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Biomedical subjects

F Balsano

Publications and source records attributed to F Balsano.

At least 73 records · Page 4Linked to original sources
PubMed1990

Plasma atrial natriuretic peptide in young normotensive subjects with a family history of hypertension and in young hypertensive patients.

Plasma atrial natriuretic peptide (ANP) behavior was evaluated in 26 untreated essential hypertensives, 21 normotensives, and 20 normotensives with hypertensive heredity under normal sodium intake (120 mEq of Na+/day). All subjects were men, mean age 22.1 +/- 1.9 years. Plasma ANP was evaluated by radioimmunoassay on samples collected in supine position upon waking and again after 1 h of orthostatism. Resulting data showed that ANP in hypertensives (supine = 44.5 +/- 19.4 pg/mL, orthostatism = 24.1 +/- 11.6 pg/mL) was at higher levels than in controls (supine = 38.3 +/- 19.4 pg/mL, orthostatism = 19.9 +/- 10.6 pg/mL) or in normotensives with hypertensive heredity (supine = 42.1 +/- 16.8 pg/mL, orthostatism = 23.2 +/- 10.8 pg/mL). Mean ANP level was higher in the latter group than in the control group (supine = +9%; orthostatism = +14.2%). In conclusion, plasma ANP is raised in young essential hypertensives, resulting in slightly elevated levels in normotensives with hypertensive heredity.

Adult↗
PubMed1990

Antiplatelet treatment with ticlopidine in unstable angina. A controlled multicenter clinical trial. The Studio della Ticlopidina nell'Angina Instabile Group.

We conducted a controlled multicenter trial with central randomization and evaluation of events under blind conditions involving 652 patients with unstable angina. Patients were treated either with conventional therapy alone (group C) (n = 338) or with conventional therapy combined with an inhibitor of platelet aggregation, ticlopidine 250 mg b.i.d. (group C + T) (n = 314). Patients were assigned randomly within 48 hours of admission and followed up for 6 months. With the "intention-to-treat" approach, the primary end points, vascular death and nonfatal myocardial infarction, were observed in 13.6% of the patients in group C and in 7.3% of the patients in group C + T, which is a reduction in risk of 46.3% (p = 0.009). Vascular mortality was 4.7% in patients in group C and 2.5% in patients in group C + T, which is a reduction in risk of 46.8% (p = 0.139). The risk of nonfatal myocardial infarction was reduced by 46.1% (p = 0.039), with a frequency of 8.9% in patients in group C and 4.8% in patients in group C + T. New Q wave myocardial infarction occurred with a frequency of 6.8% in patients in group C and 3.8% in patients in group C + T, which is a reduction in risk of 44.1% (p = 0.091). Fatal and nonfatal myocardial infarction was 10.9% in patients in group C and 5.1% in patients in group C + T, which is a reduction in risk of 53.2% (p = 0.006). These findings confirm the importance of platelets in the pathogenesis of unstable angina and the usefulness of antiplatelet treatment for the prevention of cardiovascular events.

Angina Pectoris↗
PubMed1990

Circadian variation in the frequency of ischemic stroke.

The frequency of myocardial infarction and sudden death is increased between 6 AM and noon. To determine whether the same is true for the onset of ischemic stroke, we studied 426 consecutive patients within 12 hours after the onset of their first hemispheric stroke. The frequency of onset of hemispheric stroke was significantly (p = 0.0001) higher from 6:01 AM to noon (56.1%) than from 12:01 PM to 6 PM (20.2%), from 6:01 PM to midnight (8.2%), and from 12:01 AM to 6 AM (15.5%). The identification of periods of high risk for vascular events may have important therapeutic implications, such as matching drug effects with vulnerability.

Aged↗
PubMed1990

[Monitoring of respiratory exchange during ergometric test in patients with heart failure: current aspects and prospects].

