Conjugate gradient minimization of the energy functional: A new method for electronic structure calculation.
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Biomedical subjects
Publications and source records attributed to S Baroni.
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Central dopaminergic activity (CDA) may be involved in blood pressure control as a negative modulator of sympathetic outflow. In this study the plasma PRL changes produced by mental stress (a colour-word conflict test, CWT) were investigated in normals (NT, n.15) and stable hypertensives (HT, n.16) and the PRL response, as a possible index of CDA was correlated to the cardiovascular and the plasma renin activity (PRA) responses as indexes of peripheral sympathetic outflow. A significant (p less than 0.05) slight decrease in mean values of PRL was observed in normals after the CWT but no change was found in hypertensives. No correlation was found between the PRL responses to CWT and the maximal mean arterial pressure changes or the PRA changes whether the groups were considered separately or together. These findings indicates that PRL does not appear to be a reliable index of the CDA involved in blood pressure control.
Von Willebrand factor (vWF) is known to play a relevant role in the development of atherosclerotic lesions by promoting platelet adhesion to injured endothelial cells. An increase in cytosolic calcium has been shown to be associated with the in vitro release of vWF from endothelial cells. The aim of our investigation was to examine the effect of some calcium channel blockers on the release of vWF antigen (vWF:Ag) induced by exercise in two groups of eight healthy subjects during a randomized crossover study between placebo and calcium channel blockers. Placebo and verapamil (80 mg) or nicardipine (10 mg) were given orally at an interval of 2 weeks three times on the day before and once on the morning of the study day. Measurements of plasma vWF:Ag were made at rest and after a progressive maximal exercise on a cycloergometer. A significant increase in absolute values of vWF:Ag was observed after exercise in the subjects given a placebo in both verapamil (0.397 +/- 0.074 U/ml) and nicardipine (0.327 +/- 0.036 U/ml) groups, p less than 0.05. With use of verapamil the rise in vWF:Ag was blunted and not significant (0.123 +/- 0.081 U/ml) whereas a larger increase in vWF:Ag was found in the subjects given nicardipine in comparison with placebo (0.593 +/- 120 U/ml; p less than 0.05). No correlations were observed between exercise-induced changes in systolic or diastolic blood pressure, heart rate, blood lactate level, or pH and vWF:Ag changes in the subjects given a placebo or in those given calcium channel blockers.(ABSTRACT TRUNCATED AT 250 WORDS)
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The antihypertensive effect of a single dose of 240 mg sustained-release (S-R) verapamil was investigated by ambulatory blood pressure (BP) monitoring in 13 patients with mild to moderate essential hypertension. Following a 2-week washout period, 24-hour BP monitoring was carried out with a Spacelabs ICR 5300 device following random administration of a tablet of S-R verapamil or placebo; BP recording was repeated after crossover 3 to 7 days later. Average whole-day systolic and diastolic BPs were significantly lower after verapamil (130.1 +/- 2.6/87.1 +/- 1.2 mmHg) than after placebo (142.1 +/- 3.3/95.8 +/- 2.1 mmHg) (p less than 0.01). Mean waking BP was 146.4 +/- 3.6/99.1 +/- 2.2 mmHg after placebo and 135.2 +/- 3.3/90.5 +/- 1.7 mmHg after verapamil (p less than 0.01); during sleeping hours BP was 133.8 +/- 3.1/88.7 +/- 2.6 mmHg following placebo and 122.2 +/- 2.3/80.9 +/- 1.8 mmHg following verapamil (p less than 0.01). Blood pressure profile was significantly reduced by verapamil up to 20 hours after tablet administration, while from 21 to 24 hours after drug intake BP values were similar to placebo. Response to verapamil was not correlated to the pretreatment BP values and to the patient's age. In summary, this study suggests that acute administration of 240 mg S-R verapamil in hypertensive patients produces a BP reduction during 24-hour, daytime, and nighttime periods. The hypotensive efficacy is preserved for many hours after tablet intake and seems to be due to individual variation in cardiovascular reactivity to the drug.
