The role of ATP-magnesium in ischemia and shock.
Although much is known about the role of Mg in cardiomyopathies of different etiology, very little is known about the changes in hepatic Mg levels following hemorrhagic shock or ischemia to the liver. Information available indicates that tissue and mitochondrial Mg levels may be altered following shock and ischemia and that such alterations may be responsible for the depressed cellular function during those conditions. MgCl2 administration following shock or ischemia was ineffective in improving tissue and mitochondrial Mg levels and cellular functions. Administration of ATP complexed with MgCl2, however, increased tissue and mitochondrial Mg levels, tissue ATP stores and cellular functions and proved beneficial for the survival of animals. ATP-MgCl2 administration also increased cardiac output while decreasing myocardial as well as total body O2 consumption. The potential mechanisms of the beneficial effects of ATP-MgCl2 are discussed. ATP-MgCl2 can be given safely to humans and it decreases myocardial O2 consumption and increases cardiac output without producing hypotension. A clinical trial of ATP-MgCl2 in patients with various adverse circulatory conditions is underway at our institution.
D000255:Adenosine Triphosphate / Q000032:analysis / Q000627:therapeutic use*; D000818:Animals; D002118:Calcium / Q000032:analysis; D004285:Dogs; D005230:Fatty Acids, Nonesterified / Q000032:analysis; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007511:Ischemia / Q000188:drug therapy* / Q000378:metabolism; D008102:Liver Circulation / Q000187:drug effects; D008274:Magnesium / Q000032:analysis; D008928:Mitochondria / Q000032:analysis; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D012769:Shock / Q000188:drug therapy* / Q000378:metabolism
D005230:Fatty Acids, Nonesterified; D000255:Adenosine Triphosphate; D008274:Magnesium; D002118:Calcium