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Biomedical subjects

H Leblanc

Publications and source records attributed to H Leblanc.

At least 55 records · Page 3Linked to original sources
PubMed1982

Echocardiographic study of the left auricular function and its influence on left ventricular performance in normal and diseased heart. I. Normal subjects.

Despite some limitations of the echocardiographic estimation of ventricular volume, previous studies have proved its utility in clinical practice. Assuming that the variation of ventricular volume during atrial contraction represents the atrial output, we have tried to study atrial function, its variations and its contribution to ventricular function in physiological states. For this purpose, an echocardiogram of good quality was recorded in 60 normal African subjects, mean age: 26.5 +/- 9.2. Various atrial parameters were derived from the echocardiographic dimension. Correlation was good between these indexes and the time parameters with the highest value for heart rate and the percentage of total diastolic duration of the auriculo-ventricular conduction. In order to test atrial contribution to ventricular function, ventricular and auricular indexes were correlated. Atrial systolic volume (ASV), calculated as the difference between end diastolic volume and preauricular volume on the left ventricular echocardiogram, and atrial index (ASV/BSA), have been found to have a good correlation with the ventricular stroke volume and cardiac index.

Adult↗
PubMed1982

[Effect of long-term administration of clonidine on growth hormone secretion in hypertensive diabetics].

The anti-hypertensive effect of clonidine is closely related to its central alpha-agonist action. In acute administration, the drug provokes a significant increase in the plasma concentrations of growth hormone (GH). In chronic administration, the effects of clonidine on GH secretion are not well documented. Clonidine was administered at a daily dose of 0,15 to 0,30 mg to 10 non-obese diabetic hypertensive male subjects for at least 3 months. Blood glucose and GH plasma concentrations were determined 15 times during the 24-hour cycle. Blood glucose and GH values recorded before the intake and after stopping the drug, in the basal state, after meals, after measured muscular exercise and during the first stage of sleep could be superimposed when on and off clonidine. The effects of prolonged administration of clonidine on GH secretion thus differ markedly from the effects of acute administration as in non diabetic subjects. The long-term use of clonidine does not induce a chronic increase of GH plasma concentrations which might worsen the evolution of the diabetic microangiopathy.

Adult↗
PubMed1977

The effect of dopamine infusion on insulin and glucagon secretion in man.

The effect of dopamine on the release of insulin and glucagon was investigated in eight adult subjects. Dopamine infused iv at a rate of 4 mug/kg/min X 2 hr, unaccompanied by cardiovascular changes, induced a prompt and significant increase in plasma insulin and glucagon and in plasma glucose levels. These findings suggest that dopamine may stimulate both alpha and beta cells.

Adult↗
PubMed1977

The inhibitory effect of dopamine agonists on LH release in women.

Our demonstration of an inhibitory effect of dopamine on LH release prompted us to examine whether a similar action exists for dopamine agonists, such as L-dopa and 2-bromo-alpha-ergocryptine (CB-154). Following the administration of L-dopa (0.5 g, orally) to 6 normal women in the early follicular phase, a significant fall in mean LH levels after 1 h which lasted for 5 h was observed (P less than 0.00005). This was followed by a significant rebound above basal levels between the 7th and 10th h (P less than 0.00005). The expected fall in mean PRL levels which lasted for 4 h (P less than 0.00001) was followed by a significant rebound above basal levels after the 6th h (P less than 0.00001)). There was no significant change in mean FSH levels. Following the administration of CB-154 (2.5 mg. orally) to 6 women with hyperprolactinemic amenorrhea, there was also a significant fall in LH levels (P less than 0.00001) and in FSH levels (P less than 0.00001) from 5 h until the study ended at 10 h. The anticipated PRL suppression was also observed and persisted for the duration of the 10 h study. The demonstration of an inhibitory effect of L-dopa and CB-154 on LH release adds further support to the role of dopaminergic control of pituitary LH secretion.

Amenorrhea↗
PubMed1976

The effect of L-dopa and chlorpromazine on prolactin and growth hormone secretion in normal women.

The time course of simultaneous changes in prolactin (PRL) and growth hormone secretion in response to a single dose of L-dopa and chlorpromazine was determined in normal women. L-Dopa induced greater, but shorter (30 minutes), growth hormone release than concomitant suppression of PRL secretion. The PRL peak following chlorpromazine occurred at the same time as the nadir of PRL after L-dopa (3.5 hours). The quantity of PRL release inhibited by L-dopa equaled the amount of PRL secretion during the period of rebound, suggesting L-dopa inhibits PRL release, but not synthesis, by the pituitary.

