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Biomedical subjects

G Tamburino

Publications and source records attributed to G Tamburino.

At least 19 recordsLinked to original sources
PubMed1996

Plasma endothelin-1 concentrations during cold exposure in essential acrocyanosis.

To assess endothelin-1 (ET-1) response to cold stimulation in essential acrocyanosis (EA), the authors measured ET-1 plasma concentrations in 6 patients with EA (6 women, age range seventeen to thirty-seven years) and in 6 controls (5 women, 1 man, age range twenty-one to thirty-seven years) before and after cold challenge by unilateral hand immersion in water bath at 13 degrees C for five minutes. The contralateral upper limb was considered as control. Blood samples were simultaneously drawn from an antecubital vein in the cooled side and in the contralateral upper limb at baseline, at the end of cooling, and at ten and ninety minutes after cooling was begun. Plasma ET-1 was determined by a radioimmunoassay system. Results are mean +/- SD. Baseline ET-1 was higher in patients with EA (5.1 +/- 0.3 pmol/L) than in controls (1.9 +/- 0.1 pmol/L, P < 0.001). After hand cooling, ET-1 in the cold-exposed upper limb rose in patients with EA to a peak value of 7.2 +/- 0.7 pmol/L, which was greater than that observed in healthy subjects (2.7 +/- 0.4 pmol/L, P < 0.001). The absolute increase in ET-1 plasma concentrations from baseline to peak value was significantly higher in patients with EA than in controls (2.1 +/- 0.3 vs 0.8 +/- 0.2 pmol/L, respectively, P < 0.001). In patients with EA, but not in controls, the rise in ET-1 plasma concentrations was still detected ninety minutes after cooling. The same time course of the plasma ET-1 concentrations was observed in the noncooled upper limb, but the increases in ET-1 at different times after cold stimulus were smaller than in the cold-challenged upper limb in both groups (P < 0.001). In conclusion, the results demonstrate that in patients with EA, baseline plasma levels of ET-1 are enhanced and are further increased by cooling until ninety minutes after cold challenge. This rise in plasma ET-1 could contribute to potentiating and prolonging cold-induced vasoconstriction/vasospasm and/or could be a marker for endothelial damage in EA.

Adolescent↗
PubMed1996

Raised plasma endothelin-1 concentrations in patients with primary hypercholesterolemia without evidence of atherosclerosis.

The present study was designed to investigate the pattern of circulating endothelin-1 (ET-1), a potent vasoconstricting mitogenic endothelium-derived peptide, in relation to primary increase in serum cholesterol in humans. We measured plasma ET-1 concentrations by radioimmunoassay (Amersham, UK) in 8 patients (6 females and 2 males, aged 42-62 years) with primary hypercholesterolemia, non-smokers, without evidence of cardiovascular disease, and in 8 healthy sex-and age-matched control subjects. The mean (+/- SD) values of serum total cholesterol, low-density-lipoprotein (LDL) cholesterol, high-density-lipoprotein (HDL) cholesterol and triglycerides in the hypercholesterolemic subjects were 7.2 +/- 1.1 mmol/L, 5.1 +/- 1.1 mmol/L, 1.0 +/- 0.1 mmol/L and 2.4 +/- 0.9 mmol/L, respectively. The lipid profile of the controls showed a total cholesterol of 4.6 +/- 0.3 mmol/L, LDL cholesterol of 3.0 +/- 0.2 mmol/L, HDL cholesterol of 1.0 +/- 0.1 mmol/L and triglycerides of 1.2 +/- 0.2 mmol/L. The mean ET-1 plasma levels in the hypercholesterolemic patients were significantly higher than in the controls (4.2 +/- 0.1 pmol/L and 2.2 +/- 0.7 pmol/L, respectively, p < 0.001). Our data of raised circulating ET-1 in hypercholesterolemic patients without evidence of atherosclerosis suggest that an exaggerated release of ET-1 could contribute: 1) to impair endothelium-dependent vasodilation; 2) to promote the atherogenic process in hypercholesterolemia. Finally, it could represent a marker for hypercholesterolemic endothelial damage.

Adult↗
PubMed1993

Atrial natriuretic peptide response to postural changes and upright exercise in patients with venous valvular insufficiency.

To investigate the effects of postural changes and upright exercise on atrial natriuretic peptide release and renin-angiotensin-aldosterone system behavior in patients with venous valvular insufficiency, plasma ANP, plasma renin activity and aldosterone were measured in 11 patients with venous disease and in 11 age-matched controls. In patients with large varicose veins and venous valvular dysfunction, standing was associated with a greater fall in circulating ANP levels (p < 0.05) and upright exercise was accompanied by a smaller rise in ANP concentrations (p < 0.05) as compared with controls. A significant (p < 0.001) inverse relationship was found between the number of venous segments with reflux and both upright and exercise plasma ANP concentrations (r = -0.91; r = -0.84, respectively). In the two groups the response of the renin-angiotensin-aldosterone system to upright position and physical stress was similar. These results suggest that a decreased atrial stretch, due to a reduced venous return, could account for the blunted ANP response to erect posture and exercise in patients with venous valvular incompetency.

Adult↗
PubMed1992

Transient myocardial ischemia stimulates atrial natriuretic factor release.

