[Cardiopulmonary baroreceptors and peripheral resistance in patients with obliterating arteriopathies of the lower limbs].
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Adult↗
Biomedical subjects
E Arosio
Publications and source records attributed to E Arosio.
[Patients with vascular diseases undergoing training physical exercise: urinary nitrites/nitrates and platelet adhesiveness].
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Aged↗
Prevalence of morphological alterations in cervical vessels: a colour duplex ultrasonographic study in a series of 3300 subjects.
BACKGROUND: In order to define the morphological variants involved in carotid elongation in terms of their clinical implications, we have analysed the prevalence of morphological alterations in patients routinely subjected to carotid colour duplex ultrasonography evaluation. METHODS: From January 1, 1993 to June 30, 1996, 3300 subjects were examined for central nervous system symptoms (41% of cases) or for screening related to ischaemic heart disease, lower limb arterial disease, hypertension or major dyslipidaemia (59% of cases). The chi(2)-test was used for statistical analysis. RESULTS: Morphological alterations increased with age. While kinking was more prevalent in females (female:male ratio 58% vs 42%), sharp kinking was significantly more frequent in males (39% vs 15%, p<0.001). Atheromatous plaques predominated in males (79% vs 46%, p<0.001), as well as cases with haemodynamically significant involvement (16% vs 7%, p<0.001). In patients with kinking there was a prevalence of haemodynamically significant lesions (chi(2)=52.7, p<0.001). A possible link between conformational abnormalities and hypertension appeared highly significant owing to a very different prevalence of high blood pressure in the group of subjects with kinking (chi(2)=239, p<0.001). We did not find a significant association between major neurological symptoms and the presence of kinking (chi(2)=0.215, p=0.643), but we found an association with transient ischaemic attacks (chi(2)=6.9, p<0.01). CONCLUSIONS: Conformational abnormalities like kinking, seem much more prevalent in subjects suffering from arterial hypertension. Even though high blood pressure is an important risk factor for transient ischaemic attacks, it is possible that the prevalence of atheromatous lesions and the flow turbulence linked to kinking may also play a role in their pathophysiology.
Adult↗
Decrease of platelet intracellular pH and adhesion by ticlopidine in patients with vascular disease.
BACKGROUND: Ticlopidine inhibits platelet aggregation by preventing the binding of fibrinogen to its platelet receptor. We examined whether this inhibition involved platelet transduction system such as Na+/H+ pump and platelet intracellular calcium. METHODS: Platelet adhesion in 13 patients with peripheral vascular disease treated with ticlopidine, 250 mg b.i.d for 30 days, was measured in culture microplates before and after therapy. The microplate wells were coated with human plasma, fibrinogen or collagen, and platelet adhesion was studied in the resting condition and after stimulation with 1 and 10 microM ADP. At the same time, platelet intracellular calcium and ADP-induced calcium increases were measured with the fluorescent indicator Fura 2. In addition, intracellular pH and thrombin-induced pH variations were measured with the fluorescent probe BCECF. RESULTS: Platelet adhesion to plasma and fibrinogen was significantly reduced (about 50%) after treatment with ticlopidine, while adhesion to collagen was not modified. Basal calcium and ADP-induced calcium increase were not significantly different before and after ticlopidine. Platelet basal intracellular pH was reduced (from 7.44+/-0.009 to 7.41+/-0.017, p<0.05), but agonist-induced alkalinisation was not significantly different. Early acidification, not dependent on Na+/H+ exchange, was also reduced (p<0.05). CONCLUSIONS: These data do not seem to support the hypothesis that ticlopidine-induced reduction of platelet adhesion depends on alteration of the mechanisms determining signal transduction, at least as far as basal and post-stimulation intracellular calcium is concerned. On the contrary, the possibility that ticlopidine inhibits the Na+/H+ antiport remains open to consideration.
Aged↗
Postischemic hyperemia in subjects with lower limbs obstructive arteriopathy: role of PGI2 and endothelin.
