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Biomedical subjects

A Pierucci

Publications and source records attributed to A Pierucci.

At least 19 recordsLinked to original sources
PubMed1992

Describing and interpreting 24-hour blood pressure patterns in physiologic pregnancy.

The time course of blood pressure in clinically healthy (pregnant and nonpregnant) women was followed by automatic ambulatory monitoring. Chronobiologic methods revealed the time course of dynamic rhythm characteristics as a function of gestational age. Differences were found between nonpregnant and pregnant women with an overall lowering during pregnancy of the rhythm-adjusted midline estimating statistic of rhythm (mesor).

Blood Pressure↗
PubMed1992

Selective decrement of anionic immunoglobulin clearance after induced renal hemodynamic changes in diabetic patients.

The charge permselectivity of proteins was evaluated in diabetic patients after systemic and renal hemodynamic changes induced by an intravenous injection of an angiotensin-converting enzyme inhibitor (captopril) or of clonidine. Anionic immunoglobulin clearance (IgG4) was compared with that of total immunoglobulins, which have the same size but are mostly cationic, and of albumin. Ten type I hypertensive diabetic patients (group 1), 10 type 2 hypertensive diabetic patients (group 2), 5 type 1 normotensive diabetic patients (group 3), 10 subjects with essential hypertension (group 4), and 7 normal volunteers (group 5) received an intravenous injection of captopril (25 mg/100 ml in 5 min). Twelve of the hypertensive diabetic patients underwent a second provocative test with clonidine (150 micrograms/100 ml) (group 6) or placebo (100 ml saline) (group 7) with the same procedure. None of the patients had clinical nephropathy or other disorders. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured before and during the tests. A significant decrease in diastolic blood pressure was observed in groups 1, 2, 4, and 6, together with an increase in the GFR and RPF values in groups 1, 2, 3, and 4 only, as well as a decrease in renal vascular resistances in groups 1, 2, 3, 4, and 6. Both clearances and fractional clearances of IgG4 and IgG decreased after captopril in groups 1 and 2.2+ The decrease in IgG4 clearance was correlated to that of renal vascular resistances in group 1 patients. A significant decrease in the anionic-cationic immunoglobulin ratio (IgG4/IgG) was observed in groups 1, 2, and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Potassium canrenoate and the combination of potassium canrenoate-butizide in the therapy of light to moderate arterial hypertension].

The aim of the study was to evaluate the antihypertensive effect of K-canrenoate, alone or in combination with butizide, in mild to moderate essential hypertensives. Fifteen patients (supine diastolic blood pressure ranging from 95 to 114 mmHg) received K-canrenoate 50mg/die (step 1). In patients with supine diastolic blood pressure greater than 90 mmHg therapeutic regimen was modified at two-week intervals according to the following design: K-canrenoate 100 mg/die (step 2), K-canrenoate 50 mg + butizide 5 mg/die (step 3), K-canrenoate 100 mg + butizide 10 mg/die (step 4). Blood pressure control was achieved in 2 patients treated with K-canrenoate alone (step 2) and in 8 patients on a combined regimen (step 3), and it was maintained throughout the whole trial period (12 weeks); step 4 did not achieve the goal of therapy in the remaining 5 subjects. A statistically significant increase in triglyceridemia (123.2 +/- 42.1 vs 158.3 +/- 62 mg/dl) and uricemia (4.6 +/- 0.9 vs 5 +/- 0.9 mg/dl) was observed at the end of the follow-up period. Serum potassium levels remained stable in all patients. Therefore, K-canrenoate in combination with butizide is an effective and well tolerated drug in the treatment of mild to moderate essential hypertension.

Adult↗
PubMed1990

The use of antiplatelet agents in glomerulonephritis: a pharmacological approach.

The use of antiplatelet agents in chronic glomerular disease is reviewed, with emphasis on drugs affecting thromboxane A2 synthesis or action. The results of short-term and long-term studies in human as well as animal models suggest a role for enhanced intrarenal synthesis of thromboxane A2, though not clearly defining the potential platelet vs glomerular targets of drug action. The availability of novel inhibitors and antagonists may provide new therapeutic strategies against thromboxane-A2-dependent loss of renal function.

Animals↗
PubMed1989

[Nicardipine, alone or in combination with enalapril, in the therapy of arterial hypertension secondary to chronic nephropathy].

The aim of the study was to evaluate the long term antihypertensive effect of nicardipine in hypertensive patients with chronic renal disease. Eight patients (creatinine clearance ranging from 51 to 78 ml/min/1.73 m2) received nicardipine (20 mg t.i.d.). Four weeks later, patients with diastolic blood pressure greater than or equal to 90 mmHg in recumbent position, were given enalapril (10 mg/day) as well. Blood pressure control was achieved in 3 patients treated with nicardipine alone and in 5 patients on a combined nicardipine-enalapril regimen, and it was maintained throughout the whole trial period (52 weeks). In two cases serum creatinine rose from 2.3 to 3.3 and from 1.4 to 2.2 respectively. However, the slope of the creatinine ratio, plotted against time, showed a significant reduction in renal function loss as compared to expected values. In conclusion, nicardipine, alone or in combination with enalapril, is an effective and well tolerated drug for use in treatment of hypertension secondary to chronic renal disease.