Atrial natriuretic factor release during transient myocardial ischemia was investigated in 29 patients with coronary artery disease and symptoms of angina (Canadian Cardiovascular Association classes II-III). Eleven patients (group I) underwent single-vessel percutaneous transluminal coronary angioplasty. Repeat determinations of mean pulmonary artery wedge pressure and blood sampling from pulmonary artery for atrial natriuretic factor measurements were performed at baseline, and at 2, 5, and 15 minutes after percutaneous transluminal coronary angioplasty was begun. Baseline atrial natriuretic factor levels (34.6 +/- 4.5 pg/ml) rose to 56.3 +/- 7.3 pg/ml (p = 0.02) and decreased at 5 minutes (43.7 +/- 5.7 pg/ml, not significant) and 15 minutes (35.3 +/- 4.4 pg/ml, not significant). Changes in atrial natriuretic factor concentrations were significantly correlated with those in mean pulmonary artery wedge pressure (2 minutes: r = 0.69, p = 0.02; 5 minutes: r = 0.90, p less than 0.001). In group II (n = 10) the increase in atrial natriuretic factor after dye load occurred later (baseline: 25.8 +/- 2.1; 60 minutes: 40.6 +/- 2.6 pg/ml; p = 0.005) than that observed in group I after percutaneous transluminal coronary angioplasty. In group III, atrial natriuretic factor during angina rose as early (baseline 11.3 +/- 1.3; 5 minutes: 20 +/- 2.3 pg/ml; p = 0.006) as after percutaneous transluminal coronary angioplasty. Results indicate that transient myocardial ischemia stimulates atrial natriuretic factor release, probably through changes in cardiac function.

Angina Pectoris↗
PubMed1990

Comparison of ketanserin and enalapril in the treatment of mild-to-moderate essential hypertension.

In a double-blind 3-month study in mild-to-moderate essential hypertensive patients over 50 years of age, ketanserin, a selective S2-serotoninergic antagonist with additional alpha 1-adrenergic blocking properties, has been compared with enalapril, an angiotensin-converting enzyme inhibitor. Supine and upright blood pressures and heart rates were recorded for placebo and during active treatment (-4, -2, 0, 2, 4, 6, 8, 10, and 12 weeks). Metabolic profile (plasma glucose, creatinine, sodium, potassium, total and HDL-cholesterol, triglycerides, uric acid) was monitored during treatment with placebo and at the end of the study. Mean blood pressure was equally and significantly (p less than 0.001) lowered by both drugs from 2 weeks of treatment, whereas no changes occurred in mean heart rate or in biochemical variables. Dizziness was observed in three patients on ketanserin and in one patient on enalapril, whereas headache occurred in only one patient on enalapril. These data indicate that ketanserin is as effective and well tolerated as enalapril in hypertensive patients over 50 years of age.

Aged↗
PubMed1990

Baseline and post-atrial pacing release of atrial natriuretic factor in mitral stenosis.

To investigate the release of atrial natriuretic factor (ANF) in mitral stenosis and the influence of the increase on the frequency of atrial contraction or atrial distention on ANF secretion, we studied 10 patients with symptoms of congestive heart failure (New York Heart Association classes II and III) in sinus rhythm, who were undergoing cardiac catheterization as part of an evaluation workup for mitral stenosis. Echocardiographic tracings, repeat determinations of mean pulmonary artery wedge pressure (MPAWP) and mean right atrial pressure, and blood sampling from the pulmonary artery for measurements of ANF were performed at baseline, during atrial pacing (pacing rate of 125 beats/min for 5 minutes), and 5 minutes after the pacing protocol was completed. Baseline ANF levels were closely related to right atrial pressure (r = 0.89; p less than 0.001) and increased markedly after atrial pacing from 205.6 +/- 39.8 (SEM) to 343.9 +/- 57.9 (SEM) pg/ml. A similar pacing-induced increase was shown for MPAWP and left atrial size. Our data indicate that pacing-induced increases in atrial distention and intracavitary pressure further stimulate release of ANF. However, an independent effect of frequency of atrial pacing on plasma ANF in humans could not be identified.

Adult↗
PubMed1989

Evidence for a further stimulation of atrial natriuretic factor release by atrial pacing in patients with mitral stenosis.

To investigate the release of atrial natriuretic factor (ANF) in mitral stenosis and the effect of an increased atrial contraction frequency on atrial distension and ANF secretion, we studied 14 patients [New York Heart Association (NYHA) grades II-III] in sinus rhythm, undergoing cardiac catheterization for mitral stenosis. Echocardiographic tracings, repeat determinations of mean pulmonary artery wedge pressure and blood samples from the pulmonary artery for ANF measurements were taken at baseline, during atrial pacing (125 beats/min for 5 min) and 5 min after pacing. After pacing, ANF levels rose markedly with a parallel increase in mean pulmonary artery wedge pressure and left atrial size. These data indicate that atrial pacing is capable of further stimulating ANF release, even in patients with elevated baseline ANF and left atrial pressure and an increased left atrial dimension.

Adult↗
PubMed1987

Acute effects of salmon calcitonin in man include stimulation of the renin-angiotensin-aldosterone system.

The present double-blind placebo-controlled cross-over study was designed to evaluate the renin-angiotensin-aldosterone system behavior after a short-term infusion of a pharmacological dose (100 MRC U) of salmon calcitonin. Overall, a significant increase in plasma renin activity, aldosterone and serum angiotensin-converting enzyme was seen throughout. This effect may be, at least in part, due to the renal loss in sodium and calcium ions, while the increased kaliuresis could be interpreted as a consequence of the stimulation of aldosterone release.

Adult↗