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Biomedical subjects

G Di Minno

Publications and source records attributed to G Di Minno.

At least 19 recordsLinked to original sources
PubMed1992

Fibrinogen and mechanisms of thrombosis. A difficult link.

Epidemiological observations indicate that high plasma fibrinogen levels are strongly correlated to the frequency of two major thrombotic complications of atherosclerosis: stroke and myocardial infarction. Thrombosis is increasingly recognized as a central mechanism in stroke and myocardial infarction, and fibrinogen is involved in events thought to play a major role in thrombosis. Therefore, elucidation of the relationship between fibrinogen and thrombosis may strengthen the predictive value of this protein and define new interventions against stroke and myocardial infarction. In addition, advances in the understanding of the atherogenic potential of several risk factors of coronary heart disease took advantage of information emerging from the measurement of the factor in population-based studies. Thus, it is conceivable that measuring plasma fibrinogen to predict stroke and myocardial infarction is a major direction to be followed to gain insight into the thrombogenic potential on this protein and inspire new strategies against thrombotic complications of atherosclerosis.

Blood Viscosity↗
PubMed1991

In vitro inhibition by defibrotide of monocyte superoxide anion generation: a possible mechanism for the antithrombotic effect of a polydeoxyribonucleotide-derived drug.

In an attempt to elucidate the antithrombotic potential of defibrotide (D) we have evaluated several functions of monocytes from 7 healthy subjects before and after in vitro incubation of the cells with increasing concentrations of this drug. At concentrations as high as 40 micrograms/ml, D hardly affected the expression of both the procoagulant activity of monocytes and the formation of superoxide anion in response to 1 mg/ml zymosan (STZ). In contrast, at concentrations that may be achieved in vivo following the administration of the drug (5-20 micrograms/ml), D impaired in a dose-dependent manner (p less than 0.05) the generation of O-2 in response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP, 1 microM) or calcium ionophore A23187 (10 microM). Regardless of the agonist employed, at concentrations between 1 and 5 mM, extracellular Ca2+ had little effect on the impairment of superoxide anion generation by D. In contrast, the inhibitory effect was time-dependent, the maximum impairment (greater than 30%) being observed when the cells were preincubated with the drug for 20 h. These data support the concept that the antithrombotic potential of D involves the ability of the drug to affect the generation of free radicals by leukocytes and suggest that future in vivo studies for the evaluation of the activity of D should take into account the role of monocytes in hemostasis and thrombosis.

Adult↗
PubMed1990

[Impairment of diuresis in surgical intervention. Role of urinary prostaglandins].

In 8 patients who underwent abdominal surgery for non-neoplastic reasons, we have evaluated some parameters of renal function (PRP, NaU, GFR and diuresis) plasma levels of PRA and ADH and urinary prostaglandins PGE2 and 6-keto-PGF1 alpha. In 4 patients we found that surgery per se was associated with enhancements of PRA, ADH and 6-keto-PGF1 alpha. In other 4 patients, Indomethacin, a specific inhibitor of prostaglandin synthesis was given and this was followed by impairment of natriuresis and RPF. These data confirm the central role of prostaglandins in the control of diuresis and natriuresis and suggest that use of drugs affecting prostaglandin synthesis should be avoided in patients who are undergoing surgery.

Adult↗
PubMed1988

Aggregation of human peripheral blood mononuclear cells by calcium ionophore A23187. Comparison with the aggregation of platelets and defective response in Glanzmann's thrombasthenia.

Following exposure to calcium ionophore A23187, washed peripheral blood mononuclear cells (MNC) aggregated and formed thromboxane, like platelets. However, while aspirin strongly inhibited platelet aggregation and thromboxane formation, it had a little effect on the aggregation of MNC. In about 50% of the samples studied, aggregation of MNC was associated with the secretion of ATP. However studies in which exogenous ATP or ADP were used, suggested that the aggregation of MNC is independent of the secretion of nucleotides. MNC from 2 thrombasthenic patients failed to aggregate and bound 9-10 fold less radiolabelled fibrinogen than those from normals when challenged with A23187. However, fibrinogen, which plays a major role in the aggregation of platelets, did not appear to be involved in the aggregation of MNC. A differing behavior of these two types of cells was also found when the effect of plasma was studied on the aggregation response to A23187. Indeed, citrated plasma greatly enhanced the aggregation of platelets while it suppressed the response to MNC. This inhibitory effect of plasma was not detected when heparinized plasma was substituted for citrated plasma. We conclude that the aggregation of MNC in response to A23187 does not involve basic events known to play a major role in the aggregation of platelets. The response to A23187 may be an important probe for understanding basic mechanisms and pathophysiological significance of the aggregation of MNC.