Adult↗
PubMed1989

Fractional conversion of thromboxane B2 to urinary 11-dehydrothromboxane B2 in man.

Thromboxane (TX) B2, the chemically stable hydration product of pro-aggregatory TXA2, undergoes two major pathways of metabolism in man, resulting in the formation of 2.3-dinor-TXB2 and 11-dehydro-TXB2, respectively. We have measured the excretion of the latter during the infusion of exogenous TXB2 over a 50-fold dose range in order to examine the fractional conversion of TXB2 to urinary 11-dehydro-TXB2 and to re-assess the rate of entry of endogenous TXB2 into the circulation. Four healthy male volunteers received 6-h intravenous infusions of the vehicle alone and TXB2 at 0.1, 1.0 and 5.0 ng.kg-1.min-1 in random order. They were pretreated with aspirin 325 mg/d in order to suppress endogenous TXB2 production. Urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2 were measured before, during and up to 24 h after the infusions and in aspirin-free periods, by means of NICI-GC/MS-validated radioimmunoassays. Aspirin treatment suppressed urinary 11-dehydro-TXB2 by 91%. The fractional elimination of 11-dehydro-TXB2 was independent of the rate of TXB2 infusion and averaged 6.8 +/- 0.7%, as compared to 6.4 +/- 0.9% for 2,3-dinor-TXB2. Interpolation of 11-dehydro-TXB2 values obtained in aspirin-free periods onto the linear relationship between the quantities of infused TXB2 and the amount of metabolite excreted in excess of control values (y = 0.0058x, r = 0.94, P less than 0.001) permitted calculation of the mean rate of entry of endogenous TXB2 into the circulation as 0.12 ng.kg-1.min-1. We conclude that: (a) urinary 11-dehydro-TXB2 is at least as abundant a conversion product of exogenously infused TXB2 as 2,3-dinor-TXB2; (b) its excretion increases linearly as a function of the rate of entry of TXB2 into the circulation up to approx. 40-fold the calculated rate of secretion of endogenous TXB2; (c) the latter is consistent with previous estimates based on monitoring of the beta-oxidation pathway of TXB2 metabolism.

Adult↗
PubMed1989

Improvement of renal function with selective thromboxane antagonism in lupus nephritis.

To test the hypothesis that the vasoconstrictor thromboxane A2 may affect renal hemodynamics in lupus nephritis, we examined the short-term effects of a selective thromboxane-receptor antagonist, BM 13,177, and of low-dose aspirin. In a randomized, double-blind, crossover study, 10 patients with biopsy-proved lupus nephritis were given a 48-hour continuous infusion of BM 13,177 or placebo. At base line, seven patients had markedly elevated urinary levels of thromboxane B2, the breakdown product of thromboxane A2. During the infusion of BM 13,177, the inulin clearance rate, which was 68 ml per minute per 1.73 m2 of body-surface area at base line, increased by an average of 24 percent (range, 12 to 47 percent; P less than 0.01). Para-aminohippurate clearance was increased to the same extent, with no change in the filtration fraction. The bleeding time doubled, indicating an occupancy of platelet thromboxane receptors of more than 95 percent. The hemodynamic changes were associated with a significant increase in sodium excretion from 76 to 118 mmol per day (P less than 0.01) but with no change in arterial blood pressure. In another study, 10 additional patients with lupus nephritis were randomly assigned to receive either placebo or 20 mg of aspirin twice daily for four weeks. The aspirin regimen produced a selective, cumulative inhibition of platelet cyclooxygenase activity and a doubling of bleeding time. However, there was no change in the inulin clearance rate and no change in urinary levels of thromboxane B2 or 6-keto-prostaglandin F1 alpha, which are indicators of renal synthesis of thromboxane A2 and prostacyclin, respectively. We conclude that in lupus nephritis, impairment of renal function is at least in part mediated hemodynamically and is reversible with a thromboxane antagonist. Platelets, however, are not a major source of thromboxane A2 synthesis and action within the kidney.

Adolescent↗
PubMed1989

Angiotensin converting enzyme inhibition delays the progression of chronic renal failure in hypertensive patients with immunoglobulin A nephropathy.

Ten hypertensive, non-nephrotic patients with immunoglobulin (IgA) nephropathy treated with conventional therapy (vasodilators, beta-blockers, diuretics) were observed for 21.4 +/- 9 months. Treatment was then changed to an angiotensin converting enzyme (ACE) inhibitor alone for an additional 22.6 +/- 9 months. The ACE inhibitor therapy was associated with a lower diastolic blood pressure and a slowing in the rate of decline in renal function, but no change in proteinuria.

