[Effect of aortic valve replacent for aortic stenosis on cervical arterial blood flow]. / Incidence sur les flux des artères cervicales d'un remplacement valvulaire pour sténose aortique.

Aortic stenosis is known to modify initial upstroke time (IUT) of velocity in peripheral arteries and carotid velocities. The authors conducted a prospective study in 30 patients scheduled for aortic valve replacement for aortic stenosis. The goal was to establish postoperative correction of carotid flow disorders. In the preoperative period, a positive correlation (p < 0.01) was observed between IUT and mean pressure gradient, and a negative correlation (p < 0.02) between IUT and aortic valve area. Post-operatively, the authors observed a large decrease (p < 0.0001) of IUT, and higher (p < 0.05) systolic peaks of velocity (PSV) in all studied arteries. In this article, the authors confirmed the few previous studies which described preoperative velocity modifications in aortic stenosis population, but they also described for the first time their postoperative correction. Therefore, identifying these patterns of peripheral circulatory alterations is important and underestimation of carotid stenosis, currently estimated preoperatively, must be avoided.

Effect of insulin on basal pancreaticoduodenal output of somatostatin in normal and diabetic dogs.

The effect of insulin on basal pancreaticoduodenal output of SRIH was investigated in vivo and compared in normal and alloxan diabetic dogs. The experiments were performed on anesthetized dogs having a T-shaped catheter inserted into the pancreaticoduodenal vein just at the exit of the pancreas for blood sampling. In normal dogs, an insulin infusion (1 IU/kg for 20 min) or an iv insulin injection (0.2 IU/kg over 30 sec) produced, before any change in glycemia, an immediate reduction of the venous pancreaticoduodenal output of SRIH. Then pancreaticoduodenal output of SRIH rose close to starting values and decreased again when blood glucose level became very low. In alloxan-diabetic dogs, insulin infusion (1 IU/kg for 20 min) also induced an immediate inhibitory effect on pancreaticoduodenal SRIH output; the effect was more transient and from 20 min, unlike in normal dogs, an increase in pancreaticoduodenal output of SRIH was observed. In conclusion, exogenous insulin induces an immediate reduction in pancreaticoduodenal SRIH secretion both in normal and diabetic dogs, independently of basal blood glucose level and before any change in glycemia. In contrast, the delayed effect is different: SRIH secretion is reduced in normal dogs, whereas it is enhanced in diabetic dogs.

In vivo study of glucose-induced somatostatin secretion: comparison in normal and alloxan-diabetic dogs.

This work was undertaken to study the effect of glucose on pancreaticoduodenal and peripheral venous somatostatin-like immunoreactivity (SLI) levels in dogs. Our experiments were performed in normal and alloxan diabetic dogs, conscious or anesthetized. The response of somatostatin was studied following intravenous (0.2 g/kg) or oral (1 g/kg) glucose administration. SLI levels were assayed in peripheral venous blood and in superior pancreaticoduodenal venous blood. An interplay of the cholinergic nervous system was challenged both after oral and intravenous glucose load by a prior administration of atropine sulfate (0.2 mg/kg i.v.). Our results show that (a) peripheral venous SLI levels do not reflect pancreatic D-cell activity in alloxan diabetic as in normal animals. (b) Increase of peripheral venous SLI level after oral glucose is under cholinergic nervous system control. (c) In alloxan diabetic dogs, the response of pancreaticoduodenal venous SLI to intravenous glucose was decreased, whereas peripheral SLI response to oral glucose was increased.

Effects of dietary fiber on postprandial glycemic profiles in diabetic patients submitted to continuous programmed insulin infusion.

Conventional (C) or fiber supplemented (F) test breakfast and lunch were given on 3 successive randomized days to six insulin-dependent diabetic patients treated with continuous programmed insulin infusion. Meal distribution was as follows: day 1 (C breakfast and C lunch), day 2 (F breakfast and C lunch), day 3 (F breakfast and F lunch). No rise in blood glucose (BG) was observed after F breakfast (days 2 and 3) while a small rise in BG occurred after the C breakfast (day 1). Significant differences were observed between day 1 and days 2 and 3 for absolute BG values as well as for BG changes (delta BG) from base-line. At lunch slight differences in delta BG were only noted at 45 min (p less than 0.05) between days 2 and 3, while there was no difference between days 1 and 2. Our results indicate that fiber supplementation is useful even in pump-treated insulin-dependent diabetics but that F breakfasts have no influence on the carbohydrate tolerance to the subsequent lunch.

