XPS study of graphene oxide reduction induced by (100) and (111)-oriented Si substrates.

The reduction of graphene oxide (GO) has been extensively studied in literature in order to let GO partially recover the properties of graphene. Most of the techniques proposed to reduce GO are based on high temperature annealing or chemical reduction. A new procedure, based on the direct reduction of GO by etched Si substrate, was recently proposed in literature. In the present work, we accurately investigated the Si-GO interaction with x-ray photoelectron spectroscopy. In order to avoid external substrate oxidation factors we used EtOH as the GO solvent instead of water, and thermal annealing was carried out in UHV. We investigated the effect of Si(100), Si(111) and Au substrates on GO, to probe the role played by both the substrate composition and substrate orientation during the reduction process. A similar degree of GO reduction was observed for all samples but only after thermal annealing, ruling out the direct reduction effect of the substrate.

Correlation between peripheral hemodynamic changes and left ventricular diastolic function in hypertensive patients treated with urapidil.

We evaluated the modifications induced by chronic treatment with an alpha 1-adrenolytic hybrid drug, urapidil, on the hemodynamic parameters in peripheral artery and left ventricle diastolic function. Fifteen mild to moderate essential hypertensive patients (13 men, 2 women; mean age 42 years, range 32-54 years) received urapidil (60 mg b.i.d.) for 6 months. Peripheral hemodynamic and cardiac parameters were evaluated by duplex scanner, coupled with a plethysmographic method, basally (T0) and after 6 weeks' (T1) and 6 months' treatment (T2). Mean blood pressure (BP) showed a reduction after 6 weeks of -9.07 mm Hg (confidence intervals [CI] 95%: -9.21; -8.92; P < 0.01), which was maintained after 6 months (-8.21 mm Hg, CI 95%: -8.97; -7.43; P < 0.01), while no significant change was seen in heart rate. Compliance showed highly significant changes after both 6 weeks (+1.073 dyn-1.cm4.10(-7), 95% CI: +0.965; +1.181, P < 0.001) and 6 months (+0.933 dyn-1.cm4. 10(-7), 95% CI: +0.903; +0.963, P < 0.001), as well as characteristic impedance (T1:-16.689 dyn.s.cm-5/10(2), 95% CI: -16.914; -16.463 P < 0.001; T2: -15.98 dyn.s.cm-5. 10(2), 95% CI: -18.186; -13.784; P < 0.001) and forearm resistances (T1: -26.153 mm Hg.ml-1.s, 95% CI: -34.553; -17.753, P < 0.01; T2: -43.587 mm Hg.ml-1.s, 95% CI: -52.711; -34.464, P < 0.01). Similarly, we have recorded a similar change in left ventricular end-diastolic posterior wall thickness (T1: -1.067 mm, 95% CI: -1.099; -1.035, P < 0.01; T2: -2.866 mm, 95% CI: -3.044; -2.688, P < 0.01), end-diastolic interventricular septum thickness (T1: -0.921 mm, 95% CI: -1.511; -0.289, P < 0.05; T2: -2.711 mm, 95% CI: -3.211; -2.199, P < 0.01), end-diastolic volume (T1: +6.4 ml, 95% CI: +6.343; +6.456, P < 0.01; T2: +19.867 ml, 95% CI: +18.564; +21.170, P < 0.01), and mass/volume index (T1: -0.11, 95% CI: -0.118; -0.101, P < 0.01; T2: -0.218, 95% CI: -0.221; -0.217, P < 0.01). Changes in arterial compliance have shown a statistically significant correlation with changes in mass/volume index (r = -0.468; P < 0.03), end diastolic volume (r = 0.501; P < 0.02), as well as left ventricle rapid filling phase (r = 0.426; P < 0.05) and left ventricle end diastolic posterior wall thickness (r = -0.478, P < 0.03). Our results suggest that the antihypertensive efficacy of urapidil coupled with the restoration of the dumping function of the large arteries, and the reduced activation of reflex sympathetic activation, may play a considerable role among the mechanisms allowing the regression of the functional modifications affecting the left ventricular diastole.

Tolerability and antihypertensive efficacy of Fosinopril on 24-hr ambulatory blood pressure in hypertensive elderly subjects.

