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Biomedical subjects

B Marasini

Publications and source records attributed to B Marasini.

At least 37 records · Page 2Linked to original sources

Platelet and plasma serotonin in patients with liver cirrhosis.

To evaluate the role of serotonin in liver cirrhosis, serotonin was determined by high-performance liquid chromatography in plasma, platelets and ascitic fluids from 14 cirrhotic patients. Plasma-free serotonin was within the normal range, but intraplatelet serotonin was significantly low in cirrhosis (p less than 0.001) and this decrease paralleled the severity of the disease. The concentration of serotonin in ascitic fluids was 12% of the corresponding plasma concentrations. Our data indicate that serotonin levels are influenced by hepatic injury, but the reasons for these changes are still unclear.

Ascitic Fluid↗

Ketanserin treatment and serotonin in patients with primary and secondary Raynaud's phenomenon.

In a double-blind, placebo cross-over study in 14 patients with Raynaud's disease, oral ketanserin 40 mg b.d. for two months reduced the number of digital ischaemic attacks in 36% of the patients, with no difference between primary or secondary cases. Intraplatelet and circulating serotonin concentrations were significantly higher in patients than in controls. During treatment there was a significant decrease in intraplatelet serotonin, but no change in circulating serotonin or in the amount of serotonin released by platelets in vitro. The results suggest that oral ketanserin is of minor help in Raynaud's phenomenon and they support a role for serotonin in the disorder.

Adolescent↗

Plasma free and intraplatelet serotonin in patients with Raynaud's phenomenon.

Plasma free and intraplatelet serotonin concentrations were measured by high-performance liquid chromatography coupled with electrochemical detection, in 30 patients with Raynaud's phenomenon of various etiologies. Serotonin was significantly higher in plasma (P less than 0.005) and in platelets (P less than 0.005) from Raynaud's patients than from normal controls. Moreover, plasma circulating serotonin could differentiate primary from secondary Raynaud's phenomenon, with significantly higher levels (P less than 0.05) for patients with an underlying connective tissue disease. Our data indicate a role for serotonin in Raynaud's phenomenon.

Adolescent↗

Circulating dopamine in Raynaud's phenomenon.

Plasma free and conjugated and intraplatelet free dopamine, norepinephrine, and epinephrine levels were determined by high-performance liquid chromatography coupled with electrochemical detection for 20 subjects with Raynaud's phenomenon of various etiologies. Circulating free dopamine and epinephrine were significantly lower in Raynaud's patients than in controls (dopamine 26.0 +/- 13.6 vs 56.3 +/- 39.6 pg/ml, p less than 0.005; epinephrine 25.8 +/- 16.9 vs 56.9 +/- 40.9 pg/ml, p less than 0.005), while the corresponding conjugated forms in plasma and the intraplatelet contents were within normal limits. There were no abnormalities in plasma free, conjugated, or intraplatelet free norepinephrine. All of the levels were independent of the etiology, the duration, and the severity of the disease. The reduced plasma levels of free dopamine and epinephrine might be due to impaired adrenal release in response to some kinds of sympathetic stimulation or to rapid tissue uptake and peripheral metabolism. A possible role for a postischemic dopaminergic vasodilating system is discussed.

Adolescent↗

Cigarette smoking and platelet function.

To assess the influence of cigarette smoking on platelet activation, we studied the changes in intraplatelet and platelet-released serotonin (5-HT) and plasma levels and platelet-associated production of thromboxane B2 (TXB2), in 6 non smokers and 6 habitual smokers, before and after acute exposure to smoke. Before smoking, habitual smokers showed slightly higher, albeit not significantly, 5-HT platelet concentrations and TXB2 plasma levels, as well as lower TXB2 platelet production after collagen and even more after ADP stimulation (0.59 +/- 0.27 vs 1.35 +/- 0.46 and 0.99 +/- 0.47 vs 2.08 +/- 0.51 ng/10(8) platelets for habitual smokers vs controls, 4 and 10 min after ADP, p less than 0.02). No significant differences in platelet 5-HT release were observed. Acute smoking did not induce any significant change from baseline in either 5-HT or TXB2 for controls, while significantly reduced TXB2 production from ADP-challenged platelets from habitual smokers (0.30 +/- 0.15 vs 0.59 +/- 0.27 ng/10(8) platelets, immediately after smoking vs baseline, p less than 0.01). Ninety min after the completion of the smoking, the values had returned to baseline. Immediately after smoking, significant differences were found between habitual smokers and controls for TXB2 platelet production (2.76 +/- 1.78 vs 6.42 +/- 1.60, p less than 0.025 and 3.01 +/- 1.90 vs 6.44 +/- 2.26 ng/10(8) platelets, p less than 0.05, for habitual smokers vs controls, 4 and 10 min after the addition of collagen; 0.30 +/- 0.15 vs 1.20 +/- 0.84 and 0.79 +/- 0.50 vs 1.70 +/- 0.74 ng/10(8) platelets, p less than 0.05, after ADP stimulation). Differences were no longer significant 90 min after smoking. Our data indicate that cigarette smoking is associated with platelet dysfunction, which seems due to impairment of metabolic platelet capacity rather than increased platelet activation in vivo.

