Rr. Russell et al., Cardiac responses to insulin-induced hypoglycemia in nondiabetic and intensively treated type 1 diabetic patients, AM J P-ENDO, 281(5), 2001, pp. E1029-E1036
Citations number
34
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Insulin-induced hypoglycemia occurs commonly in intensively treated patient
s with type 1 diabetes, but the cardiovascular consequences of hypoglycemia
in these patients are not known. We studied left ventricular systolic [lef
t ventricular ejection fraction (LVEF)] and diastolic [peak filling rate (P
FR)] function by equilibrium radionuclide angiography during insulin infusi
on (12 pmol.kg(-1).min(-1)) under either hypoglycemic (similar to2.8 mmol/l
) or euglycemic (similar to5 mmol/l) conditions in intensively treated pati
ents with type 1 diabetes and healthy nondiabetic subjects (n=9 for each).
During hypoglycemic hyperinsulinemia, there were significant increases in L
VEF (Delta LVEF = 11 +/-2%) and PFR [Delta PFR = 0.88 +/-0.18 end diastolic
volume (EDV)/s] in diabetic subjects as well as in the nondiabetic group (
Delta LVEF = 13 +/-2%; Delta PFR = 0.79 +/-0.17 EDV/s). The increases in LV
EF and PFR were comparable overall but occurred earlier in the nondiabetic
group. A blunted increase in plasma catecholamine, cortisol, and glucagon c
oncentrations occurred in response to hypoglycemia in the diabetic subjects
. During euglycemic hyperinsulinemia, LVEF also increased in both the diabe
tic (Delta LVEF = 7 +/-1%) and nondiabetic (Delta LVEF = 4 +/-2%) groups, b
ut PFR increased only in the diabetic group. In the comparison of the respo
nses to hypoglycemic and euglycemic hyperinsulinemia, only the nondiabetic
group had greater augmentation of LVEF, PFR, and cardiac output in the hypo
glycemic study (P<0.05 for each). Thus intensively treated type 1 diabetic
patients demonstrate delayed augmentation of ventricular function during mo
derate insulin-induced hypoglycemia. Although diabetic subjects have a more
pronounced cardiac response to hyperinsulinemia per se than nondiabetic su
bjects, their response to hypoglycemia is blunted.