The current techniques of respiratory gas-exchange monitoring during stress testing in patients with congestive heart failure have provided new physiopathologic and clinical data. The "breath-by-breath" measurement of oxygen consumption and carbon dioxide production and the evaluation of the relationship between these parameters and respiratory volumes, allow to determine both ventilatory and metabolic responses during exercise, thus giving a precise estimate of the effective cardiopulmonary functional capacity. The demonstration of peripheral vascular and metabolic abnormalities by these techniques have provided new insights into the mechanism of dyspnea and fatigue in patients with heart failure. Although the relationship between respiratory and metabolic parameters and hemodynamics has been extensively studied, its mechanisms are still unclear. Moreover, controversy still exists as to the link between functional capacity and prognosis. Finally, recent studies on the cardiopulmonary adaptations to exercise training in patients with left ventricular dysfunction, have clearly demonstrated clinical and hemodynamic improvement after conditioning. These data, if confirmed, may provide a new approach in the management of patients with this disorder.

Anaerobic Threshold↗
PubMed1989

Recognition of hepatitis B virus envelope proteins by liver-infiltrating T lymphocytes in chronic HBV infection.

The Ag specificity and cytotoxic function of human T cell clones, generated from lymphocytes infiltrating the liver of a chronic hepatitis B patient, were studied. Both class I- and class II-restricted T clones specifically proliferated to hepatitis B virus envelope proteins, but not to hepatitis B core Ag. The fine specificity of T cells was studied by using rAg having different composition in relation to HBV-envelope proteins or synthetic peptides of preS regions. The antigenic determinant recognized by T cell clones mapped to the preS2 region based on the response to r(preS1+preS2+S) and to r(preS2+S) and the failure to respond to S or preS1 alone. More precise epitope mapping was based on synthetic preS2 peptides 120-150 or 120-134, which stimulated both class I- and class II-restricted T clones, whereas preS2 153-171 or preS1 1-110 peptides did not; thus, the preS2 120-134 appears to contain both the residues binding to class I molecules and the residues binding to class II molecules. Moreover, strong and specific cytotoxic responses of these clones were observed only when HLA-matched EBV-lines, used as target cells, were previously sensitized with r(preS1+preS2+S) or preS2 peptides, which were shown to stimulate the clones. Thus, a preS2 epitope can represent a target Ag for liver-infiltrating T cells, which could kill the hepatocytes expressing the Ag plus the appropriate MHC molecule.

Adult↗
PubMed1989

Inhibition of cyclooxygenase-independent platelet aggregation by sodium salicylate.

The effect of acetylsalicylic acid (ASA) on platelet aggregation (PA) and thromboxane A2 (TxA2) formation was investigated in vitro and ex vivo after 1 g or 300 mg ASA administration to healthy subjects. 50-100 microM ASA inhibited PA by single aggregating agent such as platelet aggregating factor (PAF) or epinephrine and reduced to less than or equal to 5% of control platelet TxB2 formation, but did not influence PA by epinephrine plus PAF. The latter was inhibited by increasing ASA concentration. In samples incubated with 100 microM ASA and stimulated with epinephrine plus PAF, PA could be inhibited by the addition of 100-300 microM sodium salicylate. After 300 mg-1 g ASA administration to healthy subjects, the inhibition of PA by epinephrine plus PAF was more marked by highest doses of ASA. This study suggests that aspirin inhibits PA with a cyclooxygenase-independent mechanism; this effect is mediated, at least in vitro, by salicylic acid.

Adult↗
PubMed1989

Inhibition of tissue plasminogen activator inhibitor by defibrotide in atherosclerotic patients.

Defibrotide, an antithrombotic drug, was previously shown to activate fibrinolysis. In order to elucidate the relationship between defibrotide treatment and fibrinolysis, ten atherosclerotic patients were given 1200 mg/day defibrotide intravenously for 7 days and then 400 mg/day intramuscularly for another 20 days. t-PA antigen assessed before and after venous occlusion was not affected by the treatment. Tissue PAI activity significantly decreased and t-PA activity, measured after venous occlusion, increased after 8 and 28 days of treatment; both these changes disappeared after defibrotide was discontinued. No particular side effects were detected throughout the investigation. The study suggests that defibrotide increases t-PA activity by reducing PAI activity.

