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Biomedical subjects

A Antonello

Publications and source records attributed to A Antonello.

At least 37 records · Page 2Linked to original sources
PubMed1996

Carotid artery lesions in patients with nondiabetic chronic renal failure.

Atherosclerotic complications are the leading cause of death in chronic renal failure (CRF) patients. Therefore, we wished to investigate the prevalence of carotid artery lesions (CALs) in these subjects. Two groups were evaluated by high-resolution echo Doppler: group 1 included 103 patients (68 males and 35 females) affected by nonnephrotic CRF and group 2 included 100 control subjects (60 males and 40 females). The prevalence of hypertension was 84% in both groups. The exclusion criteria included diabetes mellitus and symptoms of cerebrovascular disease. In the two groups we evaluated clinical history, physical examination, total cholesterol, triglycerides, fibrinogen, blood cell counts, blood urea nitrogen, creatinine, 24-hour proteinuria, and urine analysis. In group 1 patients the following lipid profile parameters were also evaluated: low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, lipoprotein(a), ApoAI, ApoAII, and ApoB. Group 1 had higher triglycerides and fibrinogen than group 2. A lower body mass index was found in group 1 than in group 2. The prevalence of CALs was significantly higher in the CRF patients than in the control subjects (62% v 47%; P = 0.04). The difference between the two groups was more striking among normotensive patients (62% v 19%; P = 0.03). All CRF patients affected by peripheral arterial disease and 86% of those having coronary artery disease had associated CALs. In CRF patients the severity of CALs was positively correlated to age, white blood cell count, triglycerides, and fibrinogen. Nondiabetic CRF patients have a higher prevalence of carotid artery lesions than control subjects. Several factors besides hypertension, including lipids, blood coagulation, and leukocytes, could contribute to the accelerated atherosclerosis of CRF patients.

Adult↗
PubMed1996

Increased urinary NO2-/NO3- and cyclic guanosine monophosphate levels in patients with Bartter's syndrome: relationship to vascular reactivity.

Nitric oxide (NO) is a potent endogenous vasodilator and plays a pivotal role in the control of vascular tone by the formation of cyclic guanosine monophosphate (GMP). Patients affected by Bartter's syndrome have lower than normal vascular reactivity with normohypotension and decreased peripheral resistances in spite of biochemical and hormonal abnormalities typical of hypertension, and it is possible that increased production of NO may be involved in maintaining this reduced vascular response and vasodilatation. We have examined this possibility by studying NO2-/NO3- and cyclic GMP urinary excretions to assess NO production in vivo in seven patients affected by Bartter's syndrome compared with seven healthy controls. A group of five patients with hypokalemia other than Bartter syndrome (pseudo-Bartters) was also included in the study to evaluate the effect of hypokalemia on NO production. NO2-/NO3- urinary excretion (0.45 +/- 0.14 v 0.25 +/- 0.04 micromol/micromol urinary creatinine [controls], P < 0.005, v 0.28 +/- 0.05 [pseudo-Bartters], P < 0.01) and cyclic GMP urinary excretion (0.057 +/- 0.028 v 0.022 +/- 0.01 micromol/micromol of urinary creatinine [controls], P < 0.009, v 0.024 +/- 0.004 [pseudo-Bartters], P < 0.02) were increased in patients with Bartter's syndrome in comparison with controls and pseudo-Bartters, and a linear correlation between these two parameters was also present (P < 0.001). We conclude that in Bartter's syndrome the increased NO2-/NO3- and cyclic GMP urinary excretions point to an increased NO synthesis, which could account for the reduced vascular response of the disease, therefore adding its role in determining the vascular hyporeactivity of Bartter's syndrome.

Adolescent↗
PubMed1996

Intracellular calcium signalling and vascular reactivity in Bartter's syndrome.

We investigated patients affected by Bartter's syndrome in the attempt to localize the intracellular defect mediating the reduced intracellular Ca2+ mobilization that may be responsible for the decreased vascular reactivity characteristic of Bartter's syndrome. Using the formylmethionyl-leucyl-phenylalanine (fMLP) receptor system, which causes, intracellular calcium release, we investigated fMLP-stimulated intracellular inositol 1,4,5-trisphosphate (IP3) production as well as the number and affinity of fMLP receptors in neutrophils from Bartter's syndrome patients and healthy controls. Scatchard plot analysis of radioactive fMLP binding to neutrophils indicated that there were no differences in either cell receptor number and affinity for ligand between healthy controls (n = 5) and patients with Bartter's syndrome (n = 5): 6,151 +/- 1,431 vs. 7,112 +/- 2,566 receptors/cell; K(D): 0.446 +/- 0.14 vs. 0.454 +/- 0.09 pM of fMLP. 5- and 10-second fMLP-stimulated intracellular IP3 production was instead reduced in patients affected by Bartter's syndrome: 2.479 +/- 1.07 vs. 4.073 +/- 1.04 nmol/10(7) cells at 5 s (n = 8; p < 0.01); 1.673 +/- 0.741 vs. 3.766 +/- 1.348 nmol/10(7) cells at 10 s (n = 8; p < 0.005). The results of this study indicate that the anomaly of intracellular calcium mobilization in patients with Bartter's syndrome arises from a defect at the postreceptor level. The anomalous calcium signalling that takes place in Bartter's syndrome may provide a mechanism for the hyporesponsiveness to pressor stimuli characteristic of these patients.

