Iron, platelet function, and coronary heart disease: a possible link?
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Blood Platelets↗
Biomedical subjects
F Balsano
Publications and source records attributed to F Balsano.
Atrial natriuretic peptide in non-modulating essential hypertension.
To evaluate the atrial natriuretic peptide response to angiotensin II (Ang II) infusion in non-modulating hypertension, we studied 31 men with essential hypertension. These patients were subdivided into groups of low renin patients (n = 8), non-modulators (n = 11), and modulators (n = 12) according to their renin profile and ability to modulate renin and aldosterone responses to a graded infusion of Ang II (1.0 and 3.0 ng/kg per minute) on a low Na+ intake (10 mmol Na+ per day). During basal conditions, plasma atrial natriuretic peptide was higher (p < 0.05) in low renin patients (16.34 +/- 2.67 fmol/mL) than in both modulators (10.59 +/- 4.29 fmol/mL) and non-modulators (9.85 +/- 2.64 fmol/mL). During Ang II infusion, plasma atrial natriuretic peptide significantly increased in both low renin (27.67 +/- 2.61 fmol/mL at 60 minutes, p < 0.01) and modulating (20.36 +/- 3.07 fmol/mL at 60 minutes, p < 0.05) patients, whereas it did not change in non-modulators (13.94 +/- 4.39 fmol/mL, NS). After 5 days on a high sodium intake (200 mmol Na+ per day), plasma atrial natriuretic peptide rose in modulating (20.61 +/- 2.31 fmol/mL, p < 0.01 versus low sodium intake), non-modulating (20.11 +/- 6.48 fmol/mL, p < 0.01 versus low sodium intake), and low renin (26.13 +/- 3.81 fmol/mL, p < 0.001 versus low sodium intake) hypertensive patients. When the Ang II infusion was repeated with a high sodium intake, plasma atrial natriuretic peptide increased again in low renin and modulating patients, whereas it did not change in non-modulators.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Enhanced blood pressure response to cyclooxygenase inhibition in salt-sensitive human essential hypertension.
To evaluate the influence of salt sensitivity on the blood pressure response to oral indomethacin treatment, we studied 35 hospitalized essential hypertensive patients (24 men and 11 women, aged from 40 to 55 years). During a normal NaCl intake (120 mmol Na+ per day), patients were assigned to receive in a randomized double-blind fashion either 200 mg indomethacin (25 patients) or placebo (10 patients) for 5 days. Two weeks after the interruption of indomethacin treatment, during which the normal NaCl intake was continued, salt sensitivity was assessed by giving each patient a high (220 mmol Na+ per day for 10 days) and then a low (20 mmol Na+ per day for 10 days) NaCl diet. Blood pressure changes were evaluated, and the measurement taken at the end of the 2 weeks under normal sodium intake was considered baseline blood pressure. Patients were classified as salt sensitive when a diastolic blood pressure change of 10 mm Hg or more occurred after both low and high periods of sodium intake. In salt-resistant patients treated with indomethacin (n = 12, nine men and three women, mean age 50.5 +/- 3.7 years), neither blood pressure (systolic blood pressure from 150.8 +/- 11.2 to 154.6 +/- 9.3 mm Hg, NS; diastolic blood pressure from 99.3 +/- 2.1 to 101.1 +/- 4.4 mm Hg, NS) nor the urinary Na+ excretion (from 108.1 +/- 20.9 to 97.9 +/- 9.1 mmol/24 hr, NS) was significantly affected by the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Urinary kallikrein excretion and plasma atrial natriuretic peptide in human salt-sensitive hypertension.
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Adult↗
Effects of short-time insulin suppression on renal sodium excretion in type II diabetic hypertensives.