Adult↗
PubMed1989

Blood lipid peroxides in TIA: relation to platelet function and metabolic profile.

Patients with transient ischemic attacks (TIA) were previously shown to have high plasma values of thiobarbituric acid-reactive substances (TBA-RS). To study whether these changes could be related to platelet activability, TBA-RS was investigated in 24 TIA patients before and 24 h after 1 g aspirin, an inhibitor of platelet cyclooxygenase pathway. Baseline TBA-RS values were significantly higher in TIA than in controls. Conversely, TIA patients had TBA-RS values after aspirin similar to controls, suggesting that the increase of plasma TBA-RS was not attributable to platelet hyperfunction. The evaluation of metabolic profile showed that patients with highest TBA-RS had hypercholesterolemia, hypertriglyceridemia, and/or diabetes mellitus. This study suggests that the increase of plasma TBA-RS in TIA could be an epiphenomenon of altered metabolic pathway.

Administration, Oral↗
PubMed1989

Interrelation between factor VII, prekallikrein, and hyperfibrinolysis in advanced cirrhosis.

Factor VII and prekallikrein activities were studied in 37 patients with liver cirrhosis who were in a decompensated state. Sixteen of them died 30-70 days after admission; 21 survived and were discharged after 30-80 days. Seven who died and six survivors had signs of hyperfibrinolysis: factor VII activity differentiated the two groups independently of the presence of hyperfibrinolysis. The presence of hyperfibrinolysis significantly reduced prekallikrein activity, which did not differentiate clearly survivors from non-survivors. Long term follow up of survivors showed a good correlation between factor VII and prekallikrein activities with long term survival. Hyperfibrinolysis seemed to influence the clinical course of patients: 87% of patients with hyperfibrinolysis who died had fatal haemorrhagic episodes. Low factor VII activity may be a precursor of terminal liver insufficiency.

Adult↗
PubMed1989

Conjunctival provocation test as a model for the study of allergy and inflammation in humans.

The clinical response after allergen challenge and immunologic mechanisms leading to tissue inflammation have been extensively studied in the skin, nose and lung of allergic subjects. The present paper reviews personal studies aimed at evaluating clinical, cellular and humoral events after administration of specific allergen to the eye. Specific conjunctival provocation tests performed in grass-sensitive patients caused persisting inflammatory changes in conjunctival scrapings and tear fluid with a significant accumulation of different inflammatory cells depending on the time of observation (neutrophils, 20 min; eosinophils, 6 h; neutrophils, eosinophils and lymphocytes, 12-24 h after provocation). Increasing the dose of allergen resulted in a dose-dependent increase in the number of inflammatory cells recruited. When high doses of allergen were used, the challenge not only induced late-phase histological changes, but also clinical symptoms 6-10 h after provocation. Several mediators of allergic inflammation, such as histamine, C3a des-Arg, leukotrienes B4 and C4, were also present and could be measured in tears after allergen challenge. Our studies represent the first evidence in humans that a late phase of allergic reaction occurs in the eye. They also suggest that the conjunctival provocation test may represent a model for the study of cells and mediators involved in the pathophysiology of allergic inflammation as well as of its pharmacologic modulation.

Allergens↗
PubMed1989

[Holiday heart syndrome: spontaneous reversibility of the electrocardiographic and echocardiographic alterations].

The holiday heart syndrome is characterized by symptomatic arrhythmias more often supraventricular, elicited by alcohol ingestion, typically during the week-end period. After admission, electrocardiographic changes, which disappear in few days, are often reported. A case of an alcoholic with syncopal episodes related to alcohol ingestion is described. In this patient, remarkable changes of ventricular repolarization on the electrocardiogram associated with impairment of ventricular diastolic function on the Doppler echocardiographic study are showed. ECG and echo-Doppler data reversed to normality after few days of alcohol withdrawal.

