[Plasma renin activity after the cold pressor test in arterial hypertensive syndromes].
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Adult↗
Biomedical subjects
A Saitta
Publications and source records attributed to A Saitta.
Serum and urinary activities of beta-N-acetylglucosaminidase and beta-glucuronidase in diabetic patients.
Serum and urinary activities of two acid glycohydrolases, beta-n-acetyl-glucosaminidase and beta-glucuronidase, were significantly higher in a group of diabetic patients when compared to a control group. No significant differences were found between patients without vascular complications and those with retinopathy and/or large vessel disease, while the highest enzyme levels were present in diabetics in poor metabolic control. In diabetics with nephropathy, urinary excretion of both enzymes was further increased, so that the serum/urine activity ratio (greater than 1 in normal subjects and in diabetics without nephropathy) was inverted (less than 1). These data seem to show that the high activity of these enzymes, commonly observed in diabetes mellitus, is related to the illness rather than to its vascular complications, being higher in patients in poor metabolic control. Furthermore serum/urine activity ratio may be a useful indicator in the monitoring of diabetic nephropathy.
Acetylglucosaminidase↗
Serum activity of beta-N-acetylglucosaminidase in obese hyperinsulinemic subjects.
We have measured serum activity of beta-N-acetylglucosaminidase (NAG, fluorimetric method) in some groups of obese subjects with similar degrees of overweight but with different insulin secretion and glucose tolerance (GT) during OGTT. In the control group (35 normal subjects, mean body weight 102% of ideal body weight, normal GT) NAG was 282 +/- 77 nmol S/h/ml; in group I (11 subjects, body weight 149%, normal GT and insulin levels) NAG was 304 +/- 55; in group II (19 subjects, body weight 142%, normal GT and high insulin levels) NAG was 453 +/- 90 (p less than 0.001 vs group I and controls); in group III (14 subjects, body weight 154%, impaired GT and high insulin levels) NAG was 481 +/- 108 (p less than 0.005 vs group I and controls); in group IV (16 subjects, body weight 153%, diabetic GT and high insulin levels) NAG was 657 +/- 109 (p less than 0.001 vs other groups). Moreover in the whole series NAG levels and insulin areas, but not NAG levels and degree of overweight, were significantly correlated (r=0.46, p less than 0.001). These data show that hyperinsulinism (especially when there is also pathological glucose tolerance) can positively affect NAG levels, probably through altered glycoprotein turnover, of which NAG serum levels are a sensitive indicator.
Adolescent↗
Effects of gallopamil on epinephrine and norepinephrine plasmatic levels and on TxB2 and beta-tg release in patients with coronary artery disease during adrenergic stimulus with cold pressor test.
We investigated the effect of gallopamil administration during a cold pressor test (CPT) in 18 patients suffering from chronic angina (CA) and in 21 healthy subjects. CA patients showed increased basal levels of beta-thromboglobulin and thromboxane B2 compared to control patients and normal plasma levels of catecholamines. CPT caused plasma catecholamines, beta-thromboglobulin and TxB2 levels to rise. This rise was greater in CA patients than in control patients. Administration of gallopamil (50 mg kg-1 three times a day for 30 days) reduced plasma levels of catecholamines, beta-thromboglobulin and TxB2 blood concentrations either under basal conditions or after CPT. Our data suggest that gallopamil is able to modulate the response induced by adrenergic stress.
Adult↗
Soluble E-selectin levels in acute human myocardial infarction.
It has been suggested that leukocyte adhesion mechanisms play a key role in experimental myocardial infarction. We have recently shown that E-selectin, an adhesion molecule belonging to the selectin family, is involved in the pathogenesis of experimental myocardial ischemia. We investigated the circulating levels of E-selectin, studied as a marker of endothelial dysfunction, in acute myocardial infarction. Our study was carried out in 60 patients, 20 hospitalized for acute myocardial infarction, 20 suffered from angina pectoris and 20 healthy control subjects. Patients with acute myocardial infarction had increased serum levels of soluble E-selectin (sE-selectin = 255 +/- 12 ng/ml) compared to both patients with angina pectoris (sE-selectin = 51 +/- 14 ng/ml). Thrombolytic therapy with urokinase (1,000,000 IU as an intravenous bolus in 5 min, followed by producing reperfusion and reduced the serum levels of sE-selectin (71 +/- 19 ng/ml). Our results confirm previous experimental data and indicate that adhesion mechanisms supporting leukocyte-endothelium interaction may also be operative in human acute myocardial infarction.
Adult↗
Recombinant human granulocyte colony-stimulating factor reverts vascular dysfunction.
The aim of our study was to investigate the vascular effects of recombinant human granulocyte colony-stimulating factor (rh G-CSF) in a rat model of irreversible vascular failure. Male anesthetized rats were subjected to the clamping of the splanchnic arteries for 45 min. This surgical procedure resulted in an irreversible state of shock (splanchnic artery occlusion shock) characterized by high mortality rate (0% survival, 120 min following the release of clamps), a profound hypotension and vascular dysfunction consisting of a marked hyporeactivity to phenylephrine (PE 1 nM-10 microM) of aortic rings. Administration of recombinant human granulocyte colony-stimulating factor (20 micrograms/kg i.v. 5 min after the release of occlusion) increased survival rate (90% 4 h after the release of occlusion), blunted the profound hypotension and reverted the marked vascular dysfunction. Finally, rh G-CSF inhibited the activity of inducible nitric oxide synthase in peritoneal macrophages activated with endotoxin. Our data suggest that rh G-CSF may influence vascular function when low-flow states occur.
Acute Disease↗
[Elevated levels of lipoprotein(a) are present in subjects with early ischemic cardiopathy and with a familial history of ischemic cardiopathy].
BACKGROUND: Elevated levels of lipoprotein(a) are associated with a greater risk of atherothrombotic cardiovascular diseases. Since the Lp(a) levels are genetically determined and fairly stable in the course of life and a family history appears to be an independent risk factor of cardiovascular diseases, we evaluated the behavior of Lp(a) levels in patients with early events of coronary heart disease (CHD) and also in subjects with positive family history of ischemic heart diseases. METHODS: The levels of lipoprotein (a) [Lp(a)] were measured in 254 subjects, 138 males and 116 females with an average age of 48.6 +/- 13.8 years (range 20-76 years). Diabetic subjects, females submitted to oestrogen treatment and those already in treatment with hypolipidaemic drugs were excluded from the study. Forty of the 254 patients (15.7%), 27 males and 13 females, had CHD (29 a previous myocardial infarction and 11 a stable angina). A positive family history for CHD was considered present (102 of the 254 patients) if one or more first degree relatives had angina or myocardial infarction before the age of 60 years in men and 65 in women. RESULTS: The levels of Lp(a) were higher (p < 0.01) in women (25.1 +/- 28.3 mg/dl) compared to men (17.6 +/- 18.4 mg/dl), without differences in relation to age. The Lp(a) plasmatic levels were not correlated with age, body mass index, total cholesterol, LDL and HDL, triglycerides, apo B, apo AI, fibrinogen and there were no differences in Lp(a) levels in presence or absence of other known cardiovascular risk factors such as hypertension and smoking. The Lp(a) levels were not different between subjects with CHD (28.15 +/- 31.7 mg/dl) and controls (20.3 +/- 22.8 mg/dl). The subjects with CHD were older and had higher levels of fibrinogen and a significantly greater prevalence of hypertension and family history of CHD. Fifteen of the 40 subjects with CHD had an early onset of CHD (before 50 years of age) and only in such patients the Lp(a) levels were significantly greater compared to controls (35.8 +/- 33.2 mg/dl vs 20.3 +/- 22.8 of the controls, p < 0.01), independently of other variables (age, BMI, smoking, hypertension, cholesterol, triglycerides, HDL-c, LDL-c, fibrinogen). Furthermore the Lp(a) plasmatic levels were higher in subjects with a family history of CHD (28.3 +/- 27.6 mg/dl vs 16.3 +/- 18.6 mg/dl of the subjects without a family history of CHD, p < 0.01) even if they had or not had a previous coronary ischemic event. CONCLUSIONS: Such data confirm the importance of high levels of Lp(a) above all for the early events of CHD and for the subjects with a family history of CHD, which could be expression of a greater predisposition for cardiovascular events.
Adult↗
Clinical investigation on hyaluronic acid in the treatment of gonoarthrosis.
The clinical efficacy and tolerance of the sodium salt Hyaluronic acid (HA) 20 mg/2 ml administered through the intraarticulation every week, for a four week period in a group of 12 patients with gonoarthrosis were investigated. Such a treatment has brought about a bettering of the baseline clinical parameters considered, i.e., spontaneous, stiffness, walking time and analgesics consumption.
Arthritis↗
[Evaluation of arteriolar reactivity and blood coagulation parameters during picotamide treatment].
Thirty-two patients, nineteen males and thirteen females, mean age 59.4 +/- 11.9 years, 18 with peripheral arteriopathy Fontaine stage II and 14 with cerebral vasculopathy were submitted to treatment with picotamide, 900 mg/die. In basal conditions and after 30 and 60 days of treatment, we evaluated some blood clotting parameters concerning both platelets (circulating platelet aggregates, beta-thromboglobulin, TxB2, 6-keto-pgF1 alpha) and plasma (fibrinogen, plasminogen, ATIII, Factor VIII-C and VIII Ag, prothrombin time, activated thromboplastin time) and some instrumental parameters such as walking distance and Doppler with a post-ischaemic hyperaemia test in patients with peripheral arteriopathy and Doppler of epiaortic vessels with resistance and pressure-perfusion index evaluation in patients with cerebral vasculopathy. Treatment with picotamide significantly reduced circulating platelet aggregates, beta-TG and TxB2 levels, without change of 6-keto-PGF-alpha values, with reduction of F VIII-C and slight increase of plasminogen and ATIII levels. In patients with peripheral arteriopathy after two months, a significant increase in distance and an improvement of arteriolar reactivity were observed, as shown by increase of the perfusion-index and by reduction of the post-ischaemic recovery time. These observations, together with the good tolerance of the drug, justify the use of picotamide in the treatment of patients with atherosclerotic vasculopathy at different localizations.
Aged↗
[Effects of adrenergic stimulation on transmembrane transport of Na+ in patients with essential hypertension].
BACKGROUND: It has been studied whether an adrenergic stimulation induced by the cold pressor test (CPT) could influence the behaviour of the transmembrane transport systems of sodium in hypertensive subjects compared to a normotensive control population. MATERIALS AND METHODS: Twenty-two hypertensive subjects (average age 43.2 +/- 5.7 years), with normal weight, without signs of cardiovascular and metabolic diseases, underwent the cold pressor test. The dynamic behaviour of sodium erythrocytic transport systems and plasmatic norepinephrine was evaluated basally, at the third minute during the cold pressor test and 20 minutes after the end of the test. The same test was carried out in a control population made up of 20 normotensive subjects (average age 41.9 +/- 4.8 years), selected on the basis of the absence of any cardiovascular or metabolic pathology and without family history of arterial hypertension. RESULTS: The cold pressor test did not cause significant changes in the sodium transmembrane transport systems in normotensive subjects, while in the hypertensive subjects a significant reduction was observed, during the test, in the total efflux of sodium and in the sodium/potassium pump, respectively from 2636 +/- 296 mumol/l/red blood cells/hr to 2032 +/- 178 mumol/l/red blood cells/hr (p < 0.0001) and from 2156 +/- 149 mumol/l/red blood cells/hr to 1610 +/- 101 mumol/l/red blood cells/hr (p < 0.0001); the intraerythrocytic sodium increased from 6.5 +/- 1.0 mmol/l/cells to 7.2 +/- 1.1 mmol/l/cells (p < 0.04) and the passive permeability decreased from 0.039 +/- 0.004 hr-1 to 0.018 +/- 0.006 hr-1 (p < 0.0001). During cold pressor test the increase in the plasma norepinephrine levels was correlated to the reduction in the total efflux of sodium (r = -0.60; p < 0.003) and in the sodium/potassium pump (r = -0.59; p < 0.003) only in hypertensive subjects. CONCLUSIONS: Our data show that an adrenergic stimulation, induced by the cold pressor test, is able to significantly influence the behaviour of transmembrane fluxes of sodium in hypertensive subjects, and it causes an inhibitory effect on the sodium/potassium pump and an increase in the intraerythrocytic sodium. Such data show the existence in hypertensive subjects of an interrelationship between adrenergic activity and sodium transport systems that could cooperate in causing and/or in maintaining the hypertensive syndrome.