Adult↗
PubMed1989

[Multicenter clinical study of the antihypertensive activity of lisinopril].

One-hundred patients suffering from slight-moderate hypertension (53 m, 47 f, aged between 18 and 78, average 49.08) have been studied in order to assess the effectiveness and tolerance of lisinopril ("Zestril", ICI-Pharma), a new ACE inhibitor in a single daily administration at doses of between 10 and 80 mg in relation to pressure values. Monotherapy with Lisinopril proved effective in 84 patients (88.4%), in 74 of whom (7.9%) pressure values were returned to normal. 11 patients (11.6%) did not respond to treatment. In most cases, the result was obtained with a dose of 20 mg in a single administration (32.6%). The incidence of side-effects was limited and in no case required the withdrawal of the drug.

Adolescent↗
PubMed1987

Effects of sulindac on renal and extrarenal eicosanoid synthesis.

We measured the renal and extrarenal synthesis of prostacyclin and thromboxane A2, as reflected by the urinary excretion of the stable hydration products 6-keto-prostaglandin F 1 alpha and thromboxane B2 and the corresponding 2,3-dinor-derivatives, during chronic administration of sulindac (200, 400, 600, and 800 mg/day, each dose given for 7 days in successive weeks) in seven healthy subjects. Urinary eicosanoids were measured by negative ion, chemical ionization-GC/MS-validated RIA techniques. Both 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-prostaglandin F 1 alpha showed a dose-dependent reduction, ranging between 45% and 85%. In contrast, the urinary excretion of 6-keto-prostaglandin F1 alpha and thromboxane B2 did not change significantly throughout the study. These results extend previous observations of a selective sparing of renal cyclooxygenase activity by sulindac in humans and demonstrate that this selectivity is not related to an overall weaker enzyme inhibition.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Renal effects of nonsteroidal anti-inflammatory drugs in chronic glomerular disease.

In contrast to a variety of clinical conditions characterized by ineffective circulatory volume, chronic glomerular disease is not usually associated with increased circulating levels of vasoconstrictor hormones. However, a reduction in glomerular prostacyclin production can possibly account for the prostaglandin dependence of renal function in these patients by virtue of the enhanced constrictor effects of angiotensin II on glomerular arterioles and mesangium. The reduction of renal function induced by a nonselective cyclo-oxygenase inhibitor is inversely related to the basal prostacyclin production. Increased renal synthesis of vasoconstrictor thromboxane A2, as noted in patients with systemic lupus erythematosus, might contribute to the cyclo-oxygenase dependence of renal function. Aspirin as well as a variety of structurally unrelated nonsteroidal anti-inflammatory drugs reduce renal function in systemic lupus erythematosus patients. However, the functional consequences of renal cyclo-oxygenase inhibition are partially attenuated in patients with lupus nephritis vis-à-vis other forms of chronic glomerular disease because of concomitant suppression of enhanced glomerular thromboxane A2 production. Animal data consistent with a prevailing functional significance of vasodilator prostaglandins have also been reported. Short-term administration of sulindac at the recommended dosage is relatively safe in patients with chronic glomerular disease because of selective sparing of glomerular cyclo-oxygenase activity. The long-term consequences of selective versus nonselective cyclo-oxygenase inhibition remain to be established in humans. The beneficial effects of a combination of aspirin and dipyridamole in slowing the deterioration of renal function in patients with membranoproliferative glomerulonephritis does provide a rationale for exploring the effects of low-dose aspirin (i.e., 0.5 to 1.0 mg/kg per day), which most effectively suppresses platelet thromboxane A2 production without interfering with renal prostacyclin synthesis.

Animals↗
PubMed1986

Effect of prostacyclin on renal kallikrein release in man.

The aim of this research was to study exogenous prostacyclin effect on urinary kallikrein excretion (UKK) in man, to define whether prostacyclin-induced renin release and/or endogenously released cyclooxygenase products were responsible for prostacyclin-induced enhancement of UKK, to determine furosemide effect on UKK. Prostacyclin was infused in eight healthy men and repeated after propranolol and indomethacin treatment. Prostacyclin caused a dose-dependent increase of UKK. Pretreatment with propranolol and indomethacin did not affect prostacyclin-induced enhancement of UKK, although it reduced absolute values of plasma renin activity. Furosemide increased UKK and simultaneously urinary 6-keto-prostaglandin F1 alpha. We conclude that prostacyclin induces an increase in UKK in a dose-dependent manner; furosemide-induced renal prostacyclin synthesis is temporally related to enhancement of UKK; partial dissociation of UKK from plasma renin activity under propranolol and indomethacin treatment and in response to furosemide might suggest a direct effect of prostacyclin on UKK.

6-Ketoprostaglandin F1 alpha↗