000627:therapeutic use
D016207:Cytokines; D009479:Neuropeptides; D017382:Reactive Oxygen Species; D014810:Vitamin E; D013373:Substance P; D015740:Calcitonin Gene-Related Peptide