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Biomedical subjects

L Scapellato

Publications and source records attributed to L Scapellato.

30 records · Page 2Linked to original sources
PubMed1985

The role of endogenous opioids in the baroreflex dysfunction of dialysis patients.

We studied the effect of the opiate antagonist naloxone on the response to Valsalva manoeuvre in nine dialysis patients, in six diabetics with normal renal function whose response to Valsalva manoeuvre was similar to that of dialysis patients and in eight healthy subjects. Naloxone caused a progressive increase in the subnormal Valsalva ratio in dialysis patients but it did not cause any change in diabetics nor in healthy subjects. The increase in Valsalva ratio observed in dialysis patients was due to restoration of the parasympathetically mediated reflex bradycardia of the release phase of the manoeuvre. Endogenous opioids may be responsible for the baroreflex dysfunction of dialysis patients.

Adult↗
PubMed1981

Defective platelet aggregation and increased platelet turnover in patients with myelofibrosis and other myeloproliferative diseases.

In 9 patients with myeloproliferative diseases (MPD) (6 with myelofibrosis, MF, 1 with Ph1 positive chronic granulocytic leukaemia, CGL, 1 with primary eosinophilia, PE, 1 with pre-leukaemia syndrome, preL) collagen, epinephrine, and ADP-induced aggregation, N-ethylmaleimide-induced malondialdehyde (MDA) production, beta-thromboglobulin (beta-TG) plasma levels, and platelet turnover were studied. Collagen-induced aggregation was found to be normal in 7 patients, absent in 1, and reduced in 1. In all but 3 patients, aggregation with ADP was markedly reduced. Epinephrine-induced aggregation was decreased in 7 patients. No difference was found between mean MDA production in MPD (3.21 +/- 0.50 nmol/10(9) PLTs) and in control group of 21 normal subjects (3.04 +/- 0.26 nmol/10(9) PLTs). Mean beta-TG levels were significantly higher (P less than 0.01) in MPD patients (165.00 +/- 28.29 ng/ml) than in healthy controls (81.76 +/- 14.63 ng/ml). Mean platelet production half-time was significantly shorter in MPD (2.48 +/- 0.24 d) than in the control group (3.43 +/- 0.17 d), after adjustment for age by covariance analysis (P less than 0.005). Our data do not indicate an abnormal prostaglandin synthesis and are consistent with the hypothesis that a disseminated intravascular platelet aggregation might take place in MPD patients.

Adult↗
PubMedDate not supplied

Monoclonal antibody-defined T lymphocyte subpopulations in monoclonal gammapathy of undetermined significance.

We used monoclonal antibodies of the OK series to study T lymphocyte subpopulations in 55 patients with monoclonal gammapathy of undetermined significance (MGUS) and in 40 healthy control subjects, with the aim to investigate if alterations in T lymphocyte subpopulations occur also in MGUS. Mean OKT3+ and OKT8+ cell counts were higher (p less than 0.01 and p less than 0.001, respectively) and the mean OKT4/OKT8 ratio was lower (p less than 0.02) in MGUS patients than in the control subjects. MGUS with the IgM-type monoclonal immunoglobulin (IgM-MGUS) showed the most evident derangement of T lymphocyte subpopulations, i.e., a significant increase of OKT8+ cells and a significant reduction of the OKT4/OKT8 ratio. OKT4+ and OKT8+ cells were significantly increased in patients with high paraprotein concentration (above 16 g/l). Our data suggest that alterations of T lymphocytes are present in MGUS, and that they are similar to those observed in malignant lymphoproliferative disorders.

Adult↗
PubMedDate not supplied

Hemodynamic and humoral interactions between captopril and nifedipine.

Nine patients with uncomplicated essential hypertension received, according to a randomized sequence, captopril (25 mg three times daily), nifedipine (10 mg three times daily), and both drugs for 1 week, with each treatment period separated by a 1-week interval during which a placebo was given. Captopril significantly reduced blood pressure and plasma aldosterone, increased plasma renin activity (PRA), and did not change heart rate. Nifedipine exerted a similar effect on blood pressure and PRA, but it increased heart rate and did not change aldosterone. Captopril plus nifedipine further reduced blood pressure and increased PRA, did not change heart rate, and reduced aldosterone to values similar to those after captopril alone. The hypotensive effect of captopril was highly predictable by basal PRA values, and that of nifedipine by age, while PRA increments induced by captopril were unrelated to those induced by nifedipine. These data indicate that: 1) captopril and nifedipine exert an additive effect on blood pressure and renin; 2) captopril counteracts the heart rate increase induced by nifedipine; 3) nifedipine does not influence the aldosterone inhibition induced by captopril. It is suggested that the association of the two drugs can be usefully employed in the treatment of hypertension.

Adult↗