Alcoholism↗
PubMed1989

Ticlopidine in the treatment of intermittent claudication: a 21-month double-blind trial.

After a 3-month, single-blind, run-in period, 151 patients with intermittent claudication were randomly allocated to receive the antiplatelet agent ticlopidine (250 mg twice per day) or an identical placebo. One hundred and twenty patients completed the double-blind phase of the trial, which lasted 21 months. The primary analysis was performed according to the "intention-to-treat principle" in all 151 enrolled patients. There was, continuing on from the third month after randomization, a progressive and sustained improvement of the pain-free and maximum walking distances in the two treatment groups that was significantly greater in the ticlopidine group. The ankle-arm systolic blood pressure ratio at rest and after exercise increased in a significant manner in the ticlopidine group only. In a secondary analysis, with exclusion of 25 patients because of protocol violations at selection, consistently significant differences in favor of the ticlopidine group were still observed for maximum walking distance and systolic ankle-arm blood pressure ratio, both at rest and after exercise. No major side effects were reported in the treated group. It is concluded that long-term treatment with ticlopidine improves walking ability and ankle systolic blood pressure in patients with claudication.

Blood Pressure↗
PubMed1989

Allergy and asthma: distinguishing the causes from the triggers. An eye model for the study of inflammatory events following allergen challenge.

The study of the late-phase reaction to allergen challenge has greatly contributed to increasing understanding of the relationship existing between immunoglobulin E (IgE) triggering, allergic inflammation and bronchial hyperreactivity, as well as to changing our concept from "causes" to "triggers" of asthma. This paper reviews personal studies on a model of conjunctival provocation in allergic subjects. These studies represent the first evidence of a late-phase reaction in the human eye and contribute to a better knowledge of the network of cells and mediators involved in allergic inflammation which are responsible for heightened bronchial reactivity in allergic asthma.

Asthma↗
PubMed1988

Effect of angiotensin converting enzyme inhibition on platelet angiotensin II content.

The effect of captopril treatment on platelet angiotensin II levels was evaluated in 12 patients with essential hypertension. Captopril significantly lowered (p less than 0.01) mean arterial blood pressure in seven patients (Group 1) and was ineffective in five (Group 2). In Group 1, a marked decrease in plasma angiotensin II levels in both the supine (from 5.5 +/- 0.5 to 2.8 +/- 0.9 pg/ml) and the upright positions (from 17.5 +/- 4.7 to 3.9 +/- 1.6 pg/ml; p less than 0.0025) and a significant increase in platelet angiotensin II levels (from 10.5 +/- 5.3 to 22.4 +/- 17 pg/ml; p less than 0.05) after captopril treatment was observed. In Group 2, no variation was found in plasma angiotensin II levels, whereas platelet angiotensin II levels increased slightly (from 10.8 +/- 3.1 pg/ml to 16.9 +/- 5.2 pg/ml; NS). These findings suggest that the decrease in plasma angiotensin II levels can lead to an increase in platelet angiotensin II receptors or can lead to angiotensin II production in platelets through activation of a feedback mechanism. The second hypothesis suggests that platelets have alternative enzymatic pathways leading to angiotensin II production not inhibited by captopril.

Adult↗
PubMed1988

Inhibition by picotamide of thromboxane production in vitro and ex vivo.

The effect of picotamide on platelet function has been studied in vitro and ex vivo. Picotamide at micromolar concentrations inhibited platelet aggregation induced by ADP, arachidonic acid and collagen, and it also inhibited the production of thromboxane A2 (TxA2). Unlike aspirin, picotamide did not affect the synthesis of prostacyclin by blood vessels. In eight healthy subjects who took picotamide 1200 mg/d platelet aggregation and TxA2 production were inhibited. Picotamide appears to be an antiplatelet drug that reduces TxA2 synthesis without affecting cyclo-oxygenase activity.

Adult↗