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Biomedical subjects

R Pippi

Publications and source records attributed to R Pippi.

8 recordsLinked to original sources
PubMed1989

[Results of a questionnaire on malignant tumors of the oral cavity].

A set of 23 questions on malignant neoplasms of oral cavity has been submitted to a group of 38 graduate in dentistry and dental prosthesis, at the time of their qualifying examination. The answers reveal a sufficient degree of knowledge of the problem but also indicate that some specific aspects of this important question should be probed.

Education, Dental, Continuing↗
PubMed1988

Pancreatic A- and D-cell response to arginine during acute alloxan-induced intra-islet insulinopenia.

This study was performed to investigate the role of pancreatic B-cell function on glucagon and somatostatin response to arginine. Isolated perfused rat pancreas was used for the experiment. Acute B-cell destruction was induced in vitro by 0.56 mM alloxan infused directly into the vascular system of the perfused pancreas. This resulted in a fall in basal insulin release and in a complete absence of hormone response to 20 mM arginine. Glucagon and somatostatin release during metabolic stimulus was superimposable on that observed in the control experiments (no alloxan infusion). We conclude that a normal B-cell function is not required for glucagon and somatostatin response to arginine.

Alloxan↗
PubMed1986

Effects of beta non-selective and beta 1 selective adrenergic blocking agents on glucagon secretion from isolated perfused rat pancreas.

To characterize beta-receptors which affect pancreatic A-cell activity, the effects of propranolol (beta non-selective blockade) and metoprolol (beta 1 selective blockade) were evaluated on epinephrine modulated insulin (IRI) and glucagon (IRG) release both in basal state and during metabolic stimulus (arginine 20 mM). The isolated perfused rat pancreas model with the exclusion of stomach and duodenum was used. Epinephrine infusion (at 10(-7) M) caused a prompt and sustained increase in basal IRG secretion and significantly potentiated glucagon release in response to metabolic stimulus. Insulin secretion was markedly suppressed by epinephrine both in basal conditions and during metabolic stimulus. Propranolol (at 10(-7) M) and metoprolol (at 10(-7) M) infusion clearly and similarly counteracted epinephrine stimulatory effects on IRG secretion but failed to elicit any significant effect on the epinephrine inhibited IRI release either in basal state or during the metabolic stimulus. These results suggest that, at least in the rat, the adrenergic stimulation of IRG release is mediated through a beta 1 receptor.

Animals↗
PubMedDate not supplied

Alpha-adrenergic system in the modulation of pancreatic A and B cell function in normal rats.

The role of the alpha-adrenergic system in the control of pancreatic A and B cell function was investigated in an isolated perfused rat pancreas model. Two experimental procedures were performed. In the first one we evaluated the effects of two distinct concentrations (10(-8) M and 10(-7) M) of five adrenergic substances, with varying degrees of potency on the alpha-adrenergic presynaptic receptor, on insulin (IRI) and glucagon (IRG) release induced by arginine (20 mM) plus glucose (6.6 mM). In the second procedure we studied the effects of the two alpha-blocking agents yohimbine (alpha 2-blocker) and prazosin (alpha 1-blocker) at 10(-7) M on epinephrine-modulated IRI and IRG response to the same combined metabolic stimulus. The inhibitory activity on basal and metabolically induced IRI secretion of the agonists was superimposable on their potency on the presynaptic alpha 2-adrenergic receptors. Similarly, the alpha 1-blocking agent prazosin was less effective than the alpha 2-blocker yohimbine in counteracting the inhibitory effects of epinephrine on basal and arginine plus glucose-induced insulin release. The alpha-cell activity was clearly stimulated by epinephrine, whereas selective alpha-adrenergic drugs showed no significant action on IRG secretion. Both alpha-blockers were ineffective on basal IRG release, while they had some potentiating effect on the epinephrine-induced glucagon release in basal state and during the metabolic stimulus, without a significant difference between the two drugs. We conclude that, at least in the isolated perfused rat pancreas, alpha 2-adrenergic receptors are involved in the inhibition of IRI release induced by catecholamines. On the contrary, the alpha-adrenergic system does not seem to play an essential role in the regulation of IRG secretion; the potentiation of the epinephrine-induced stimulation of A cell function by the alpha-adrenergic blockade could be accounted for by a greater availability of the catecholamine at the beta-receptor binding sites.

Adrenergic alpha-Agonists↗