Adult↗
PubMed1988

A retrovirus carrying the polyomavirus middle T gene induces acute thrombocythemic myeloproliferative disease in mice.

Mice inoculated with an artificially constructed retrovirus carrying the middle T gene of polyomavirus develop acute myeloproliferative disease with severe thrombotic and hemorrhagic disorder and impaired platelet function. The megakaryocytic lineage appears to be a target for polyoma-murine leukemia virus infection and middle T gene expression. This newly described disease represents a unique model system for studying disorders of the megakaryocytic lineage.

Adenosine Triphosphate↗
PubMed1988

The effect of tiaprofenic acid on uric acid excretion in man.

The uricosuric effect of tiaprofenic acid was evaluated in a group of normouricaemic inpatients with various rheumatic disorders. Six patients aged 26 to 60 years were maintained on a standardised low-purine diet and, after a washout period of 72 hours, tiaprofenic acid was administered in 3 oral doses of 300 mg 12-hourly. A normal renal function, as assessed by serum creatinine and creatinine clearance determinations, was considered mandatory for entry into the study. The following parameters were evaluated before and after treatment: haematological values, blood urea nitrogen (BUN), serum and urinary creatine concentrations, serum uric acid concentration and the fractional excretion rate of uric acid. Our preliminary results showed a substantial increase of urinary uric acid excretion in the samples collected after treatment, especially in the first 4 hours.

Adult↗
PubMed1987

Renal handling of urea in subjects with persistent azotemia and normal renal function.

Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechanism(s) responsible for their azotemia. During constant alimentary protein, urea nitrogen appearance was normal and urea clearance was much lower than in 10 age-matched control subjects (23.3 +/- 2.1 ml/min and 49.6 +/- 2.6 ml/min per 1.73 m2, P less than 0.001). Inulin and para-aminohippurate clearances, blood volume and plasma concentration of antidiuretic hormone were within normal limits. During maximal antidiuresis, in spite of greater urea filtered load, the urinary excretion of urea was less, and both the maximum urinary osmolality and the free-water reabsorption relative to osmolar clearance per unit of GFR were greater than in control subjects. After sustained water diuresis, the plasma urea concentration markedly decreased to near normal levels in azotemic subjects. The basal urinary excretion of prostaglandins E2 was significantly reduced in azotemic subjects and was directly correlated with fractional urea clearance (r = 0.857, P less than 0.001). An additional group of control subjects (N = 8) showed a marked reduction of fractional clearance of urea after inhibition of prostaglandin synthesis (P less than 0.01). These data suggest that azotemia is due to increased tubular reabsorption of urea in the distal part of nephron, presumably because of increased back diffusion in the papillary collecting duct, accounting for the enhanced maximum urinary osmolality and free-water reabsorption. Renal prostaglandin E2 may participate in the pathogenesis of azotemia by altering recycling of urea in the medulla.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effects of PGE2 infusion on renal function in normal man before and after angiotensin II inhibition by captopril.

Increasing doses of prostaglandin E2 (PGE2) (5, 10, 20, 40, 60 ng/kg/min) were infused in 7 normal volunteers before and after angiotensin II synthesis inhibition by captopril (100 mg by mouth). PGE2 infusion alone did not alter blood pressure, while it increased the urinary excretion of both epinephrine and norepinephrine, enhanced p-aminohyppuric clearance (CPAH), inulin clearance (CIn), sodium and water excretion and decreased urinary osmolality. No changes of CIn, CPAH and catecholamines were observed after captopril alone, whilst there was a significant increase in urine output and sodium excretion and a decrease in urinary osmolality. In the presence of captopril, the infusion of PGE2 caused a significant fall in blood pressure and CIn, enhanced epinephrine excretion and sodium excretion, while it did not significantly reduce CPAH. Our findings suggest that an intact renin-angiotensin system is necessary to maintain GFR during PGE2 infusion.

