Insulin resistance and its reversal by in vivo infusion of ATP in hermorrhagic shock.
Hemorrhagic shock in rats was produced by bleeding the animals to a mean arterial pressure of 40 mmHg, which was maintained for 2 h. Muscles from these animals ('shock' muscles) demonstrated basal glucose uptake values unchanged from control values but, unlike the control muscles, the "shock' muscles showed resistance to the stimulation of glucose uptake by insulin. Infusion of ATP-MgCl2, ADP-MgCl2, adenosine-MgCl2, or GTP-MgCl2 to animals following shock had no effect on basal glucose uptake; however, ATP-MgCl2 but not the other nucleotides permitted insulin to exert its stimulatory effect on such muscles. An optimal insulin effect in ATP-MgCl2 treated 'shock' muscles occurred at an insulin concentration of u.001 U/ml, which is also the concentration required to produce optimal insulin effect in control muscles. Following 1-h incubation in Krebs-HCO3 medium, intracellular ATP contents of 'shock' muscles were about 50% lower than in control muscles. Treatment with ATP-MgCl2 following shock, however, resulted in ATP contents in such muscles similar to those in control muscles. Possible mechanisms for this reversal of insulin resistance by in vivo infusion of ATP-MgCl2 in shock are discussed.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D005947:Glucose / Q000378:metabolism; D006160:Guanosine Triphosphate / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D007333:Insulin Resistance; D009132:Muscles / Q000378:metabolism; D009711:Nucleotides / Q000494:pharmacology; D051381:Rats; D012771:Shock, Hemorrhagic / Q000503:physiopathology*
D007328:Insulin; D009711:Nucleotides; D000244:Adenosine Diphosphate; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate; D005947:Glucose