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Biomedical subjects

M Cinquegrani

Publications and source records attributed to M Cinquegrani.

26 records · Page 2Linked to original sources
PubMed1987

Effects of oral labetalol on forearm and hepatic circulations in normotensive humans.

The effects of single oral labetalol doses (100, 200, and 400 mg) on forearm and hepatic circulations were studied over a 2-hour period in 27 normotensive human subjects by using a double-blind, placebo-controlled design. Labetalol administration resulted in a dose-dependent beta-receptor blockade as determined by an isoproterenol sensitivity test. It also produced a dose-dependent decrease in mean arterial blood pressure that was of greater duration at larger doses. At the lowest dose labetalol produced a transient decrease in arterial pressure followed by a decrease in forearm blood flow and increase in forearm vascular resistance. As the dose of labetalol increased, the hypotensive response became more prolonged, but the changes in forearm blood flow and vascular resistance no longer occurred. Heart rate did not change significantly after any of these doses. Hepatic blood flow also did not change significantly after labetalol. Our results suggest that the increase in forearm vascular resistance after the lowest dose of labetalol probably was caused by unopposed alpha-receptor activation because the agent had a relatively greater beta-receptor blocking action at the low doses, but as the dose increased the alpha-receptor blocking action of the drug became more pronounced and abolished the vasoconstrictor effect in the forearm. Furthermore, our study indicates that despite the significant drop in arterial pressure at doses greater than 100 mg, blood flow is well maintained to the skeletal muscle and splanchnic circulations during labetalol therapy.

Administration, Oral↗
PubMedDate not supplied

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↗
PubMedDate not supplied

[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↗
PubMedDate not supplied

[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↗
PubMedDate not supplied

[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↗