The physiological basis of postischemic hyperemia is not yet fully understood. The present study investigated the effects of pharmacologic manipulation of the prostaglandin system on local hemodynamics. Strain-gauge plethysmography was used to study 8 normal subjects and 9 patients with obliterating arterial disease of the lower limbs. Hemodynamic evaluations were performed before treatment, after seven days of low-dose acetylsalicylic acid (100 mg/day) to inhibit platelet thromboxane synthesis, and after acute infusion of 1 g of acetylsalicylic acid to inhibit endothelial prostacyclin synthesis. In patients with arterial disease, the hemodynamic study was also carried out after infusion of iloprost, a synthetic prostacyclin analogue. Acute infusion of acetylsalicylic acid significantly reduced basal blood flow in normal subjects, but not in patients with arterial disease. In the latter group, iloprost affected neither basal nor maximal postischemic flow. The study also evaluated the role of endothelin in musculocutaneous hemodynamic regulation, both in physiological conditions and in atherosclerosis. This part of the study addressed the possibility that the hemodynamic effects of vasodilator prostanoids like prostacyclin might affect endothelin release in vivo. During reactive hyperemia, plasma endothelin was reduced in normal subjects (-1.02 pg/mL, 95% CI: -2.23, 0.08), but not in patients with atherosclerosis (-0.35 pg/mL, 95% CI: -1.45, 0.75). In both groups, plasma endothelin was not affected by aspirin. These findings confirm the role of prostacyclin in local hemodynamic regulation. In the normal subject, musculocutaneous blood flow seems to depend at least in part on the action of vasodilator prostanoids and endothelin. This is not the case in patients with arterial disease, in whom plasma endothelin does not seem to be affected by postischemic changes in blood flow. A possible explanation for this difference could be alteration of the endothelial function in patients with arterial disease, related to the functional and structural characteristics of the artery wall in atherosclerosis.
Aged↗
Changes in peripheral hemodynamics and vasodilating prostaglandins after high-dose short-term ibuprofen in chronically treated hypertensive patients.
The use of cyclooxygenase inhibitors has been seen to reduce the efficacy of many antihypertensive drugs. However, cyclooxygenase inhibitors are normally non-selective because they affect both vascular tissue, where the endothelial prostanoids exert principally a vasodilatory action, and the kidneys, where they also play an important role in regulating hydroelectrolytic metabolism by redistribution of intraparenchymal flow. To evaluate the relative importance of vascular district in the hypertensive patient, we administered ibuprofen - a drug acting with only a minimal antagonist activity. A group of 20 male hypertensives were randomly allocated, according to a single-blind protocol, to treatment with amlodipine (A, 10 mg/day) or lisinopril (L, 20 mg/day). Blood pressure was significantly reduced after 30 days, with a mean difference of -21.75 mmHg for systolic blood pressure (SBP) (95% confidence interval (Cl): -27.46 to -16.04; P< 0.0001) and -14.15 mmHg for diastolic blood pressure (DBP) (95% Cl: -17.13 to -11.17; P< 0.0001). Brachial artery compliance showed a mean increase of 1.657 x 10(-7) dyn-1 cm(4) (95% Cl: 1.188 to 2.126; P<0.001), and forearm resistances showed a mean decrease of -41.973 mmHg ml(-1)s (95% Cl: -75.479 to -8.467; P = 0.017). Changes in compliance were significantly related to those in SBP (r= -0.546; P= 0.013). The administration of ibuprofen (400 mg, three times a day for 3 days) was accompanied by a slight but significant increase in SBP, but not in brachial artery compliance or forearm resistances. Only SBP was affected, showing a mean increase of 4.25 mmHg (95% Cl: 1.26 to 7.24; P = 0.008). There was also reduced urinary excretion of PGI(2) and TXA(2) metabolites. The mean change in 6-keto-PGF(1 alpha) and 2,3-dinor-6-keto-PGF(1 alpha) was 45.71 ng per g urinary creatinine (uCr) (95% Cl: -0.16 to-91.25; P= 0.049) and -73.17 ng (g uCr)(-1) (95% Cl: -38.81 to -107.53; P<0.001), respectively. The mean decrease in TXA(2) catabolites was highly significant: -39.2 ng (g uCr)(-1) (95% Cl: -18.17 to-60.22; P< 0.001) and -102.87 ng (g uCr)(-1) (95% Cl: -61.86 to -143.88; P< 0.001) for TXB(2) and 2,3-dinor-TXB(2), respectively. Our study highlighted an inverse correlation between changes in blood pressure and those in urinary 2,3-dinor-6-keto-PGF(1alpha) excretion, irrespective of antihypertensive regimen. This suggests that, in the hypertensive patient treated with NSAIDs, inhibition of vascular prostanoid synthesis may play an important role in countering the efficacy of an important vascular tone regulatory mechanism.
