title: Cardiac responses to insulin-induced hypoglycemia in nondiabetic and intensively treated type 1 diabetic patients.
abstract: Insulin-induced hypoglycemia occurs commonly in intensively treated patients with type 1 diabetes, but the cardiovascular consequences of hypoglycemia in these patients are not known. We studied left ventricular systolic [left ventricular ejection fraction (LVEF)] and diastolic [peak filling rate (PFR)] function by equilibrium radionuclide angiography during insulin infusion (12 pmol. kg(-1). min(-1)) under either hypoglycemic (approximately 2.8 mmol/l) or euglycemic (approximately 5 mmol/l) conditions in intensively treated patients with type 1 diabetes and healthy nondiabetic subjects (n = 9 for each). During hypoglycemic hyperinsulinemia, there were significant increases in LVEF (DeltaLVEF = 11 +/- 2%) and PFR [DeltaPFR = 0.88 +/- 0.18 end diastolic volume (EDV)/s] in diabetic subjects as well as in the nondiabetic group (DeltaLVEF = 13 +/- 2%; DeltaPFR = 0.79 +/- 0.17 EDV/s). The increases in LVEF and PFR were comparable overall but occurred earlier in the nondiabetic group. A blunted increase in plasma catecholamine, cortisol, and glucagon concentrations occurred in response to hypoglycemia in the diabetic subjects. During euglycemic hyperinsulinemia, LVEF also increased in both the diabetic (DeltaLVEF = 7 +/- 1%) and nondiabetic (DeltaLVEF = 4 +/- 2%) groups, but PFR increased only in the diabetic group. In the comparison of the responses to hypoglycemic and euglycemic hyperinsulinemia, only the nondiabetic group had greater augmentation of LVEF, PFR, and cardiac output in the hypoglycemic study (P < 0.05 for each). Thus intensively treated type 1 diabetic patients demonstrate delayed augmentation of ventricular function during moderate insulin-induced hypoglycemia. Although diabetic subjects have a more pronounced cardiac response to hyperinsulinemia per se than nondiabetic subjects, their response to hypoglycemia is blunted.
authors.affiliation: Department of Internal Medicine, School of Medicine, Yale University, New Haven, Connecticut 06520, USA.
authors.forename: R R
authors.initials: RR
authors.lastname: Russell
authors.forename: D
authors.initials: D
authors.lastname: Chyun
authors.forename: S
authors.initials: S
authors.lastname: Song
authors.forename: R S
authors.initials: RS
authors.lastname: Sherwin
authors.forename: W V
authors.initials: WV
authors.lastname: Tamborlane
authors.forename: F A
authors.initials: FA
authors.lastname: Lee
authors.forename: M A
authors.initials: MA
authors.lastname: Pfeifer
authors.forename: F
authors.initials: F
authors.lastname: Rife
authors.forename: F J
authors.initials: FJ
authors.lastname: Wackers
authors.forename: L H
authors.initials: LH
authors.lastname: Young
mesh_terms: D000328:Adult; D002302:Cardiac Output; D002395:Catecholamines / Q000097:blood; D011232:Chemical Precipitation; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy*; D003971:Diastole; D004837:Epinephrine / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005934:Glucagon / Q000097:blood; D015309:Glucose Clamp Technique; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000139:chemically induced* / Q000503:physiopathology*; D007328:Insulin / Q000009:adverse effects* / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D011092:Polyethylene Glycols; D013318:Stroke Volume; D013599:Systole; D016277:Ventricular Function, Left
chemical_list: D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D019344:Lactic Acid; D011092:Polyethylene Glycols; D005934:Glucagon; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine