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Biomedical subjects

F Massara

Publications and source records attributed to F Massara.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Practolol inhibition of some salbutamol-induced metabolic and hormonal responses.

The effect of practolol (a selective beta1-adrenergic receptor blocking agent) on increased blood insulin, sugar, lactate and FFA and decreased blood phosphorus and potassium induced by salbutamol (a primarily beta2-adrenergic stimulant) was studied in 6 normal volunteers. Practolol abolished the rise of lactate and glucose, suggesting that changes in these parameters due to salbutamol are mediated by beta1-receptors. The rise of insulin and the fall of potassium were only partially inhibited, and the possible involvement of the beta2-receptors as well in these 2 cases cannot be ruled out. The decrease of phosphorus and the FFA rise were not affected and thus appear to be primarily dependent on beta2-receptors.

Adult↗
PubMedDate not supplied

Effect of propranolol on some adrenaline- and insulin-induced metabolic changes in man.

The effect of propranolol on adrenaline- and insulin-induced changes in blood glucose pyruvate, lactate, phosphorus and potassium were examined in 29 apparently healthy volunteers. A slight, but significant reduction in adrenaline-induced hyperglycaemia was noted, along with suppression of both the increase in pyruvate and lactate and the decrease in phosphorus and potassium attributable to this catecholamine. There was no significant change in the blood glucose curve after insulin whereas insulin-induced increases in pyruvate and lactate were reduced by 44% +/- 17.7 (mean +/- SEM) and 78% +/- 5.4 respectively, and the fall in phosphorus by 48% +/- 3.1; the decrease in potassium, however, was not significantly modified. These findings suggest that changes in plasma pyruvate, lactate and inorganic phosphates induced by insulin, and regarded as espressions of its peripheral metabolism, are greatly dependent on the beta-adrenergic effect of the endogenous catecholamines released during the time when blood glucose values are low.

Adult↗
PubMedDate not supplied

Some metabolic and hormonal effects of salbutamol in man.

The effect of i.v. infusion of a beta-adrenergic stimulant, salbutamol on blood insulin, glucose, lactate, phosphates, potassium and NEFA was studied in 9 normal subjects. The effect of the drug on the blood sugar and insulin response to i.v. glucose was also examined in 4 subjects. Salbutamol was followed by increases in insulin, glucose and lactate, and a fall in blood phosphorus and potassium. NEFA values did not change significantly. These effects of salbutamol were abolished by propranolol and may thus be attributed to its beta-adrenergic stimulating action. Salbutamol also induced a reduction in glucose tolerance, in spite of the presence of enhanced blood insulin levels.

Adult↗
PubMedDate not supplied

The effect of somatostatin on plasma insulin and growth hormone levels in basal conditions and after glucagon in normal and acromegalic subjects.

The effect of low-dose somatostatin (2.5 mug/min i.v.) on blood sugar, insulin and GH levels (basal and after i.v. 1 mg glucagon) was studied in 7 normal and 10 acromegalic subjects. No changes in basal values were noted in normal subjects, whereas the insulin response to glucagon was partly inhibited and the glucose response enhanced. Basal blood glucose was likewise unaltered in the acromegalics. There was, however, a significant, though unrelated, fall in both insulin and GH. The insulin response to glucagon was inhibited to a greater degree than in normal subjects. It is clear, therefore, that somatostatin can inhibit the insulin response to glucagon, as well as that to the other stimuli for which data are given in the literature. Acromegalic subjects appear to be more sensitive to inhibition of insulin secretion by somatostatin, though no relation between this and the drug's parallel inhibition of GH secretion can be shown.

Acromegaly↗
PubMedDate not supplied

The hypophosphatemic and hyperkalemic effect of arginine in man.

The effects of a 0.5 g/kg body weight arginine infusion on plasma inorganic phosphate and potassium were examined in 15 normal subjects, and 6 recently diagnosed insulinopenic diabetics. Plasma phosphorus displayed a highly significant (p less than 0.001) fall in normal subjects, with a maximum fall below the baseline of 1.11 +/- 0.15 mg/100 ml or 33 + 3% (mean +/- SE). In addition, there was a highly significant correlation (p less than 0.01) between these falls and the insulin peaks induced by arginine. Plasma potassium levels, on the other hand, displayed a distinct and significant increase in 7 of the 8 subjects studied in this connection. The maximum increase over the baseline was 1.23 +/- 0.17 meq/l or 33 +/- 6% (p less than 0.01). In diabetic patients, arginine too led to a fall in phosphorus. While this was still significant, it was clearly less than in normal subjects: maximum fall = 0.64 +/- 0.09 mg/100 ml or 15 +/- 3%. Plasma potassium increased to a greater extent than in normal subjects: maximum increase = 1.63 +/- 0.21 meq/l or 42 +/- 6%. These findings show that arginine is responsible for a fall in plasma phosphorus that may well be partly related to the insulin response, and an increase in plasma potassium of clinical significance, whose mechanism(s), however, are still obscure.

Adolescent↗
PubMedDate not supplied

Effect of the somatostatin analog D-Trp8,D-Cys14 on glucose insulin, pancreatic glucagon and growth hormone plasma levels in acromegalics and mild diabetics.

The effect of the somatostatin analog (GHRIH-A) D-Trp8, D-Cys14 on plasma levels of growth hormone, pancreatic glucagon, insulin and glucose was studied in four acromegalic patients and in four maturity-onset mild diabetics. Acromegalics received a bolus iv injection of 25 microgram of GHRIH-A, followed by a continuous infusion of 25 microgram in saline over an hour. Mild diabetics were submitted in two different days to two tests: arginine (30 g in 30 min) +/- GHRIH-A (bolus iv injection of 25 microgram followed by an infusion of 25 microgram/h over 120 min) and arginine + saline. GHRIH-A lead to a significant (2 p less than 0.01) fall in GH basal secretion in acromegalics, and significantly reduced the GH response to arginine in maturity-onset diabetics. The inhibitory effect of insulin secretion was less impressive, but significative in both groups. No significant changes in plasma pancreatic glucagon values were noted. In mild diabetics, GHRIH-A infusion induced a small but significant increase in the blood glucose increment due to arginine. Our data suggest that this somatostatin analog may be potentially useful only when GH suppression is the main therapeutic goal to be reached, as in acromegaly and in severe diabetic retinopathy, but not in metabolic control of mild diabetic patients with a good residual insulin secretion.

Acromegaly↗
PubMedDate not supplied

Partial remission of hyperprolactinemic amenorrhea after bromocriptine-induced pregnancy.

Clinical and/or biological improvement has been observed in 7 out of 17 patients with hyperprolactinemic amenorrhea followed for 6-15 months after the successful outcome of bromocriptine (Parlodel, Sandoz)- induced pregnancy. The ovulatory cycle was resumed in 2 out of these 7 patients (with subsequent spontaneous conception in 1); in 3 others the medroxyprogesterone acetate test became positive. In all cases, post-partum prolactin values were considerably reduced. The possible causes of this improvement are discussed, examining the present data and those in the literature. Regressive lesions, due for example to vascularization defects or hemorrhage occurring in the prolactin-secreting tissue, as a result of the hyperplastic stimulus of estrogens during pregnancy, are suggested as a possible explanation.

Adult↗