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Biomedical subjects

B Marasini

Publications and source records attributed to B Marasini.

At least 19 recordsLinked to original sources
PubMed1992

Tissue-type plasminogen activator and von Willebrand factor plasma levels as markers of endothelial involvement in patients with Raynaud's phenomenon.

In order to investigate the significance of high circulating levels of von Willebrand factor (vWF), recently observed in patients with vascular diseases, we compared the plasma levels of vWF with those of tissue-type plasminogen activator (t-PA) and the platelet content of serotonin (5-HT) in 40 patients with Raynaud's phenomenon (RP), primary or associated to systemic sclerosis (SSc), and in 14 patients with chronic peripheral obstructive disease due to arteriosclerosis (PAOD). VWF and t-PA plasma levels were significantly increased (p < 0.001) in SSc (vWF: 158.2, range 116.3-305.0%; t-PA: 10.2, range 6.4-17.8 ng/ml). By contrast, normal plasma levels of both vWF (85.3, range 53.5-157.0%) and t-PA (6.5, range 2.7-9.3 ng/ml) were observed in primary RP. VWF and t-PA were normal in PAOD patients, compared with age-matched healthy controls (vWF: 143.0, range 57.0-204.0%; t-PA: 7.5, range 3.4-13.6, ng/ml). The platelet content of 5-HT was within the normal range (37.3-99.7 ng/10(8) platelets) in RP patients, but significantly reduced (P < 0.05) in PAOD patients (39.0, range 14.7-91.4). Our data suggest that the different pattern of circulating vWF and t-PA between SSc and arteriosclerotic patients may be related to a different endothelial cell involvement. Whether this increase may reflect active attempts of regeneration and repair, indicating endothelial cell viability rather than damage is a matter of speculation.

Adult↗
PubMed1991

L-arginine therapy in Raynaud's phenomenon?

Since L-Arginine is the substrate for nitric oxide synthesis by vascular endothelial cells the effects of L-arginine treatment on the digital vascular response to local stimuli were investigated in patients with primary or secondary Raynaud's phenomenon. After therapy, patients with Raynaud's phenomenon secondary to systemic sclerosis showed: (1) higher digital vasodilation after local warming, (2) cold-induced digital vasodilation, and (3) increase of plasma levels of tissue-type plasminogen activator.

Adolescent↗
PubMed1991

Cold-induced changes in plasma norepinephrine, epinephrine and dopamine concentrations in patients with Raynaud's phenomenon.

To investigate the role of the sympathetic system in Raynaud's phenomenon, which has not yet been elucidated, we measured the levels of norepinephrine, epinephrine and dopamine before, immediately and 30 min after the cold pressor test in plasma from 17 patients with primary, 6 with secondary Raynaud's phenomenon and 19 volunteers, matched for age and sex. Patients had significantly low baseline epinephrine (0.13 +/- 0.02 vs 0.37 +/- 0.04, nmol/l, p less than 0.001, mean +/- S.E.), but normal norepinephrine and dopamine (norepinephrine: 1.77 +/- 0.16 and 2.06 +/- 0.18; dopamine: 0.10 +/- 0.01 and 0.11 +/- 0.02, patients and controls). Immediately after the cold test norepinephrine significantly increased (p less than 0.001) in patients (2.42 +/- 0.22) and controls (3.24 +/- 0.28); epinephrine increased in patients (0.18 +/- 0.02, p less than 0.02); dopamine did not show any significant change (0.13 +/- 0.01 and 0.13 +/- 0.02, patients and controls). In the recovery period, while norepinephrine and epinephrine returned to baseline in both groups, dopamine increased in controls (0.21 +/- 0.04, p less than 0.005) but remained unchanged in patients (0.11 +/- 0.01). We conclude that there is no sympathetic overactivity in Raynaud's phenomenon and propose a role for circulating dopamine in post-ischaemic vasodilatation as an explanation for the particular behaviour of dopamine.

Adult↗
PubMed1990

Effect of chronic ketanserin treatment on serotonin-induced platelet aggregation in patients with Raynaud's phenomenon.

To investigate whether the variable efficacy in Raynaud's phenomenon of long-term oral ketanserin treatment might be related to variation in the sensitivity of 5-HT2 receptors to ketanserin, serotonin-induced platelet aggregation was measured in ten patients with Raynaud's phenomenon at various times after treatment with ketanserin. Platelet aggregation was completely inhibited 90 min after 40 mg ketanserin, but not 12-14 h after the last dose of 40 mg on the 31st day of continuous twice daily administration. However, 90 min after an additional dose of 40 mg, platelet aggregation was again completely inhibited. The present results indicate that ketanserin 40 mg b.d. does not continuously inhibit platelet 5-HT2 receptors in patients with Raynaud's phenomenon and suggest that more frequent intake might be more effective.

Administration, Oral↗
PubMed1990

Digital blood flow and 5-hydroxytryptamine receptor blockade after ketanserin in patients with Raynaud's phenomenon.

1. The effect of ketanserin on digital blood flow and 5-hydroxytryptamine (5-HT)-induced platelet aggregation was studied in 18 patients with Raynaud's phenomenon. 2. Measurements were made before and after a single dose of 20 mg ketanserin and again after 1 month of continuous treatment with 20 mg ketanserin three times a day. 3. Digital blood flow was assessed by changes in digital pulse volume; platelet aggregation by changes in light transmission after challenge with 10(-5) M 5-HT. 4. Ketanserin induced a rise in digital blood flow and blocked the platelet response to 5-HT; the two events were not correlated and were independent of subjective improvement. 5. These data do not support the suggestion that 5-HT2-receptor blockade is of major importance in the dilatory effect of ketanserin in Raynaud's phenomenon.

Adult↗
PubMed1989

Abnormal platelet aggregation in patients with Raynaud's phenomenon.

Platelet aggregation in vitro to several aggregating agents (serotonin (5-HT), adenosine diphosphate, adrenaline and collagen) was studied in 16 patients with primary and secondary Raynaud's phenomenon and compared with that in 13 normal volunteers. Platelets from patients with Raynaud's phenomenon had significantly greater responses to all the 5-HT concentrations tested (p less than 0.001 for 10 microM; p less than 0.01 for 1 microM; p less than 0.05 for 0.1 microM; p less than 0.02 for 0.025 microM) and to low doses of adenosine diphosphate (p less than 0.01 for 1 microM; p less than 0.02 for 0.5 microM) but normal responses to collagen, adrenaline, and high doses of adenosine diphosphate. Patients with secondary Raynaud's phenomenon were significantly more hypersensitive to 0.5 microM adenosine diphosphate than patients with primary Raynaud's phenomenon. In patients with secondary Raynaud's phenomenon there was a significant correlation between the extent of 5-HT aggregation and the duration of the disease. The finding that platelets from patients with Raynaud's phenomenon have enhanced responses to 5-HT and adenosine diphosphate, but normal responses to adrenaline and collagen, is consistent with a role for 5-HT in this disease.

Adenosine Diphosphate↗
PubMed1989

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1987

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↗
PubMed1986

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↗
PubMed1986

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↗
PubMed1980

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↗