The effects of a short-time insulin suppression on Na+ excretion were evaluated in 9 type II diabetic hypertensive males. All patients had a body mass index < 26 and normal plasma lipid levels. After 2 weeks under constant NaCl intake (120 mEq of NaCl daily) either octreotide, a somatostatin analogue, or its vehicle were infused in a forearm vein during acute volume expansion (0.20 ml/kg/min isotonic saline given intravenously over a period of 30 min). A double blind randomized cross-over design was followed, and each patient was given both infusions at one week interval. Blood and urine samples for the evaluation of plasma insulin and serum and urine Na+ were taken at time-30, 0, 30, 60, 90, 120, and 240 min. Our data showed that octreotide completely suppressed insulin levels (from time 0 to 60 min). During acute volume expansion+octreotide, Na+ excretion was 0.20 +/- 0.15 mEq/min at time 0, 0.23 +/- 0.21 mEq/min at time 30, 0.64 +/- 0.24 mEq/min at 60 (p < 0.05 vs time 0), 0.71 +/- 0.35 mEq/min at 90 (p < 0.05 vs time 0), 0.78 +/- 0.10 mEq/min at 120 (p < 0.01 vs time 0) and 0.71 +/- 0.12 mEq/min at 240 min (p < 0.05 vs time 0). As compared to acute volume expansion alone, octreotide induced a significant increase of Na+ excretion at 60 and 90 min (p < 0.05). In conclusion, a short-time insulin suppression, as obtained by the somatostatin analogue octreotide, enhances the natriuretic response to intravenous saline load in lean type II diabetic hypertensives.
Adult↗
Hyperfibrinolysis resulting from clotting activation in patients with different degrees of cirrhosis. The CALC Group. Coagulation Abnormalities in Liver Cirrhosis.
This study explored the relationship between clotting activation and tissue plasminogen activator and its inhibitor in cirrhotic patients with different degrees of liver failure. Sixty-seven patients (40 men, 27 women; age = 31-77 yr) with cirrhosis diagnosed by liver biopsy were divided into three subgroups (A, B and C) on the basis of Child-Pugh classification. Tissue plasminogen activator antigen and activity, plasminogen activator inhibitor antigen and activity, fibrin/fibrinogen degradation products, and D-dimer were measured in each patient. Forty-two patients with normal levels of fibrin/fibrinogen degradation products and D-dimer showed significant progressive decreases of plasminogen activator inhibitor antigen levels (p < 0.01) and activity (p < 0.0001) from class A to class C. This decrease was significantly related to prothrombin time (p < 0.003). Tissue plasminogen activator values were not different in the three Child classes. Twenty-five patients (7 class B and 18 class C) with high circulating values of fibrin/fibrinogen degradation products and D-dimer had higher values of tissue plasminogen activator antigen (20.0 +/- 10.1 ng/ml vs. 5.9 +/- 3.0 ng/ml; p < 0.0001) and activity (6.9 +/- 2.2 U/ml vs. 2.1 +/- 1.3 U/ml; p < 0.0001) and lower values of plasminogen activator inhibitor antigen (6.9 +/- 4.1 ng/ml vs. 14.8 +/- 5.6 ng/ml; p < 0.0001) and activity (4.1 +/- 2.8 U/ml vs. 9.8 +/- 3.7 U/ml; p < 0.0001) than did patients with normal values of fibrin/fibrinogen degradation products and D-dimer.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[The diagnosis and therapy of hyperprolactinemia].
Hyperprolactinaemia is the most common result of pituitary dysfunction and is characterized by alteration on the reproductive function. After a review of the hypothalamic control mechanisms and of the local paracrine and autocrine factors regulating prolactin secretion, the most common physiological, pharmacological and pathological causes of hyperprolactinaemia are described. The clinical pictures of hyperprolactinaemia in man and woman are then summarized. The diagnostic protocol used in this Institute is then described: confirmation of the existence and entity of hyperprolactinaemia by means of a prolactin profile; exclusion of pharmacological or extra pituitary causes (cirrhosis, primitive hypothyroidism, chronic renal failure, etc.); neuro-radiological evaluation of the sella region, by means of standard X-ray, computer tomography scan, nuclear magnetic resonance. The drugs commonly used in medical treatment of hyperprolactinaemia such as a bromocriptine, other-derived compounds and then recent CV 205-502, and the surgical approaches (trans-sphenoidal and transcranial routes) are reported. The indication of medical or surgical treatment and the relevance of radiotherapy are finally considered.
