title: Glucose-insulin-potassium (GIK) prevents derangement of myocardial metabolism in brain-dead pigs.
abstract: Brain death is associated with neuroendocrine changes resulting in reduced myocardial glycogen content. The purpose of this study was to investigate the effects of glucose-insulin-potassium (GIK), on myocardial metabolism in brain-dead pigs. Sixteen brain-dead pigs were given GIK infusion (n = 8), or Ringer solution (n = 8). At end-point (7 h post brain death) arterial concentrations and myocardial arteriovenous (a-v) concentration differences of glucose, lactate and free fatty acids (FFA) were assessed, and myocardial biopsy specimens were taken from the right atrium and left ventricle. Biopsies were also taken from five normal pigs. Myocardial glycogen content in the GIK group was significantly higher compared to the control group, but comparable to the non-brain-dead animals. There was a higher and significant myocardial uptake of glucose and lactate in the GIK group compared to the controls. Plasma levels of FFA were significantly lower in the GIK group, and the myocardial uptake of FFA was 5 times higher in the control group compared to the GIK group. There were no significant differences in hemodynamic variables among the groups. In conclusion, intravenous supply of GIK to brain-dead pigs results in increased myocardial glycogen content and seems to prevent abnormal myocardial metabolism, which may have clinical implications for the myocardial protection of donor hearts.
authors.affiliation: Department of Cardiothoracic Surgery, Sahlgrenska Hospital, Göteborg, Sweden.
authors.forename: B
authors.initials: B
authors.lastname: Nilsson
authors.forename: H
authors.initials: H
authors.lastname: Berggren
authors.forename: R
authors.initials: R
authors.lastname: Ekroth
authors.forename: V
authors.initials: V
authors.lastname: Mantovani
authors.forename: F
authors.initials: F
authors.lastname: Nilsson
authors.forename: S
authors.initials: S
authors.lastname: Svensson
authors.forename: L
authors.initials: L
authors.lastname: Wiklund
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001926:Brain Death / Q000473:pathology / Q000503:physiopathology*; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005947:Glucose / Q000494:pharmacology*; D006003:Glycogen / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D007328:Insulin / Q000494:pharmacology*; D007552:Isotonic Solutions / Q000494:pharmacology*; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011188:Potassium / Q000494:pharmacology*; D000077325:Ringer's Lactate; D013552:Swine
chemical_list: D001786:Blood Glucose; D002314:Cardioplegic Solutions; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007552:Isotonic Solutions; D007773:Lactates; D000077325:Ringer's Lactate; C030396:glucose-insulin-potassium cardioplegic solution; D019344:Lactic Acid; D006003:Glycogen; D005947:Glucose; D011188:Potassium