[Importance of the cholinergic nervous system in the postprandial secretion of insulin in dogs]. / Importance du système nerveux cholinergique dans la sécrétion post-prandiale d'insuline chez le chien.

This work was designed to study the evolution of blood glucose and plasma insulin after food intake. The experiments were performed on normal conscious dogs. Blood was sampled from the jugular vein. The animals had a meal consisting of meat (30 g/kg) or received a nutrient undergoing direct resorption, glucose (1 g/kg). 10 minutes before the intake of meal or glucose, some animals received an i.v. injection of atropine (0.2 mg/kg). The ingestion of meat did not change blood glucose level, but induced a biphasic increase in insulin secretion, the second phase persisted at least for 240 minutes. The previous injection of atropine totally suppressed the increase in insulinemia. The oral intake of glucose induced hyperglycemia and a biphasic increase in insulinemia. The injection of atropine suppressed the first phase of hyperinsulinemia; then the increase of insulinemia evolved in parallel to hyperglycemia. These results, observed in the dog, underline the importance of the cholinergic nervous system not only during the early phase of insulin secretion (cephalic phase), but also during a prolonged post-prandial period.

Effects of fenugreek seeds on endocrine pancreatic secretions in dogs.

The components of fenugreek seeds were separated and analyzed to determine which fraction of the seed had hypoglycemic activity. These fractions were administered orally to normal or diabetic dogs for 8 days. The effect on blood glucose and pancreatic hormones was studied in normal dogs. The lipid extract had no effect; the defatted fraction (50.2% fibers: gum 17.7%, hemicellulose 22%, cellulose 8.3%, lignin 2.2%) lowered basal blood glucose level, plasma glucagon and somatostatin levels and reduced the orally induced hyperglycemia. The addition of this fraction to the insulin treatment resulted in a decrease of hyperglycemia and glycosuria in diabetic dogs. The results indicate that the defatted part is responsible for the antidiabetic action. However, the present study does not permit one to know whether the effects are caused by an unknown pharmacological compound or by the gastrointestinal action of fibers.

[Post-hyperglycaemic hypoglycaemia: effects of somatostatin (author's transl)]. / Les hypoglycémies post-hyperglycémiques: effets de la somatostatine.

Precise recordings of reactive (post-hyperglycaemic) hypoglycaemia were ensured by continuous blood glucose monitoring during oral glucose tolerance tests. The definition of hypoglycaemia was limited to the following criteria: absence of chemical diabetes; fall in blood sugar to less than 30% of the fasting level or to less than 2.50 mmol/l (0.45 g/l); development of clinical signs of hypoglycaemia. An infusion of somatostatin over 4 hours slowed down the initial rise in blood sugar during the first 90 minutes and the rise was prolonged throughout the infusion whatever its duration. The maximum glycaemia reached was 13.3 mmol/l (2.40 g/l) at the 250th minute. Interruption of the infusion led to a rapid fall in blood sugar to a level identical (2.1 and 2.5 mmol/l) with and without somatostatin respectively. Somatostatin infusions, while frankly diabetogenic in certain circumstances, do not prevent reactive hypoglycaemia but rather delay its onset.

Effects of somatostatin added to insulin in a glucose-controlled insulin infusion system.

Five insulin treated diabetics were studied on three consecutive days. Overnight variable intravenous insulin infusions were used before each study to maintain normoglycaemia and to calculate the optimal basal insulin infusion rate (1.1 +/- 0.1 U/h) which ws then kept constant throughout the study day. A standard 400 kCal breakfast with 25 g xylose was given at 0800 h. When the blood glucose rose above 4.1 mmol/l, an external artificial pancreas was used to infuse either extra insulin (day INS) or somatostatin for either 3h (day som) or the entire 8h experimental period (day SOM). Peak post-prandial blood glucose values were similar on all three days. The blood glucose rebounded after the cessation of the somatostatin infusion on day som. Post-prandial blood xylose peaks were lowered by somatostatin on both days but rebounded after the cessation of the somatostatin infusion on day som. The area under the plasma and urinary xylose curves was lowered by somatostatin only on day SOM. Growth hormone and glucagon levels were not statistically different on all 3 days. Thus somatostatin, when added to an optimal insulin infusion, minimised the insulin requirements by slowing intestinal absorption, but led to rebound hyperglycaemia if not feed-back controlled.