Combined Modality Therapy↗
Fibrinolytic balance and lupus anticoagulant in patients with repeated spontaneous fetal loss.
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Abortion, Habitual↗
Transferrin receptor mediates uptake and presentation of hepatitis B envelope antigen by T lymphocytes.
Human activated T lymphocytes expressing class II molecules are able to present only complex antigens that bind to their own surface receptors, and thus can be captured, internalized, and processed through the class II major histocompatibility complex processing pathway. We have used the antigen-presenting T cell system to identify the viral receptor used by hepatitis B virus (HBV) to enter cells, as well as the sequence of HB envelope antigen (HBenvAg) involved in this interaction. Results show that both CD4+ and CD8+ T clones can process and present HBenvAg to class II-restricted cytotoxic T lymphocytes and that the CD71 transferrin receptor (TfR) is involved in efficient HBenvAg uptake by T cells. Moreover, we provide evidence that the HBenvAg sequence interacting with the T cell surface is contained within the pre-S2 region. Since TfR is also expressed on hepatocytes, it might represent a portal of cellular entry for HBV infection. This system of antigen presentation by T cells may serve as a model to study both lymphocyte receptors used by lymphocytotropic viruses and viral proteins critical to bind them.
Amino Acid Sequence↗
Tumor necrosis factor-alpha and interferon-gamma synthesis by cerebrospinal fluid-derived T cell clones in multiple sclerosis.
T cell clones derived from cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS) were analysed for their capacity to produce interleukin 2 (IL-2), interleukin 4 (IL-4), interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha). They were also compared with liver-infiltrating T cell clones from patients with chronic active hepatitis. All the CSF T clones (both CD4+ and CD8+) produced large amounts of IFN-gamma and particularly of TNF-alpha, that was synthesized in a significantly larger amount than compared clones. Moreover, they were capable of secreting IL-2, but not IL-4. From our results, we conclude that first, the CSF CD4+ T clones could constitute a subset with functional properties similar to the T helper 1 (Th1)/inflammatory cell subset of the mouse; and second, the large amounts of TNF produced by CSF T cell clones strongly suggests a significant role for this cytokine as well as of IFN-gamma in MS immunopathogenesis.
Adult↗
Hyperfibrinolysis increases the risk of gastrointestinal hemorrhage in patients with advanced cirrhosis.
Sixty-one patients with different degrees of liver failure, 23 with Child-Pugh class B and 38 with Child-Pugh class C, were studied and observed for 3 yr. Coagulation index analysis showed significantly lower values of prothrombin activity, more prolonged activated partial thromboplastin time, higher bilirubin and fibrinogen degradation products values in class C patients. Among all patients, 28 had fibrinogen degradation products values greater than 10 micrograms/ml, and in these patients a hyperfibrinolytic state was confirmed by higher values of circulating plasminogen activator antigen (17.3 +/- 8.7 ng/ml vs. 5.41 +/- 1.9 ng/ml; p less than 0.0001) and activity (6.6 +/- 2.1 IU/ml vs. 1.92 +/- 1.12 IU/ml; p less than 0.0001) and significantly lower plasminogen activator inhibitor antigen (6.4 +/- 3.5 ng/ml vs. 15.8 +/- 5.6 ng/ml; p less than 0.0001) and activity (3.6 +/- 2.2 IU/ml vs. 8.5 +/- 3.9 IU/ml; p less than 0.0001). Patients with positive fibrinogen degradation products had higher serum bilirubin (6 +/- 4 mg/dl vs. 2 +/- 2 mg/dl; p less than 0.0001) and lower fibrinogen (156 +/- 52 mg/dl vs. 194 +/- 62 mg/dl; p less than 0.02) than patients without hyperfibrinolysis. During the follow-up period, 41 patients died, 22 from fatal gastrointestinal hemorrhage and 19 from liver failure. Thirty patients experienced fatal (22 patients) and nonfatal (8 patients) gastrointestinal hemorrhage. Patients with positive fibrinogen degradation products or class C had a higher risk of gastrointestinal bleeding than patients with negative fibrinogen degradation products (odds ratio = 8) or class B (odds ratio = 3.5), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
T cell recognition of hepatitis B envelope proteins.