Adenosine Diphosphate↗

Serotonin levels in hypertension.

The present study examines the putative role of serotonin (5-hydroxytryptamine) in the pathogenesis of essential hypertension. Intraplatelet and plasma free serotonin levels, as well as the amounts released from aggregating platelets, were measured in six patients with untreated essential hypertension, using high performance liquid chromatography with electrochemical detection. Platelet serotonin contents were similar to those in age-matched controls. However, hypertensive patients showed significantly higher levels of plasma free serotonin as well as a significantly higher release from aggregating platelets, stimulated by collagen or adenosine diphosphate (ADP). These data suggest that serotonin may be involved in the pathogenesis of essential hypertension.

Adult↗

Danazol and stanozolol in long-term prophylactic treatment of hereditary angioedema.

Treatment with 17 alpha-methyltestosterone and with some synthetic androgens prevents attacks of hereditary angioedema (HAE). However, the potential hepatotoxicity of 17 alpha-alkylated androgens raises the problem of long-term prophylactic use of these agents. Therefore we compared the efficacy in preventing HAE attacks of 17 alpha-alkylated steroids (danazol and stanozolol) with non-17 alpha-alkylated derivatives (quinbolone, nandrolone decanoate and mesterolone). As the latter group proved ineffective, it seems that a drug's efficacy in preventing HAE attacks is connected to its 17 alpha-alkylation. Moreover, our long-term observations with the minimum effective dose of danazol seem to indicate the absence of important collateral effects.

Adult↗

Treatment of hereditary angioedema.

The purpose of this study was to report the results of different treatments in 20 patients with hereditary angioedema. Effectiveness of tranexamic acid in preventing swellings was evaluated in 15 patients: in all but 3 subjects tranexamic acid was effective without serious side effects. 15 severe attacks of edema were managed with intravenous infusions of either kallikrein inhibitor (8 cases) or concentrate of C1 esterase inhibitor (7 cases). In only 1 case was the kallikrein inhibitor unsuccessful. C 1 esterase inhibitor concentrate proved highly effective in the treatment of acute attacks (the result was lacking in one patient because of too low dosage of the drug). No side effects were observed with both treatments, but improvement was more rapidly achieved with infusion of C1 esterase inhibitor. The serum levels of C4 and C1 esterase inhibitor and the activity of C 1 esterase inhibitor before and after long-term prophylaxis and acute attacks treatment were investigated.

Adolescent↗

Hepatic function and fibrinolysis in patients with hereditary angioedema undergoing long-term treatment with tranexamic acid.

Prophylactic treatment with antifibrinolytic agents, epsilon-aminocaproic and tranexamic acid, reduces the incidence and severity of attacks in patients with hereditary angioedema. Long-term effectiveness or risk of antifibrinolytic agents has not been established. Sixteen patients needing continuous prophylaxis because of frequency and severity of attacks were treated with tranexamic acid. In four patients this treatment was ineffective and the drug was withdrawn after 2 months. A remission or reduction in the frequency or severity of attacks was observed in 12 patients treated for a period ranging from 8 to 34 months. Hepatic tests and blood fibrinolytic activity were not influenced by long-term oral treatment with tranexamic acid.

Adolescent↗

[Study by means of enzymatic and immunochemical determination of Cl esterase inhibitor in 59 patients with hereditary angioneurotic edema].

Serum C1 esterase inhibitor was determined in 138 members of 18 italian families with hereditary angioedema by immunochemical and enzymatic assays. On the basis of quantitative and functional findings, the type A of hereditary angioedema was diagnosed in 44 subjects, and the type B in 15. Some technical devices concerning serum sample handling were identified. The influence of heparin, EDTA, and citrate on C1 esterase inhibitor activity of normal plasma was also investigated.

Adult↗

Orosomucoid contents of pleural and peritoneal effusion of various etiologies.

Orosomucoid and the contents of seven other proteins were determined by radial immunodiffusion in sera and in pleural or peritoneal fluids of 66 patients. No significant difference between concentration of individual proteins in effusions of neoplastic origin and those of nonneoplastic inflammatory origin was found. In noninflammatory fluids, the protein concentrations were lower, but their distribution was similar to distributions in the other fluids tested. These findings support the view that the protein content of effusions reflects changes in vascular permeability.

Ascitic Fluid↗