Localization of insulinomas: Comparison of conventional arterial stimulation with venous sampling (ASVS) and superselective ASVS

2000 ◽  
Vol 41 (2) ◽  
pp. 172-177 ◽  
Author(s):  
Y. Baba ◽  
N. Miyazono ◽  
M. Nakajo ◽  
I. Kanetsuki ◽  
H. Nishi ◽  
...  
Keyword(s):  
Hepatic Vein ◽  
Calcium Gluconate ◽  
Serum Insulin ◽  
Mesenteric Arteries ◽  
Venous Sampling ◽  
Insulin Levels ◽  
Pancreatic Body ◽  
Pancreatic Artery ◽  
Pancreatic Insulinoma ◽  
Detailed Evaluation

Purpose: To examine the value of superselective arterial stimulation venous sampling (ASVS) to localize insulinomas. Material and Methods: Superselective ASVS (SS-ASVS) was performed in 9 patients with insulinoma. Injection of secretagogue (calcium gluconate: 0.01 mEq Ca++/kg) was performed into the gastroduodenal, splenic (proximal and distal), and superior mesenteric arteries in 9 patients and additionally into the dorsal pancreatic artery in 6 patients. Sampling from the hepatic vein was performed to measure serum insulin concentrations at 30, 60 and 120 s after each injection of secretagogue into these arteries. SS-ASVS results were correlated with surgical findings, compared to those of conventional ASVS. Results: Insulinomas were correctly localized to the head, body or tail of the pancreas by SS-ASVS in 8 patients (89%). Conventional ASVS detected insulinomas in 7 patients (78%), although it could not distinguish whether the insulinoma was located in the pancreatic body or tail in 4 of the 7 patients. There were eight-fold or more increases in serum insulin levels in hepatic venous samples related to the artery supplying the tumor in 8 patients. Localization of the insulinomas was verified at surgery in all patients. Conclusion: SS-ASVS is a useful method for detailed evaluation of overproduction of insulin from pancreatic insulinomas and their localization. When the pancreatic insulinoma is situated in the pancreatic body or tail, the localization is more accurately made by SS-ASVS than by conventional ASVS.

Hypothalamic noradrenergic and sympathoadrenal control of glycemia after stress

1989 ◽  
Vol 256 (2) ◽  
pp. E231-E235
Author(s):  
G. A. Smythe ◽  
W. S. Pascoe ◽  
L. H. Storlien
Keyword(s):  
Insulin Release ◽  
Acute Stress ◽  
Serum Insulin ◽  
Elevated Serum ◽  
Serum Glucose ◽  
Neural Pathways ◽  
Swim Stress ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Positive Correlations

Central noradrenergic pathways play a significant role in mediating blood glucose levels after neuroglycopenia. To further investigate hypothalamic noradrenergic neuronal activity (NNA) and sympathoadrenal influences in glucoregulation, we studied the effects of acute stress on glycemia and insulin release in normal and adrenalectomized (ADRX) rats. Within 5 min of exposure of rats to ether or cold-swim stress, significant positive correlations were evident between hypothalamic NNA and serum glucose levels (r = 0.70, P less than 0.001; at 15 min r = 0.78, P less than 0.0001). Five minutes after stress in the intact rat, insulin release was inhibited and serum insulin levels inversely correlated to hypothalamic NNA (r = 0.45, P less than 0.05). This relationship between insulin and NNA was no longer present 15 min after stress, but the levels of insulin remained inappropriately low with respect to the elevated serum glucose levels (approximately 30% above basal). Blockade of sympathetic noradrenergic pathways by treatment of intact rats with guanethidine prevented the rise in glucose after cold-swim stress but did not prevent the inhibition of insulin release. Fifteen minutes after exposure of ADRX rats to cold-swim stress their hypothalamic NNA and serum glucose levels were similar to intact animals. However, in contrast to their intact counterparts, serum insulin levels were significantly elevated (P less than 0.01). These data are consistent with central noradrenergic neural pathways directly mediating hepatic glucose release and indirectly inhibiting pancreatic insulin release via activation of adrenal medullary catecholamines.

scholarly journals Endothelial dysfunction precedes hypertension in diet-induced insulin resistance

1998 ◽  
Vol 275 (3) ◽  
pp. R788-R792 ◽  
Author(s):  
Prasad V. G. Katakam ◽  
Michael R. Ujhelyi ◽  
Margarethe E. Hoenig ◽  
Allison Winecoff Miller
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Sprague Dawley ◽  
Insulin Resistant ◽  
Glucose Levels

The insulin-resistant (IR) syndrome may be an impetus for the development of hypertension (HTN). Unfortunately, the mechanism by which this could occur is unclear. Our laboratory and others have described impaired endothelium-mediated relaxation in IR, mildly hypertensive rats. The purpose of the current study is to determine if HTN is most likely a cause or result of impaired endothelial function. Sprague-Dawley rats were randomized to receive a fructose-rich diet for 3, 7, 10, 14, 18, or 28 days or were placed in a control group. The control group received rat chow. After diet treatment, animals were instrumented with arterial cannulas, and while awake and unrestrained, their blood pressure (BP) was measured. Subsequently, endothelium-mediated relaxation to acetylcholine was determined (in vitro) by measuring intraluminal diameter of phenylephrine-preconstricted mesenteric arteries (∼250 μM). Serum insulin levels were significantly elevated in all groups receiving fructose feeding compared with control, whereas there were no differences in serum glucose levels between groups. Impairment of endothelium-mediated relaxation starts by day 14 [mean percent maximal relaxation (Emax): 69 ± 10% of baseline] and becomes significant by day 18 (Emax: 52 ± 11% of baseline; P < 0.01). However, the mean BP (mmHg) does not become significantly elevated until day 28 [BP: 132 ± 1 ( day 28) vs. 116 ± 3 (control); P < 0.05]. These findings demonstrate that both IR and endothelial dysfunction occur before HTN in this model and suggest that endothelial dysfunction may be a mechanism linking insulin resistance and essential HTN.

Splanchnic blood flow in the monkey during hemorrhagic shock

1965 ◽  
Vol 208 (2) ◽  
pp. 265-269 ◽  
Author(s):  
Francis L. Abel ◽  
John A. Waldhausen ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Mesenteric Arteries ◽  
Splanchnic Blood Flow

Blood flow in the celiac and superior mesenteric arteries was measured in nine Macaca monkeys during a standardized hemorrhagic shock procedure. Simultaneous pressures were obtained from the hepatic vein, portal vein, and aorta. Each animal was bled rapidly to an arterial pressure of 40 mm Hg and maintained at this level until 30% of the bled volume had spontaneously reinfused. The remaining blood was then rapidly reinfused and the animal observed until death. The results show a lack of overshoot of venous pressure on reinfusion, grossly pale intestines with some microscopic congestive changes, and a decrease in splanchnic conductance throughout the postinfusion period. Hepatic venous pressure exceeded portal pressure in six of the nine animals during the period of hemorrhage. The results are interpreted as indicative of insignificant splanchnic pooling during hemorrhagic shock in this animal.

Effect of Exogenous Secretin on Serum Insulin Levels in Patients with Pancreatic Disease

1971 ◽  
Vol 64 (6) ◽  
pp. 724-726 ◽  
Author(s):  
L T CDR RAYMOND B. JOHNSON ◽  
JOHN SABOL ◽  
DAVID M. McCANCE ◽  
JONAS SODE ◽  
WILLIAM M. LUKASH
Keyword(s):  
Serum Insulin ◽  
Pancreatic Disease ◽  
Insulin Levels
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