We have studied the T-cell processing pathways of Hepatitis B antigens and the role of specific B lymphocytes. It could be shown that some form of processing by specific B cells is required for class I CTLs. This mechanism differs from class II endosomal processing. In addition, it could be shown that lysis of HBsAg-specific B cells may be partly responsible for chronic HBV carrier states.
B-Lymphocytes↗
Effect of oral defibrotide on tissue-plasminogen activator and tissue-plasminogen activator inhibitor balance.
Defibrotide, a polydeoxyribonucleotide of mammalian origin, has been shown to reduce the blood level of the plasminogen activator inhibitor, and so to increase the activity of tissue plasminogen activator without any adverse effect. A randomized, double-blind, placebo-controlled study has been done in 22 patients, 14 with peripheral vascular disease, 6 with coronary heart disease and 2 with cerebrovascular disease. Patients were given defibrotide 400 mg b.d. or identical placebo for 30 days and the parameters of fibrinolysis were evaluated before and after the treatment. A significant increase in tissue plasminogen activator activity at rest and after venostasis was observed after defibrotide; tissue plasminogen activator antigen at rest and after venostasis was not affected by either treatment. Defibrotide significantly reduced plasminogen activator inhibitor activity and antigen at rest. Only one patient complained of gastric pain after placebo treatment. The study shows that defibrotide has profibrinolytic property and that it could be used to explore the role of plasminogen activator inhibitor in venous and arterial thrombosis.
Administration, Oral↗
Ambulatory blood pressure recording in diabetic patients with abnormal responses to cardiovascular autonomic function tests.
The aim of our study was to analyse the 24-h periodic pattern of blood pressure (BP) in diabetic patients with abnormal responses to cardiovascular reflexes, in order to evaluate the extent of the initial autonomic damage. We studied 44 patients with diabetes mellitus (14 insulin-dependent, 30 non-insulin-dependent; mean duration of disease 6.5 +/- 1.8 years) in good metabolic control (fasting glycaemia less than 140 mg/dl, postprandial glycaemia less than 180 mg/dl, fructosamine less than 285 mg/dl), divided into two subgroups, containing 21 normotensives (13 males and 8 females aged 28-72 years) and 23 hypertensives (13 males and 10 females aged 32-70 years) respectively. All patients showed abnormal responses to at least two out of four tests: deep breathing, lying to standing, Valsalva manoeuvre and postural hypotension. Two sex- and age-matched control groups were recruited, comprising 20 normotensive and 20 hypertensive diabetic patients without dysautonomia, respectively. The reference group consisted of 248 normotensives (135 males and 113 females, aged 18-76 years) and 212 mild-moderate hypertensives (130 males and 82 females, aged 27-66 years). Each patient underwent ambulatory BP monitoring for at least 24 h, using an auscultatory automatic device. Data concerning biological rhythms were analysed by means of periodic functions. We limited the Fourier partial sums to the first three harmonics.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Free radical-mediated platelet activation by hemoglobin released from red blood cells.