The tolerability and antihypertensive efficacy of Fosinopril were assessed in 34 elderly patients with mild to moderate hypertension. Twenty-four-hour ambulatory blood pressure (BP) was measured before and after 5 months of therapy. The patients' mean age was 67 years. At the end of the treatment the mean 24-hour systolic BP (SBP) fell from 153.4 +/- 14 to 137.7 +/- 13 mmHg and the mean 24-hour diastolic BP from 91 +/- 11 to 84.2 +/- 9 mmHg (p < 0.01). The mean decrease in SBP was 15.9 mmHg during the day and 10.3 during the night, and in diastolic BP (DBP) 8.3 mmHg during the day and 10.3 mmHg during the night (p < 0.05 between day and night). There was no significant percentage difference between the SBP and DBP decreases. The mean morning maximum of SBP decreased from 171 +/- 18 to 158 +/- 19 mmHg and there was a reduction in pressure increase between the night and day. The number of SBP peaks over 180 mmHg and 160 mmHg numerically decreased to 20.1% and 37.6% versus baseline, those of DBP over 105 mmHg and 95 mmHg to 41.6% and 58.3% versus baseline, respectively. There were no variations in the blood chemistry parameters and the drug had no adverse side effects. The authors conclude that Fosinopril is useful and well tolerated in the treatment of moderate hypertension in the elderly.

Amlodipine and haemodynamic effects of cyclo-oxygenase inhibition.

1. The haemodynamic effects of calcium antagonists could depend at least in part on the activity of vasoactive prostanoids. 2. We set out to study the effect of the cyclo-oxygenase inhibitor ibuprofen, 400 mg three times daily for 3 days, by a randomised cross-over study vs placebo in 12 mild to moderate essential hypertensive patients who had been treated for 1 month with amlodipine. 3. Blood pressure, heart rate and vascular resistances in the upper limb (Doppler ultrasound) were measured. Plasma renin activity and urinary aldosterone, as well as indices of renal function, were evaluated. Urinary 2,3-dinor-6-keto-PGF1 alpha and 2,3-dinor-TXB2, as well as 6-keto-PGF1 alpha and TXB2, were measured as indices of systemic and renal PGI2 and TXA2 synthesis. 4. Amlodipine normalised blood pressure and reduced upper limb vascular resistances; it did not affect urinary prostanoid excretion. Short-term combined administration of ibuprofen resulted in, by comparison with placebo, inhibition of systemic PGI2 (-80.5 ng 24 h-1, 95% CI -99.2, -61.4; P < 0.001) and TXA2 (-216.1 ng 24 h-1, 95% CI -276.5, -155.8; P < 0.001), together with an increase in systolic (+7.8 mm Hg, 95% CI +3.1, +12.3; P < 0.01) and diastolic (+3.9 mm Hg, 95% CI +1.2, +6.6; P < 0.01) blood pressure; it had no significant effect on regional vascular resistances (+4.7 mm Hg ml-1 s, 95% CI -5.6, +15.0). Effects of ibuprofen on renal prostanoid synthesis were less marked, and there was no change in indices of renal function or hydro-electrolytic balance.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes induced by nicardipine slow release in forearm and myocardial hemodynamics of subjects with essential hypertension.

OBJECTIVE: To evaluate the modifications induced by chronic treatment with a new formulation of nicardipine (slow release) on the hemodynamic parameters in peripheral artery and left ventricle diastolic function. MATERIALS AND METHODS: Ten mild to moderate essential hypertensive male patients (mean age 42 years, range 32-54 years) received nicardipine slow release (40 mg b.i.d.) for six months. Peripheral hemodynamic and cardiac parameters were evaluated by duplex scanner, coupled with a plethysmographic method, basally (T0) and after 1 (T1) and 6 months' treatment (T2). RESULTS: Blood pressure showed a significant reduction after 1 month (mean blood pressure 109 +/- 2 vs 124 +/- 3 mmHg, M +/- SE, p < 0.001), which was maintained after 6 months (mean blood pressure 112 +/- 3 mmHg, p < 0.001), while heart rate showed only a slight, non-significant increase. There were highly significant changes in distensibility (0.29 +/- 0.02 vs 0.16 +/- 0.01 s2.cm-2, T2 vs T0, p < 0.001), characteristic impedance (55 +/- 3 vs 78 +/- 3 dyn.s.cm-5.10(2), T2 vs T0, p < 0.001) and local resistances (71 +/- 5 vs 118 +/- 4 mmHg.ml-1. s, T2 vs T0, p < 0.001) in the brachial artery, and also in left ventricle posterior wall diastolic thickness (10.2 +/- 0.4 vs 11.5 +/- 0.3 mm, T2 vs T0, p < 0.05), end diastolic volume (127 +/- 3 vs 109 +/- 3 ml, T2 vs T0, p < 0.01) and mass/volume index (1.21 +/- 0.03 vs 1.35 +/- 0.03, p < 0.05). CONCLUSIONS: The antihypertensive efficacy of nicardipine slow release, with only two daily administrations, allows the restoration of the dumping function of the large arteries, and the regression of the functional modifications affecting the left ventricular diastole.