Adult↗
PubMed1976

Glucagon secretion in late pregnancy and the puerperium.

Fasting plasma glucagon levels in late pregnancy were not significantly changed from those of nonpregnant matched control subjects, but at 6 to 8 weeks post partum a significant decrease in fasting glucagon levels was observed. Acute elevation of plasma glucose levels (via 25 Gm. intravenous glucose loading) induced a suppression of glucagon levels. This glucose-mediated glucagon suppression appeared to be less during late pregnancy which is probably related to the smaller increments of plasma glucose following intravenous loading in late pregnancy as compared to postpartum values.

Adult↗
PubMed1976

Effects of dopamine infusion on pituitary hormone secretion in humans.

Dopamine, infused at a rate of 4 mug/kg/min for 3-4 h unaccompanied by any significant changes in cardiovascular dynamics, induced a prompt and sustained suppression of circulating prolactin (PRL) levels in normal men and women as well as in patients with hyperprolactinemia. At the discontinuation of the infusion, there was a marked rebound in PRL levels in normal subjects and a rapid return to basal levels in hyperprolactinemic patients. Dopamine infusion also induced a significant fall in LH levels in the normal subjects with a marked rebound in LH levels following the infusion. No significant changes in GH, TSH, and FSH levels were observed. These data indicate that in man a dopaminergic mechanism ixists in the regulation of PRL secretion and that dopamine also exerts an inhibitory effect of LH release.

Dopamine↗
PubMed1975

Inhibitory action of somatostatin on pancreatic alpha and beta cell function.

In normal men, the administration of somatostatin almost completely abolished the glucose stimulated insulin-release seen during control studies (without somatostatin), and caused a further reduction in glucagon secretion beyond that induced by hyperglycemia. Following the infusion, there was a rapid and marked rebound for insulin but not glucagon secretion. These events were attended by a marked retardation of the glucose disappearance rate (K) which exhibited two clearly separable components; the initial slow component (mean K equals 0.64) coincided with the period of insulin suppression and was followed by a faster component (mean K equals 1.37) temporally related to the marked rebound increase in insulin release after discontinuation of the somatostatin infusion. Similarly, the addition of somatostatin infusion completely blocked the release of insulin and growth hormone and delayed the release of glucagon stimulated by arginine infusion. Following the somatostatin infusion there was a small rise in GH and a marked rebound for insulin and this was associated with a higher level of plasma glucose than that found following arginine infusion alone. These data establish that the administration of somatostatin can effectively block the release of insulin stimulated by arginine and glucose, can attenuate the release of glucagon induced by arginine and can enhance the glucose-mediated glucagon suppression. The attendance of a relative hyperglycemia during these events is probably the net result of an impediment in peripheral glucose disposition due to acute insulin lack and a decreased hepatic glucose output secondary to glucagon suppression.

Adult↗
PubMed1975

Comparison of cylic and linear forms of somatostatin in the inhibiton of growth hormone, insulin and glucagon Secretion.

The relative potency of cyclic and linear somatostatin in their inhibitory action on GH, insulin and glucagon secretion was assessed in 7 normal adult men. Administration of linear or cyclic somatostatin as a single intravenous bolus (50 mug) resulted in a prompt and concomitant decline in both insulin and glucagon. While both peptides elicited a quantitatively similar suppression of glucagon secretion, the decline in basal insulin level was greater with the cyclic than with the linear preparation. Both the linear and cyclic form of somatostatin appears to be more potent in the inhibition of insulin than glucagon. No discernable change in plasma glucose and GH levels was observed.

Adult↗
PubMed1975

The inhibitory effect of somatostatin on growth hormone, insulin and glucagon secretion in diabetes mellitus.

