Biomedical subjects

L Mattiello

Publications and source records attributed to L Mattiello.

41 records · Page 3Linked to original sources

PubMed1990

Arginine vasopressin release from human platelets after irreversible aggregation.

1. The release of arginine vasopressin from human platelets was investigated in platelet-rich plasma after irreversible aggregation induced by adenosine 5'-pyrophosphate, collagen, sodium arachidonate, thrombin and adrenaline in vitro. 2. Arginine vasopressin levels were significantly higher in the supernatant from stimulated platelet-rich plasma than from unstimulated samples, reaching 3.5 X 10(-12) (range 1.6-12.5 X 10(-12) mol/l in the absence of an aggregating agent, 8.8 X 10(-12) (range 4.2-17.5 X 10(-12) mol/l after adenosine 5'-pyrophosphate, 13.7 X 10(-12) (2.2-63.2 X 10(-12) mol/l after collagen, 7.8 X 10(-12) (2.2-14.6 X 10(-12) mol/l after sodium arachidonate, 7.8 X 10(-12) (2.2-16.3 X 10(-12) mol/l after thrombin and 12.2 X 10(-12) (4.8-32.1 X 10(-12) mol/l after adrenaline. 3. An arginine vasopressin level of 18 X 10(12) mol/l, which can be achieved physiologically, increased the sensitivity of platelets to adenosine 5'-pyrophosphate and collagen in vitro; the same concentration of arginine vasopressin caused a potentiation of the effect of catecholamines on the response of platelets to sodium arachidonate. 4. These results indicate that intraplatelet arginine vasopressin is released during aggregation and suggest that a local release of arginine vasopressin could occur after complete platelet aggregation in vivo.

Adenosine Diphosphate↗

PubMed1990

Desensitization of the platelet aggregation response to adrenaline during insulin-induced hypoglycaemia in man.

The aim of the present study was to investigate the influence of insulin-induced hypoglycaemia on platelet sensitivity to adrenaline and non-adrenergic agonists in man. Twenty-five healthy male subjects volunteered for the study. To evaluate the effects on platelets of different insulin-adrenaline interrelationships, two experimental models were used. In the first, hypoglycaemia was induced by a 60-min IV infusion of human insulin at the rate of 64 mU m-2 min-1, whereas in the other the same insulin dose was administered as an IV bolus (3.84 U m-2). Throughout the studies, plasma glucose, insulin, and adrenaline were measured together with platelet sensitivity to adrenaline, ADP, platelet activating factor, collagen, and sodium arachidonate. In both studies, hypoglycaemia induced a reduction of platelet sensitivity to adrenaline (p = 0.006 in infusion and p = 0.045 in injection study). In particular, maximal aggregation to adrenaline fell from 47.9 +/- 9.9 (+/- SE) to 31.1 +/- 11.3% at the hypoglycaemic nadir in the infusion study, and from 64.6 +/- 8.2 to 34.6 +/- 10.3% at the hypoglycaemic nadir in the injection study. In the injection study an increase of platelet sensitivity to ADP (p = 0.05), platelet activating factor (p = 0.018), sodium arachidonate (p = 0.035), and collagen (p = 0.027) was also found, in agreement with observations already published using the infusion protocol. Thus, insulin-induced hypoglycaemia increases platelet sensitivity to non-adrenergic agonists and decreases platelet response to adrenaline.

Adenosine Diphosphate↗

PubMed1989

Insulin influences the renin-angiotensin-aldosterone system in humans.

This study investigates whether insulin influences the renin-angiotensin-aldosterone system in humans. Six healthy male volunteers were placed on a 30-minute euglycemic insulin clamp at 160 microU/mL; euglycemia was maintained also in the following 60 minutes by means of appropriate dextrose infusion. Throughout the study, plasma renin activity, angiotensin II, aldosterone, and factors involved in the regulation of the renin-angiotensin-aldosterone system were measured: catecholamines, angiotensin-converting enzyme, sodium, and potassium. A significant increase of plasma renin activity and angiotensin II was observed, and a decrease of aldosterone was also detected. These changes can be ascribed to the effects of the rapid insulin-induced plasma potassium decrease on plasma renin activity and aldosterone secretion because they did not occur in a control clamp study with a potassium infusion.

Adult↗

PubMed1988

Insulin-induced hypoglycaemia increases plasma concentrations of angiotensin II and does not modify atrial natriuretic polypeptide secretion in man.

Insulin-induced hypoglycaemia causes profound haemodynamic changes, commonly ascribed to catecholamine increase. The aim of the present study was to investigate the influence of insulin-induced hypoglycaemia on non-adrenergic factors potentially involved in haemodynamic regulation: angiotensin II and alpha-human atrial natriuretic polypeptide. Fourteen healthy male subjects, aged 25.5 +/- 0.74 years, body mass index 23.81 +/- 0.68 kg/m2, received (after an overnight fast and at least 60 min rest in a supine position) an i.v. bolus injection of human regular insulin (Actrapid HM, Novo, Bagsvaerd, Denmark: 3.84 U/m2). Serial venous blood samples were drawn in the following 150 min, to measure plasma glucose, angiotensin II, alpha-human natriuretic polypeptide, and factors potentially involved in the regulation of the renin-angiotensin-aldosterone system. During the study, we observed a plasma glucose fall, reaching a nadir of 1.95 +/- 0.11 mmol/l between 25 and 30 min, and an increase of angiotensin II (from 7.6 +/- 0.8 to 13.5 +/- 1.1 pg/ml, p = 0.01, quadratic model evaluated by an analysis of the variance for repeated measures), whereas atrial natriuretic polypeptide remained unchanged. As far as the regulation of the renin-angiotensin-aldosterone system is concerned, the increase of angiotensin II is attributable to the increased plasma renin activity, whereas angiotensin converting enzyme was not modified. The increase of plasma renin activity, in turn, is attributable both to the increased catecholamine concentrations and to the decreased potassium levels. Both adrenocorticotropic hormone and angiotensin II are potentially involved in the hypoglycaemia-induced increase of aldosterone concentrations.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Phenothiazine compounds enhance phentolamine effects on platelet aggregation and thromboxane B2 production.

In the present study we investigated the influence of phentolamine and the phenothiazine compounds chlorpromazine and trifluoperazine on human platelet aggregation as well as the effect of the association of phentolamine and the phenothiazines on responses to adenosine diphosphate, collagen, thrombin, ionophore A23187 and phorbol-myristate acetate, release reaction, thromboxane B2 synthesis and intraplatelet cyclic adenosine monophosphate levels. Phentolamine and phenothiazines exerted a dose-dependent inhibitory effect on aggregation induced by different concentrations of adenosine diphosphate and decreased the response to other agonists; furthermore, the phenothiazines enhanced the inhibitory effects of phentolamine on aggregation and thromboxane B2 synthesis, without influencing intraplatelet cyclic adenosine monophosphate levels. Phorbol ester-induced platelet activation was also inhibited in a dose-dependent way by each compound and by an association of phentolamine and phenothiazines, suggesting that the antiplatelet properties of these compounds might also be ascribed to intracellular events.

Adenosine Diphosphate↗