Adult↗
[Effect of beta blockade on the erythrocyte transport of Na+: evaluation during stimulation by cold pressure test in patients with essential hypertension].
Several studies have shown in essential hypertension alterations of the transmembrane red blood cells sodium fluxes, as an involvement, especially in the early phases, also of the adrenergic system. In this study we evaluated the behaviour of red blood cells fluxes of sodium before, during and after the cold pressor test, a method used also to evoke an adrenergic stimulation, in twenty hypertensive subjects, 14 males and 6 females, with an average age of 43.2 +/- 5.7 years, with normal weight and without cardiovascular complications and metabolic diseases. The behaviour of the Na+ total efflux (Na+ TE), of the Na+/K+ pump, of the Na+K+ cotransport (Na+/K+ CT), of the Na+/Li+ counter transport (Na+/Li+ Cnt), of the Na+ passive permeability (Na+ PP), of the intracellular Na+ (I Na+) and of the plasmatic noradrenaline (NE) was evaluated basally, at the third minute during cold pressor test (CPT) and 20 minutes after the end of the test. The test, which the same method, was repeated after a 30 day treatment with propranolol at the dose of 240 mg/day in three daily administrations. The beta-blockade caused, besides the reduction of both the systolic and diastolic pressure values, a significant increase in the Na+/K+ CT (from 248 +/- 41 to 314 +/- 71 mmol/l/cells/h, p < 0.001) and a decrease in the Na+ PP (from 0.039 +/- 0.004 to 0.023 +/- 0.007 hr-1, p < 0.00001), probably directed towards the reduction of the accumulation of intracellular Na+, that could compete, among the other mechanisms, with the anti-hypertensive action of the beta-blockers. The CPT caused, before the beta-blockade, a significant depression of the Na+/K+ pump (from 2057 +/- 149 to 1610 +/- 101 mmol/l/cells/h, p < 0.00001) and of the Na+ TE (from 2640 +/- 397 to 2032 +/- 179 mmol/l/cells/h, p < 0.00001) inversely correlated to the levels of NE (r = -0.60, p < 0.003), with a consequent increase in I Na+ (from 6.2 +/- 0.6 to 7.5 +/- 1.5 mmol/l/cells, p < 0.001), showing how the adrenergic activation in hypertensive subjects is able to interfere with the systems of transmembrane transport with an inhibitory attitude, that is expressed by an increase in the levels of I Na+. The beta-blockade was able to outweigh the depression of the Na+/K+ pump (from 1843 +/- 584 to 1728 +/- 640 mmol/l/cells/h, p: ns) and the reduction of the Na+ TE, preventing the accumulation of I Na+ (from 6.3 +/- 1.6 to 6.6 +/- 1.3 mmol/l/cells, p: ns). Such data show an increased susceptibility of the Na+ transport systems to the adrenergic stimuli in hypertensive subjects with a tendency to favor the accumulation of I Na+ and that the beta-blockade is able to antagonize the effects, with a maintenance of the intracellular levels of Na+.
Adrenergic beta-Antagonists↗