S. Cardin et al., Effect of vagal cooling on the counterregulatory response to hypoglycemia induced by a low dose of insulin in the conscious dog, DIABETES, 50(3), 2001, pp. 558-564
We previously demonstrated, using a nerve-cooling technique, that the vagus
nerves are not essential for the counterregulatory response to hypoglycemi
a caused by high levels of insulin. Because high insulin levels per se augm
ent the central nervous system response to hypoglycemia, the question arise
s whether afferent nerve fibers traveling along the vagus nerves would play
a role in the defense of hypoglycemia in the presence of a more moderate i
nsulin level. To address this issue, we studied two groups of conscious 18-
h-fasted dogs with cooling coils previously placed on both vagus nerves. Ea
ch study consisted of a 100-min equilibration period, a 40-min basal period
, and a 150-min hypoglycemic period. Glucose was lowered using a glycogen p
hosphorylase inhibitor and a low dose of insulin infused into the portal ve
in (0.7 mU kg(-1) . min(-1)). The arterial plasma insulin level increased t
o 15 +/- 2 muU/ml and the plasma glucose level fell to a plateau of 57 +/-
3 mg/dl in both groups. The vagal cooling coils were perfused with a 37 deg
reesC (SHAM COOL; n = 7) or a -20 degreesC (COOL; n = 7) ethanol solution f
or the last 90 min of the study to block parasympathetic afferent fibers. V
agal cooling caused a marked increase in the heart rate and blocked the hyp
oglycemia-induced increase in the arterial pancreatic polypeptide level. Th
e average increments in glucagon (pg/ml), epinephrine (pg/ml), norepinephri
ne (pg/ mi), cortisol (mug/dl), glucose production mg . kg(-1) . min-l), an
d glycerol (mu mol/l) in the SHAM COOL group were 53 +/- 9, 625 +/- 186, 13
1 =/- 48, 4.63 +/- 1.05, -0.79 +/- 0.24, and 101 +/- 18, respectively, and
in the COOL group, the increments were 39 +/- 7, 837 +/- 235, 93 +/- 39, 6.
28 +/- 1.03 (P < 0.05), -0.80 +/- 0.20, and 73 +/- 29, respectively. Based
on these data, we conclude that, even in the absence of high insulin concen
trations, afferent signaling via the vagus nerves is not required for a nor
mal counterregulatory response to hypoglycemia.