Hemodynamic changes induced by cilazapril and atenolol during isometric stress in hypertensive patients.

We studied 16 mild to moderate essential hypertensive patients (14 male, 2 female; mean age 45 years, range 34-55 years) in order to investigate the effects of an ACE inhibitor, cilazapril (5 mg o.d.) and a selective beta-blocker, atenolol (100 mg o.d.) on the hemodynamics of the brachial and carotid arteries after an isometric stress test with a handgrip. Both drugs caused a statistically significant decrease in blood pressure after three months' treatment, but only cilazapril reduced it after the first dose. Heart rate was reduced only by atenolol (61 +/- 3 vs 71 +/- 3 bpm; p < 0.01). Changes in forearm compliance and characteristic impedance showed a difference statistically significant both for acute test and after three months of treatment. The increase in blood pressure during handgrip did not differ appreciably between the two treatment groups. On the contrary, after handgrip only cilazapril caused a significant increase of the reactive hyperemia.

Effects of sustained-release isradipine on blood pressure and peripheral hemodynamics in hypertensive patients.

In a double-blind crossover study, 16 hypertensive patients (mean age, 41 years) were randomly assigned to receive placebo or 5 mg of an extended-release formulation of isradipine for 30 days. Blood pressure and heart rate were recorded by an automatic device and hemodynamics measured by a duplex scanner and plethysmography. After the first dose and after 30 days' treatment with isradipine, blood pressure was significantly reduced (mean arterial pressure 4 hours after the first dose, 106 +/- 3 vs 120 +/- 4 mmHg, P < 0.01; 22 hours after the last dose, 108 +/- 3 mmHg, P < 0.01) with no significant changes in heart rate. The compliance of the brachial artery was significantly increased (2.823 +/- 0.358 vs 1.204 +/- 0.156 dyn-1.cm4.10(-7), P < 0.002) and the characteristic impedence decreased (49 +/- 6 vs 91 +/- 12 dyn.s.cm-5.10(2), P < 0.05) as well as local resistances (71 +/- 5.6 vs 198 +/- 18 mmHg.ml-1.s, P < 0.001). After 30 days of isradipine treatment, 22 hours after the last dose, compliance was still increased (2.575 +/- 0.453 dyn-1.cm4.10(-7), P < 0.01) whereas impedance and forearm vascular resistances were reduced (59 +/- 8 dyn.s.cm-5.10(2), P < 0.05, and 97 +/- 14 mmHg.ml-1.s, P < 0.001, respectively). The results indicate that sustained-release isradipine ensures good blood pressure control up to the time of the following dose and restores the large artery dumping function against cyclic variations in intraluminal pressure.

Changes in the haemodynamics of large arteries induced by single doses of nicardipine, enalapril, atenolol and urapidil.

Haemodynamic changes in the carotid and brachial arteries produced by single doses of four anti-hypertensive drugs (nicardipine, enalapril, atenolol, and urapidil) have been studied in 12 patients with essential hypertension. Measurements were performed noninvasively using a mechanographic method and B-mode pulsed Doppler ultrasonography. Within 7 h all of the drugs had caused a significant reduction in blood pressure, whereas heart rate showed a significant change only after atenolol. All the drugs produced a marked reduction in brachial pulse-wave velocity. Only nicardipine caused a significant reduction in vessel wall tension both in the carotid and brachial arteries, while brachial peripheral resistance was significantly reduced by all the drugs except atenolol. Neither atenolol nor enalapril caused any significant reduction in carotid peripheral resistance. The results show that all four antihypertensive drugs led to a beneficial increase in arterial compliance despite their different effects on peripheral resistance.

Effects of long-term nicardipine treatment on hemodynamics of large arteries in essential hypertension.

