Effect of vagal cooling on the counterregulatory response to hypoglycemia induced by a low dose of insulin in the conscious dog

Citation
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
Citations number
29
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
DIABETES
ISSN journal
00121797 → ACNP
Volume
50
Issue
3
Year of publication
2001
Pages
558 - 564
Database
ISI
SICI code
0012-1797(200103)50:3<558:EOVCOT>2.0.ZU;2-N
Abstract
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.