6-Ketoprostaglandin F1 alpha↗
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.
Adult↗
Primary biliary cirrhosis is associated with specific changes in liver IgG-bearing cell subpopulations.
BACKGROUND/AIMS: The density of total IgG-bearing cells and the distribution of their subclasses were studied in the liver of patients with primary biliary cirrhosis. METHODS: Immunohistochemistry and computerized image analysis were used to compare liver specimens from 18 patients with primary biliary cirrhosis and 28 with chronic hepatitis of different etiology. RESULTS: The density of total IgG-bearing cells was similar in the two groups. However, in patients with primary biliary cirrhosis the proportion of IgG3-positive cells was significantly higher than in patients with chronic hepatitis (53 +/- 7% vs. 7.5 +/- 2.4%) (p < 10(-8)). Conversely, IgG1-positive cells were significantly less prevalent in patients with primary biliary cirrhosis than in chronic hepatitis patients (27 +/- 6.9% vs. 68 +/- 7.2%, p < 10(-8)). Stratification of patients with primary biliary cirrhosis according to histology did not show any difference in the distribution of IgG subclasses associated with the progression of disease. CONCLUSION: These data suggest a pathogenetic role of local IgG3-bearing cells in primary biliary cirrhosis.
Autoantibodies↗
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)
6-Ketoprostaglandin F1 alpha↗
Micro- and macrocirculatory, and biohumoral changes after a month of physical exercise in patients with intermittent claudication.
We studied 15 subjects with intermittent claudication, classed as stage II according to Leriche-Fontaine. The patients were subjected to laser Doppler flowmetry, strain gauge plethysmography, Doppler velocimetry, and blood sampling, in basal conditions and after one month of physical training. Symptom-free walking distance at the end of the training period showed a significant increase, while there was no major change in maximal walking distance or the Windsor index. Laser Doppler flowmetry showed no significant change in cutaneous blood flow at rest, after the month of physical training. On the other hand, strain gauge plethysmography showed a significant decrease in rest flow at the end of the training period, while peak flow of postischemic hyperemia did not change appreciably. Biohumoral evaluations showed a significant decrease of white blood cell count, triglycerides and uric acid. Platelet count, prothrombin time, aPTT and plasminogen were unchanged. On the other hand, we recorded a small, but significant, rise of fibrinogen. Our study confirmed the importance of scheduled physical activity in the patient with intermittent claudication, showing that clinical improvement is not accompanied by an increase in the circulatory reserve. The unchanged levels of plasminogen suggest that the fibrinolytic activity does not vary significantly after a course of physical exercise.
Aged↗
Lipoprotein(a) and general risk factors in patients with angiographically assessed peripheral arterial disease.
High lipoprotein(a) [Lp(a)] has been observed in patients with ischemic heart disease and cerebrovascular disease. Lp(a) is actually thought to be an independent risk factor for coronary disease. We therefore carried out a case-control study, evaluating plasma Lp(a) in 61 patients with angiographically documented peripheral arterial disease (PAD) and in 61 age- and sex-matched patients with no cardiovascular disease. General risk factors for vascular disease were also taken into account. Lp(a) was significantly higher in patients than controls (257.0 +/- 34.8 vs 146.5 +/- 23.5 mg/l p < 0.05), as were cigarette smoking, diabetes, cholesterolemia, fibrinogenemia and the waist-to-hip circumference ratio. Stepwise logistic regression analysis showed that, in addition to cigarette smoking, diabetes, cholesterol and fibrinogen, Lp(a) is a significant independent risk indicator for PAD. This result suggests that high plasma Lp(a) is associated with enhanced risk of PAD and must therefore be evaluated alongside traditional risk factors.