The effects of the calcium-entry blocker nicardipine on brachial hemodynamics were studied in 22 patients (18 male, 4 female) with essential hypertension, who were treated with 20 mg tid for 1 year. Compliance, characteristic impedance, vascular resistances, and tangential tension were measured before treatment and after 1, 3, and 12 months of treatment by an automatic recording from a B-mode, high-resolution, real-time scanner and pulsed Doppler velocimetry for the calculation of the flow volume. We observed statistically significant variations in compliance and impedance after 1 month (3.21 +/- 0.59 dyn-1 cm4 10(-7) vs. 1.26 +/- 0.16 dyn-1 cm4 10(-7) and 50.6 +/- 4.7 dyn s cm-510(2) vs. 91.4 +/- 7.3 dyn s cm-5 10(2), respectively; mean +/- SEM; p less than 0.001), while tangential tension was significantly reduced after only 3 months (23.2 +/- 2.2 mmHg vs. 25.4 +/- 2.3 mmHg cm; p less than 0.05). The correlation between variations in mean blood pressure and in the hemodynamic parameters studied remained statistically significant throughout the study. Nicardipine improved the parameters of large-artery hemodynamics that favor a normal systolic pulse.

Haemodynamic parameters in hypertensive patients: changes induced by lacidipine and nifedipine.

We conducted a randomly allocated, double-blind study in 16 essential hypertensive patients, eight of whom were treated with nifedipine and eight with lacidipine. The antihypertensive efficacy was evaluated and any modifications to peripheral haemodynamic parameters were observed in the brachial artery by a mechanographic method and B-mode scanner with a 10-MHz probe. Statistically significant reductions in blood pressure from basal values were observed after 1 and 6 months' treatment. Enhanced compliance (P less than 0.005), reduced characteristic impedance (P less than 0.001) and lower peripheral resistances (P less than 0.01) were also noted. Variations in pulse wave velocity and mean blood pressure showed a statistically significant correlation as early as the first month of treatment (P less than 0.01). Our results suggest that therapy with nifedipine and lacidipine allows an improvement in peripheral haemodynamics in hypertensive patients. This response is maintained in chronic treatment, even just before the next dose administration at the end of the longest dose interval.

Defibrotide and peripheral obliterative arterial disease: preliminary data.

In a pilot study, defibrotide was administered to 22 patients with arterial occlusive disease of the lower limbs (mean age 59 years; range 48-71 years), of whom 12 were Fontaine 2nd stage and 10 Fontaine 3rd stage. In the first group, treatment enabled significant improvement in the walking distance (580 +/- 95 vs 220 +/- 65 m; M +/- SD; p less than 0.001), even 15 days after discontinuation of therapy (445 +/- 110 m; p less than 0.05). In 3rd stage patients, treatment caused reasonable reduction of pain, with elimination of resting pain in 4 patients. Both groups underwent no modification of Doppler velocimetry and Winsor index, while photoplethysmography in 8 patients at 2nd- and in 3 patients at 3rd-stage showed improvement at the end of treatment. There were no modifications of hepatic, renal, hemopoietic and hemocoagulative functions. Beta-thromboglobulin showed a statistically significant reduction (62 +/- 10 vs 116 +/- 18 ng/ml; M +/- SEM; p less than 0.001), from 2 weeks after the first dose until 15 days after discontinuation of therapy. Defibrotide proved particularly efficacious in Fontaine 2nd-stage patients, showing its suitability for treating the stages of occlusive atherosclerotic disease at which collateral circulation can still be activated.

Evolution of carotid atheromatous lesions in endarterectomized patients.

A noninvasive follow-up using duplex ultrasonography was conducted in 128 patients who had undergone carotid endarterectomy from January 1987 to December 1988. Repeated scans of the operated area revealed a distinct increase in thickened ultrasonographic features (32% vs 8%), and a stenosing lesion was detected in 8 patients. There was also a parallel increase in the number of subjects with thicknesses of the intima adjacent to the endarterectomy area exceeding 2.5 mm. In 7% of cases, dilatation was detected in the operated area and in 27% the margin of the area was raised. The study also dealt with the contralateral carotid artery, where a progression of atheromatous involvement was observed with an increased number of cases of hemodynamically significant stenosis and 3 cases of occlusion. Periodic duplex ultrasonography in endarterectomized patients proves useful for the early detection of hemodynamically significant stenoses or of structural features potentially capable of generating emboli.