Adult↗
PubMed1996

[7-year-follow up (1987-1994) of a population with asymptomatic persistent microhematuria and normal renal function].

A group od 129 patients with persistent asymptomatic microhematuria was studied for 7 years (1987-1994). At the beginning of the study, 31 patients showed mild proteinuria (less than 1 g/day) and in the rest of 98 patients, 21 showed microalbuminuria. At the end of the study none of the patients developed renal failure, urological disease, hypertension. Six patients out of 31 with mild proteinuria (less than 1 g/day), developed an increase of proteinuria over 2 and 3/day and underwent a renal biopsy while 2 out of 21 patients with altered microalbuminuria completely recovered after the follow-up period. The rest of 77 patients at the end of the study still showed isolated microhematuria. The results of this study support the hypothesis that in a population with age range between 16 and 28 years, the presence of persistent microhematuria, also associated with mild proteinuria, even for a long time, does not seem to lead to changes of renal function or to urological diseases.

Adolescent↗
PubMed1995

Endothelium-derived vasoactive substances in Bartter's syndrome.

An imbalance between endothelium-derived vasoactive substances such as endothelin and endothelium-derived nitric oxide (NO) might be viewed as a possible determinant of vascular hyporeactivity. To check this possibility the authors evaluated the role of endothelin and NO in the reduced vascular reactivity of Bartter's syndrome. Plasma immunoreactive endothelin (22.07 +/- 7.06 vs 13.80 +/- 1.43 pmol/L, P < 0.011), urinary excretion of NO2- (0.28 +/- 0.10 vs 0.15 +/- 0.02, mumol/mumol of urinary creatinine, P < 0.01) and NO3- (0.17 +/- 0.07 vs 0.09 +/- 0.02 mumol/mumol of urinary creatinine, P < 0.011), and forearm resting blood flow (FRBF) (6.67 +/- 1.69 vs 4.30 +/- 0.38 mL/m'/100 mL, P < 0.005) were increased in patients with Bartter's syndrome in comparison with normal controls (C). No difference in postischemic maximal FBF was found (34.14 +/- 4.67 vs 31.35 +/- 2.86 mL/minute/100 mL), while patients showed a slower recovery after peak flow (PF) (77.57 +/- 61.35 vs 9.42 +/- 3.69 seconds, P < 0.013). Higher plasma endothelin supports the defect in vascular reactivity of Bartter's syndrome already shown for angiotensin II and norepinephrine and is in keeping with the altered intracellular calcium signaling previously demonstrated by the authors in this syndrome. The increased excretion of NO2- and NO3- in this syndrome, together with the higher FRBF and the slower recovery of the FBF and PF, argues in favor of an increased NO synthesis in Bartter's syndrome and of assigning it a role in the vascular hyporeactivity of Bartter's syndrome.

Adolescent↗
PubMed1994

Familial hypertension in Morgagni's De Sedibus et Causis Morborum per Anatomen Indagatis.

Morgagni was a contemporary of Malpighi, but unlike the latter he concentrated on macroscopic clinical and anatomic observations. His De Sedibus et Causis Morborum per Anatomen Indagatis consists of 5 books, written as letters to other scientists and members of foreign academies. He dealt with diseases of the head, the chest and the abdomen and with surgically treatable diseases. The final book contains corrections to the previous 4 in the light of new studies and extended clinical experience. One case history presented, of a patient of Valsalva's who died with edema and a bladder stone, can probably be considered as the first description of familial hypertension. From his clinical and autopsy investigations, Morgagni concluded that the patient died of hereditary bladder stone disease and apoplexy.

Anatomy↗
PubMed1990

Assessment of tear drainage after canalicular obstruction using fluorescein dye disappearance.

Assessment of tear drainage impairment after monocanalicular obstruction can be difficult. The authors used fluorescein dye disappearance to evaluate tear drainage after experimental obstruction of upper, lower, neither, or both canaliculi in 20 subjects. Marked impairment was noted in all subjects when both canaliculi were occluded (P less than 0.004). Monocanalicular obstruction (either upper or lower) generally resulted in minimal or no impairment, though 10% of subjects showed marked impairment. Fluorescein dye disappearance proved a reliable, rapid method for assessing tear drainage and detecting lacrimal obstruction.

Fluorescein↗
PubMed1990

Is hydrochlorothiazide-induced hypocalciuria due to inhibition of prostaglandin E2 synthesis?