The inhibitory effect of somatostatin on insulin, glucagon and growth hormone secretion was studied in 5 patients with diabetes mellitus. In three maturity onset diabetics, somatostatin infusion abolished the insulin rise induced by breakfast and oral glucose, and in 2 of them, inhibited the basal insulin secretion by 50% seen during control studies. Concomitantly, there was a marked and prompt reduction of glucagon levels (50%) with a sustained effect. The plasma glucose levels were either unchanged or slightly increased. Following the somatostatin infusion, there was a prompt rebound increase in both insulin and glucagon levels with a relatively stable plasma glucose concentration. In contrast, a drastic reduction of plasma glucose in face of a relatively small fall in plasma glucagon in response to somatostatin infusion was observed in 2 insulin-dependent diabetics. In all patients, the episodic release of growth hormone seen during the control day was abolished during somatostatin infusion.

Depression, Chemical↗
PubMed1975

The response of pancreatic and pituitary hormones to pulses and constant infusion of somatostatin.

The inhibitory action of pulses and constant infusion of somatostatin on the secretion of pancreatic and pituitary hormones was studied serially in 7 normal men and 2 untreated acromegalics. In normal men, significant inhibition of basal release of insulin and glucagon was elicited by as little as 1 mug dose of a pulse of somatostatin. Increasing doses of somatostatin (5, 50, 250 and 500 mug) given as a single pulse at weekly intervals produced what appears to be a decreased inhibition of glucagon while no measurable relationship between the dose of somatostatin and the degree of inhibition of insulin was seen. Given during the same day, incremental doses (from 1 to 250 mug) of pulses of somatostain produced a progressive decline in both glucagon and insulin. The elevated basal levels of GH, insulin and glucagon seen in acromegalics, were inhibited by a pulse of somatostatin as little as 2 mug. These inhibitions were sustained during the constant infusion of somatostatin (2.5 mug/min), and a rebound in GH, insulin and glucagon appeared promptly following the infusion.

Acromegaly↗
PubMedDate not supplied

[Effect of glipizide on glycemic control and peripheral insulin sensitivity in type 1 diabetics].

To assess the effect of Glipizide on glycaemic control and peripheral insulin sensitivity, 9 type 1 (insulin dependent) diabetic patients with normal BMI, mean age 42.1 +/- 11.0 years, diabetes duration 16.3 +/- 9.2 years were studied. They were treated by continuous subcutaneous insulin infusion for a mean duration of 32.2 +/- 11.0 months, they were in good glycaemic control (mean HbA1 7.9 +/- 1.2%, upper limit of normal value 7.5%). In a double blind randomized control study they were successively allocated for a three month period to 15 mg of Glipizide daily or a Placebo. At the end of each period the following parameters were recorded: HbA1, mean plasma glucose levels, daily insulin dosage: basal rate and pre prandial bolus, peripheral insulin sensitivity assessed by euglycaemic hyperinsulinic clamp technique, the addition of Glipizide did not induce any statistically significant modification of HbA1, glycaemic values, and daily insulin dosage: basal rate 18.2 +/- 8.7 vs. 17.9 +/- 7.3 IU/24 hours and pre prandial bolus 18.6 +/- 7.0 vs 17.6 +/- 6.3 IU/24 hours. During the glucose clamp, glucose uptake was similar under Glipizide or Placebo with the 3 levels of insulin infused. These results suggest that in type 1 diabetic patients the addition of Glipizide to insulin therapy does not alter glycaemic control and peripheral insulin sensitivity.

Adult↗
PubMedDate not supplied

Dissociated effects of nicardipine on vascular tone and insulin secretion.

Because Ca2+ antagonists may alter glucose homeostasis by blocking calcium entry into pancreatic beta-cells, this risk was evaluated for nicardipine, a new dihydropyridine derivative with vasodilatory effects. It was tested in vitro for its vascular and insulinotropic effects on isolated perfused rat pancreases. In vivo, an oral glucose tolerance test (OGTT) was conducted, and blood pressure was recorded in eight hypertensive patients with glucose intolerance who were given 90 mg/day nicardipine for 2 weeks in a single-blind placebo-controlled study. In vitro, insulin output was inhibited by 10(-4) M nicardipine but not by 10(-8) M and 10(-6) M, whereas significant changes in intrapancreatic perfusate flow indicated that vascular resistance was similarly reduced by all three concentrations. In vivo, blood pressure diminished significantly after nicardipine, but neither glucose tolerance nor insulin release was further impaired during OGTT. From these in vitro data and this short-term clinical follow-up, it is suggested that nicardipine reduces vascular tone at doses lower than those required to inhibit insulin secretion.

Adult↗