It is known that the rate of thrombus formation depends on interaction between platelets and erythrocytes, but the mechanism of this process has remained obscure. We here show that nanomolar levels of hemoglobin released from damaged red blood cells can induce platelet aggregation. The molecular mechanism is not receptor-based, but involves oxidation of oxyhemoglobin by platelet-derived hydrogen peroxide, with subsequent generation of a small unknown free radical species, detected by ESR spectroscopy. Methemoglobin and carbon monoxide-treated hemoglobin are unable to cause platelet activation or radical formation. The aggregation of platelets induced by hemoglobin is completely blocked by catalase or radical scavengers. These findings indicate a role for a novel extracellular free radical second messenger in the activation of platelets.
Carbon Monoxide↗
Enhanced release of atrial natriuretic factor during exercise-induced myocardial ischaemia in patients after acute myocardial infarction.
To determine whether acute myocardial ischaemia induced by dynamic exercise can lead to changes in plasma levels of atrial natriuretic factor, we performed symptom-limited bicycle electrocardiographic tests in 20 males with recent acute myocardial infarction and in 8 control males. Ten patients developed exercise-induced myocardial ischaemia and 10 patients did not. There were no significant differences between the two groups with regard to age, site of myocardial infarction, urinary sodium, atrial sizes, radionuclide left ventricular ejection fraction, workload, baseline and peak-exercise heart rate, baseline and peak-exercise rate-pressure product, duration of exercise. Also baseline atrial natriuretic factor concentrations were similar in both groups (ischaemic patients: 34.51 +/- 15.73 pg/ml; nonischaemic patients: 27.17 +/- 8.74 pg/ml, NS), while peak-exercise atrial natriuretic factor concentrations were higher in patients with exercise-induced myocardial ischaemia (112.31 +/- 35.5 pg/ml) than in the others (80.46 +/- 23.43 pg/ml) (P less than 0.05). After 15 minutes of recovery, plasma atrial natriuretic factor levels were still raised only in the ischaemic patients (63.3 +/- 15.44 pg/ml, P less than 0.01), returning to baseline after 30 minutes in both groups. In control subjects, the behaviour of atrial natriuretic factor resembled that of the patients without exercise-induced ischaemia, with a significant increase at peak-exercise (from baseline levels of 23.1 +/- 10.5 pg/ml to peak-exercise levels of 91.3 +/- 14.5 pg/ml, P less than 0.0005) and a rapid return to baseline levels after 15 minutes of recovery (28.5 +/- 10.6 pg/ml, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Immunologic and molecular basis of viral persistence. The hepatitis B virus model.
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Hepatitis B↗
Natriuretic hormones in young hypertensives and in young normotensives with or without a family history of hypertension.
The behavior of plasma atrial natriuretic factor (ANF) and digoxin-like substance (DLS), and the daily urinary excretion of kallikrein (uKK) were evaluated in young hypertensives and in young normotensives with or without a family history of essential hypertension. Each group was also evaluated, separating those with low plasma renin activity from the total sample. The sample group was made up of 75 young males; 31 hypertensives (mean age 22.7 +/- 2.5 years), 28 normotensives with hypertensive heredity (normotensives F+) (mean age 22.2 +/- 1.9 years) and 16 normotensives (mean age 22.0 +/- 2.1 years). An inverse correlation between ANF and PRA was shown in all groups. In hypertensives, ANF was inversely correlated with uKK (r = -0.664, P less than .0001). Plasma ANF (P less than .012) and DLS (P less than .0001) were higher in hypertensives than in normotensives, while uKK excretion was lower (P less than .0001). Plasma levels of DLS were higher in F+ normotensives than in normotensives (P less than .003). Low renin hypertensives showed the lowest uKK excretion (P less than .0001 v normal-high renin hypertensives). Furthermore, low renin hypertensives showed the highest plasma levels of ANF (P less than .0001 v normal high renin hypertensives) and DLS (P less than .012 v normal-high renin hypertensives). Plasma ANF (P less than .0001) was higher, while uKK was lower (P less than .045) in low renin F+ normotensives than in normal-high renin ones. In conclusion, our data indicate that plasma ANF and DLS are elevated since the early phase of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