Adult↗
PubMed1987

The causal role of salt depletion in acute renal failure due to captopril in hypertensive patients with a single functioning kidney and renal artery stenosis.

Captopril (C) causes ARF in hypertensive patients with renal artery stenosis (RAS) with a single functioning kidney (SK). Retrospective studies in two patients showed that episodes of C-induced ARF were preceded by a rise in urinary Na+ excretion and a rapid decrease in body weight. These observations prompted us to investigate whether extracellular fluid volume depletion secondary to C-induced natriuresis can be responsible for ARF. Prospective studies were performed in four patients with RAS-SK treated with C. These studies have shown that: ARF is associated with negative Na+ balance and is corrected by salt replacement, even without interrupting C; ARF is preceded by a rise in urinary prostaglandin (PG) E2 and 6-keto-F1 alpha; ARF is prevented by either saline infusion or aspirin administration; ARF does not occur when the dose of C is not sufficient to raise PGs and urinary N + excretion. We conclude therefore that C-induced ARF in patients with RAS-SK can be secondary to salt depletion dependent on a raised secretion of PGs.

Acute Kidney Injury↗
PubMed1986

A role for steroid hormones in the variability of blood pressure determination.

Blood pressure variability was studied in eight patients with renovascular hypertension (group 1) and eight patients with hypertension and partial deficiency of adrenal zona fasciculata 11-hydroxylase (group 2). Systolic, diastolic and mean blood pressure were found to be higher in group 1 than in group 2 when measured at home (P less than 0.001), while no difference was measured when blood pressure was taken in the outpatient clinic. Heart rate was higher in group 1 than in group 2 both at home and in the clinic (P less than 0.005 and P less than 0.05, respectively); a significant increase was observed only in the hospital clinic for group 2 (P less than 0.001). No difference in systolic function and left ventricular mass was found between the two groups. Finally, group 2 exhibited a significant increase (P less than 0.0001) in systolic, diastolic and mean blood pressure in the clinic, compared with that found at home, while group 1 showed a poor increase (P less than 0.05) in systolic blood pressure only. It is suggested that the enzymatic impairment of adrenal glands in group 2 may play a role in the disparity of blood pressure levels determined at home and in the outpatient clinic. Furthermore, our data suggest that differences in blood pressure measurement at home and in the hospital clinic should be taken into account when screening patients with partial deficiency of 11-hydroxylase.

Adrenal Glands↗
PubMed1986

Angiotensin II inhibition with captopril on plasma ADH, PG synthesis, and renal function in humans.

Using captopril (C), an angiotensin (ANG) I converting-enzyme inhibitor, to increase endogenous prostaglandins (PGs) and to decrease endogenous ANG II synthesis, we studied the relationship between endogenous ANG II, PG, and antidiuretic hormone (ADH) release in seven normal volunteers before (control study) and after inhibition of PG synthesis by a single dose of aspirin (ASA study). In the control study, following the administration of 100 mg of C, there was a significant increase of plasma PGE2, plasma-renin activity (PRA), and urinary PGE2 and 6-keto-PGF1 alpha and a decrease of plasma ADH. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were unaffected by C; urine output, fractional sodium excretion (FENa), and osmolal clearance (Cosmol) increased; and urinary osmolality (Uosmol) decreased significantly after C. In the ASA study PG were undetectable in plasma and significantly reduced in urine 1 h after aspirin and did not increase when C was added. Plasma ADH decreased and PRA increased, as in the control study, after C, whereas GFR, RPF, urine output, FENa, Cosmol, and Uosmol were unchanged. These results suggest that the effect of C on ADH release may be mediated, to a large extent, by a fall in endogenous circulating ANG II, since ADH decreased in the presence of both high or undetectable levels of PGE2. The results also suggest that the increase in PGE2 induced by C may precipitate the diuretic and natriuretic effects of acute C administration.

Adult↗