Adult↗
Modifications in peripheral hemodynamics and left ventricular function in hypertensives treated with nicardipine slow release.
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Adult↗
Early agonist-induced intracellular acidification is increased in platelets from patients with essential hypertension.
Enhanced Na+/H+ exchange has been reported to be increased in patients with essential hypertension. However, early variations of intracellular pH, although influenced by the antiport, are only partially dependent on the exchange. In this study, we measured the initial platelet pH response to agonists in a group of untreated subjects with essential hypertension (EH, n = 24) and in a group of age- and sex-matched normotensive control subjects (CS, n = 24). Intracellular pH was measured with the specific fluorescence indicator 2'7'bis(carboxyethyl)-5,6-carboxyfluorescein. Measurements were performed on platelets in the presence or absence of extracellular calcium, in a carbonate-free medium. Intracellular calcium was measured by the Fura 2 method. Mean pH values were slightly higher in the platelets of EH (7.469 +/- 0.017 U) compared with CS (7.423 +/- 0.012 U, P < .05), although there was a substantial overlap. When stimulated with physiologic agonists ADP and thrombin and with the calcium ionophore ionomycin, a biphasic response consisting of early acidification followed by alkalinization was observed, the second phase not being detectable with ADP. The initial acidification was greater in EH, particularly with ADP (EH, -0.046 +/- 0.002 U; CS, -0.036 +/- 0.002 U, P < .001) and with ionomycin (EH, -0.074 +/- 0.007 U; CS, -0.051 +/- 0.005 U, P < .05). This acidification proved in some way calcium dependent, as it was reduced in the absence of extracellular calcium (EGTA) in both EH and CS. After incubation with amiloride a further decrease in intracellular pH, more marked in EH, was observed. Alkalinization induced by thrombin was increased in EH (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Diphosphate↗
Photoconversion to identify DiI-marked cells after hepatocellular transplantation.
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Animals↗
Hepatocyte injection in Gunn rats' thymus and spleen.
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Animals↗
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.
Adult↗
Erythrocyte Na(+)-H+ exchange activity in essential hypertensive and obese patients: role of excess body weight.
INTRODUCTION: Several authors have described increased Na(+)-H+ exchanger activity in essential hypertension, and an increase in activity of this transport system has also been postulated in situations of hyperinsulinism, such as obesity and essential hypertension. METHODS: We measured Na(+)-H+ exchanger activity in a group of 37 subjects with essential hypertension (18 obese, 19 non-obese), in a group of nine normotensive obese subjects and in a control group of 16 healthy volunteers. Plasma insulin and glucose values during an oral glucose tolerance test were evaluated, together with other variables such as plasma aldosterone, plasma renin activity and plasma potassium. RESULTS: Na(+)-H+ exchanger system activity did not appear to be abnormally raised in the hypertensive subjects, but was significantly increased in the normotensive obese group. Upon dividing the hypertensive subjects into two subgroups on the basis of body mass index, it was noted that, whereas the non-obese hypertensives showed Na(+)-H+ exchanger activity patterns similar to those in controls, the obese hypertensive subjects exhibited increased activity of the transport system. Na(+)-H+ activity correlates with body mass index and shows a significant inverse correlation with plasma potassium. No correlations were found between Na(+)-H+ exchanger activity and the sum of plasma insulin values during the oral glucose tolerance test. CONCLUSION: Na(+)-H+ exchanger overactivity appears to be characteristic in overweight subjects, but would not appear to be a specific feature of essential hypertension. The increased Na(+)-H+ exchanger activity observed in obese subjects may be postulated to be related to the hypermineralocorticoidism characteristic of this condition.
Adult↗
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.
Adult↗