title: [Effects of insulin and acidosis on metabolism and function of postischemic rat heart].
abstract: Isolated perfused hearts of male Wistar rats were subjected to 25-min normothermic (37 degrees C) global ischemia, then 5-min infusion of a modified perfusate (pH=7.4) and 25-min reperfusion (control). Experimental groups were treated after ischemia with: a perfusate of the same composition (pH=6.0, RA), a perfusate, containing insulin 2 U/l (pH=7.4, RI) or a perfusate with insulin 2 U/l (pH=6.0, RIA). In the RA, RI and RIA groups a 2-4 folds reduction of contracture was combined with an augmented recovery of the aortic outflow, the cardiac and stroke volumes, compared with these indices in the control during reperfusion. At the end of the reperfusion an improved ATP and phosphocreatine (PCr) recovery in the RA and RI groups was accompanied by reduction of intracellular total creatine (SigmaCr = PCr + creatine) compared with corresponding values in control. Lactate content of reperfused hearts in the RA group was 2.3-times lower than in the control one, but it was almost twice higher in the RI group because of glycolysis stimulation. The most effective recovery of high energy phosphates in the RI group corresponded to reduction of glutamate and aspartate catabolism--total myocardial pool of these amino acids was 1.5-times higher than in the control, and individual amino acid contents did not differ significantly from initial values. Infusion of the acidified perfusate with insulin (the RIA group) resulted in neither improvement of high energy phosphate recovery nor preservation of myocardial amino acid and SigmaCr pools, compared with these indices in control. The lack of augmented metabolic effects of combined treatment with acidosis and insulin in the RIA group was accompanied by nearly the same recovery of majority of functional indices as was observed in RA and RI groups. The absence of additive protective effects of insulin and acidosis on early reperfusion was probably induced by acidosis induced inhibition of insulin-stimulated glucose uptake and glycolysis.
authors.forename: O I
authors.initials: OI
authors.lastname: Pisarenko
authors.forename: V S
authors.initials: VS
authors.lastname: Shul'zhenko
authors.forename: I M
authors.initials: IM
authors.lastname: Studneva
mesh_terms: D000138:Acidosis / Q000378:metabolism*; D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000596:Amino Acids; D007004:Hypoglycemic Agents; D007328:Insulin