1. Since prostaglandin E2 could play a role in idiopathic hypercalciuria, and considering the well-established hypocalciuric action of hydrochlorothiazide, we have evaluated the effect of 15 days' treatment with hydrochlorothiazide in 10 hypercalciuric male stoneformers on urinary Ca2+ and prostaglandin E2, as well as on plasma bicyclo-prostaglandin E2, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone. 2. In addition to lowering urinary Ca2+ (P less than 0.001), hydrochlorothiazide also promoted a significant fall in urinary prostaglandin E2 (P less than 0.001), plasma bicyclo-prostaglandin E2 (P less than 0.001) and 1,25-dihydroxyvitamin D (P less than 0.01), and an increase in plasma parathyroid hormone (P less than 0.025), whereas plasma 25-hydroxyvitamin D was unchanged. 3. A positive correlation between urinary Ca2+ and prostaglandin E2 was present before (P less than 0.00005), but not after, hydrochlorothiazide. Plasma bicyclo-prostaglandin E2 and plasma 1,25-dihydroxyvitamin D were positively correlated both before (P less than 0.005) and after (P less than 0.005) hydrochlorothiazide, as was also the percentage change in each induced by the drug (P less than 0.05). Furthermore, the changes in plasma 25-hydroxyvitamin D and plasma 1,25-dihydroxyvitamin D after hydrochlorothiazide were negatively correlated (P less than 0.05). 4. It is suggested that a block of prostaglandin E2 synthesis plays a role in the effect of hydrochlorothiazide on Ca2+ metabolism, most probably through an inhibition of 1 alpha-hydroxylase activity.

Adult↗
PubMed1985

Interactions between muzolimine, PgE2 and the renin-angiotensin-aldosterone system.

UNLABELLED: The aim of our study was to determine the possible interrelation between muzolimine and the renal PG and renin-angiotensin systems by direct assay of these renal hormones. 4 groups of five rats were subdivided as follows: Group 1: controls; Group 2: rats treated with muzolimine (100 mg/kg); Group 3: rats treated with indomethacin (4 mg/kg); Group 4: rats treated with both muzolimine and indomethacin. After 3 days, the rats were transferred to metabolic cages, urine and plasma samples were taken on the 4th day and the following parameters assayed: Urine: creatinine, Na+, PGE2. Plasma: PRA and aldosterone. RESULTS AND CONCLUSIONS: Muzolimine: 1) increase PRA (11.8 +/- 1.06 vs. 8.66 +/- 1.56 AI ng/ml/h - p less than 0.01) and 2) increases PGE2 release (7.08 +/- 3.22 vs. 0.6 +/- 0.19 micrograms/mg urine creatinine - p less than 0.005). PG synthesis-inhibition (indomethacin) lowers (0.118 +/- 0.056 mmol Na+/mg urine creatinine of group 2 vs 0.043 +/- 0.019 mmol Na+/mg urine creatinine of group 4 - p less than 0.025) although not completely abolishes (0.043 +/- 0.019 nmol Na+/mg urine creatinine of group 4 vs. 0.019 +/- 0.006 mmol Na+/mg of group 3 - p less than 0.05) the natriuretic effect of muzolimine. This suggests that the natriuretic activity of the drug, at least in part, depends on PGE2 production.

Animals↗
PubMed1982

Canrenoate reversal of inhibitory effects of digoxin on basal and furosemide-stimulated renin secretion.

Changes in plasma renin activity (PRA) were monitored in six mildly hypertensive men after intravenous doses, in seven separate experiments, of placebo, digoxin, potassium canrenoate, potassium canrenoate with digoxin, furosemide, furosemide with digoxin, and potassium canrenoate with furosemide and digoxin. Potassium canrenoate has been used as a rapid source of canrenone, which has been recently shown to be a competitive antagonist of ouabain at its Na-K-ATPase receptor site. Potassium canrenoate infusion reversed the hyporeninemic effect of digoxin. This result has been taken as evidence that: (1) antialdosteronic drugs can also reverse digoxin effects at extracardiac level and (2) the Na-K-ATPase system is involved in the renin secretory mechanism. A seemingly identical reversal of the hyporeninemic effect of digoxin was induced by furosemide, which, when given alone, stimulated renin secretion. The simultaneous administration of potassium canrenoate, digoxin, and furosemide induced an increase in PRA on the same order as that after furosemide alone. This result indicates that furosemide stimulates renin release by affecting a biochemical system other than that affected by digoxin.

Adult↗
PubMed1982

Immunogenicity of serum HLA antigens in allogeneic combinations.

Immunization of patients with chronic renal insufficiency with plasma from selected donors elicited lymphocytotoxic antibodies. Analysis of these antibodies with Fab2 blocking assays showed that they are directed to HLA-A,B and to Ia-like antigens. These results indicate that serum HLA antigens are immunogenic in allogeneic combinations.

Animals↗
PubMed1980

[Antibody response to histocompatibility antigens in hemodialysis patients subjected to planned whole-blood transfusions].

In hemodialysis patients planned whole blood transfusions from single donors, induce the formation of anti HLA A, B, C and DR cytotoxic antibodies. The percentage of immunization, however, is lower than that observed in healthy subjects immunized following a similar transfusional schedule. This observation may reflect the existence in some patients of an impairment of the immune response to histocompatibility antigens. The production of lymphocytotoxic antibodies appear to be associated with severe graft rejections while anti HLA antibodies detected only by an indirect rosette assai don't seem to play a significant role in the outcome of the transplants.

Adolescent↗