One and 3 mg/kg iron as Condrofer**, a new soluble formulation of this metal, and 1 mg/kg iron as Proteoferrina*** or ferritin were given orally for 4 weeks to male rats in which severe experimental anaemia had previously been induced (by iron-deficient diet and repeated bleedings). Haematological (erythrocyte count, haemoglobin, haematocrit, mean corpuscular volume, mean corpuscular haemoglobin, reticulocytes and leukocytes) and blood chemistry (sodium, potassium, iron and total protein) parameters were checked weekly and at the end of the drug administration period. Clinical and behavioral signs, body weight, food intake and necroscopic observations were also recorded. Condrofer time- and dose-dependently improved the general blood picture, the clinical data and the autoptic findings to the point of making these animals significantly approach control rats, save for one parameter, sideremia, which after 4 weeks of treatment remained lower than normal. The most plausible explanation would seem that the severe anaemia interfered both with the physiological iron storage and with the iron-dependent mitochondrial enzymatic systems. Iron (1 mg/kg) daily as Proteoferrina or ferritin was significantly less effective than when this metal was administered as Condrofer, since all the haematological parameters and the clinical, behavioral signs and necroscopic observations were less favourable. The more complete reversal of anaemia in the rats that received Condrofer is, most probably, due to the higher bioavailability of iron administered under this formulation, as demonstrated by iron kinetics after equidoses of iron as Condrofer and Proteoferrina.
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Endothelial injury and platelet activation may be involved in the pathogenesis of hypertensive vascular disease. The aim of this study was to evaluate the change in endothelial cell and platelet activation plasma markers after an acute physiological increase in blood pressure. Plasma renin activity (PRA), serum angiotensin-converting enzyme (ACE), plasma factor VIIIR:Ag, and plasma beta-thromboglobulin (BTG) were determined before and after handgrip in subjects with borderline (n = 8) and established (n = 11) hypertension and in age-matched normal volunteers (n = 10). A significant mean increase in ACE, factor VIIIR:Ag, and BTG was observed after handgrip in all groups of subjects. A greater response in BTG changes was found in hypertensive subjects when compared with normal subjects. No correlations were found between the blood pressure response after handgrip and the handgrip-induced changes in plasma markers of endothelial cells and platelet activation. Changes in endothelial cells and platelet activity occurring after handgrip did not appear to depend on the associated blood pressure elevations.
Endothelial injury and platelet activation, mechanisms known to be involved in vascular lesions, may promote the development of cardiovascular disorders possibly associated with mental stress. Plasma markers of platelet activation (beta-thromboglobulin, BTG) and of endothelium activity (factor VIII/von Willebrand factor, FVIII/vWf) and plasma renin activity (PRA) were determined in 17 healthy normotensive volunteers and in 21 hypertensives without target-organ damage before and after mental stress (a colour-word conflict test). The aim of the study was to compare cardiovascular reactivity with the stress-induced changes in platelet and endothelium activity. Individual responses in BTG and factor FVIII/vWf after the colour-word conflict test were markedly different, but significant mean increases were observed in both groups with no difference in the degree of response and in the percentage of responders. No correlations were found among the changes in plasma variables or between cardiovascular reactivity (systolic and diastolic blood pressure and heart rate) and the changes in BTG, FVIII/vWf and PRA. These findings suggest that hypertensive patients do not have an abnormal platelet or endothelium reactivity to mental stress, at least when the disease is free of vascular complications. This dissociation of stress-induced variability in BTG and FVIII/vWf and cardiovascular reactivity indicates that these indices could be used as independent markers of mental stress.
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Seventy-eight patients with endoscopically proven duodenal ulcer were randomly allocated to be treated with a medium dose of liquid aluminum-magnesium antacid (75 ml in five daily doses) or cimetidine (400 mg twice daily) for 4 weeks in a prospective double-blind, double-dummy study. Healing rates at completion of trial were 66.7% in the cimetidine-treated group and 71.8% in the antacid group (p, ns). Both treatments were equally effective in relieving ulcer symptoms. Among the patient variables considered, only cigarette smoking was found to have a significant negative effect on ulcer healing. These results indicate that medium doses of antacids are as effective as cimetidine in the short-term treatment of duodenal ulcer.
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Cigarette smoking has been linked with duodenal ulcer disease although the mechanism of this association is unclear. This study assessed basal gastric secretory response to acute smoking of smokers with an active duodenal ulcer; in addition the possible effects of chronic smoking on gastric secretory capacity, as expressed by pentagastrin stimulated gastric acid secretion and fasting serum pepsinogen I (PG I) concentrations, were investigated in patients with active duodenal ulcer, or non-ulcer dyspepsia. In 10 smokers with duodenal ulcer smoking four cigarettes during 40 minutes did not influence basal gastric secretion of acid and pepsin, or serum PG I and gastrin concentrations. In 136 patients with duodenal ulcer and 90 controls with non-ulcer dyspepsia, pentagastrin stimulated acid secretion and fasting serum PG I concentrations were significantly higher among habitual heavy smokers than among non-smokers. These findings suggest that in heavy smokers with duodenal ulcer acid- and pepsin-secreting cell function is not affected by acute cigarette smoking. By contrast, chronic cigarette smoking seems to be associated either with an increase of parietal- and chief-cell mass, or with an enhancement of their secretory capacity.