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Biomedical subjects

C Lechi

Publications and source records attributed to C Lechi.

At least 37 records · Page 2Linked to original sources
PubMed1989

[Usefulness of several laboratory tests on prethrombotic status in arterial vascular pathology].

The Authors analyze the clinical and biological meanings of some markers of coagulative activity (beta thromboglobulin, PF4, fibrinogen, fibrinopeptide A) and their changes in some arterial diseases. The role of main atherosclerosis risk factors (dyslipidaemia, hypertension, smoking and diabetes) in promoting a thrombophylic state in these pathological conditions is also considered. Finally the Authors evaluate the usefulness of the markers of coagulative activity from both a diagnostic and a preventive point of view in the arteriopathies of atherosclerotic etiology.

Arteriosclerosis↗
PubMed1989

Plasma ouabain-like activity in essential hypertensive patients and in subjects with primary aldosteronism.

Plasma from 37 essential hypertensive patients, from 11 subjects with primary aldosteronism and from 23 normotensive subjects was tested for ouabain-like activity. Despite a very substantial overlap, hypertensive patients (both essential and secondary) showed significantly higher levels of a ouabain-like plasma factor compared to normotensive controls. No substantial differences could be detected, however, between the two forms of hypertension; in particular, no significant changes were observed in the low-PRA subgroup. Our results are hardly compatible with the hypothesis that this substance may be of crucial importance in the development either of essential hypertension or of primary aldosteronism.

Adolescent↗
PubMed1989

Platelet intracellular free Ca2+ after incubation with plasma from hypertensive patients.

Variations in intracellular free calcium were measured in platelets from normal donors, incubated with plasma from hypertensive patients and from control subjects to test the hypothesis that a circulating factor might induce an increase in calcium concentration. Before incubation, plasma was heat-inactivated or ultrafiltered. Incubation both with heat-inactivated and ultrafiltered plasma failed to result in any significant modifications in intracellular free calcium. Similarly, no significant increase was observed after incubation with ouabain at concentrations ranging from 10(-7) to 10(-4) M. No significant differences were observed between platelets incubated with plasma from hypertensive as compared with control subjects. These findings are not consistent with the hypothesis that the increase in intracellular free calcium observed in platelets of hypertensive patients may be due to a plasma ouabain-like factor.

Adult↗
PubMed1988

Altered excretion of prostaglandin and thromboxane metabolites in pregnancy-induced hypertension.

The renal and systemic metabolites (the latter as 2,3-dinor derivatives) of prostacyclin and thromboxane A2 were measured, along with renal prostaglandin E2 and kallikrein, in the urine of 15 patients with pregnancy-induced hypertension, 15 normotensive pregnant women matched for both age and gestational age, and 15 normotensive nonpregnant control women. Urinary excretion of all prostaglandin and thromboxane metabolites studied proved significantly higher in normotensive pregnant women than in controls. Prostaglandin E2, 6-keto-prostaglandin F1 alpha, and 2,3-dinor-6-keto-prostaglandin F1 alpha were significantly lower in pregnancy-induced hypertensive women than in normotensive pregnant women, whereas thromboxane B2 and 2,3-dinor-thromboxane B2 showed no significant differences in the two groups. A significant negative correlation (r = -0.636, p less than 0.01) was found between urinary 2,3-dinor-6-keto-prostaglandin F1 alpha and mean blood pressure in the two groups of pregnant women taken as a whole. These data indicate that, in pregnancy-induced hypertension, there is an imbalance between vasodilator and vasoconstrictor factors, not only in the kidneys, but also at the systemic vascular level. This imbalance, which may in itself produce vasoconstriction, may also potentiate the hypertensive effect of catecholamines and angiotensin II.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Intracellular free Ca2+ in platelets of essential hypertensive patients. Lack of correlation with clinical and laboratory data.

Platelet intracellular free Ca2+, [Ca2+]i, was found to be higher in 64 hypertensive patients than in 65 age- and sex-matched normotensive controls (142.7 +/- 3.8 nmol/l vs 126.6 +/- 2.4 nmol/l, M +/- SEM, respectively; P less than 0.001). No differences were observed in hypertensive patients in relation to age, duration of hypertension or severity of retinopathy, but a slight correlation was observed (r = 0.275, P less than 0.05) between platelet [Ca2+]i and systolic blood pressure. No correlations were found between platelet [Ca2+]i and plasma cholesterol, triglycerides, aldosterone or renin activity. These data appear to support the hypothesis that increased platelet [Ca2+]i in hypertensive patients is more likely to be related to a primary cellular abnormality than to activation by extrinsic humoral or vascular factors.

Adolescent↗
PubMed1987

Measurement by bioluminescence technique of erythrocyte membrane Na+,K+-ATPase activity in hypertensive patients.

Erythrocyte membrane Na+,K+-ATPase activity was measured using a bioluminescence technique in 28 hypertensive patients (24 with essential hypertension, 2 with renovascular hypertension and 2 with hypertension secondary to primary hyperaldosteronism) and in 28 normotensive control subjects matched for age and sex. Erythrocyte Na+,K+-ATPase activity was significantly reduced in the patients with essential hypertension (130.9 +/- 11.4 vs. 186.6 +/- 19.5 nmol ATP/mg prot per h; mean values +/- SEM; p less than 0.05) and in the patients with secondary hypertension. A significant negative correlation was found between erythrocyte Na+,K+-ATPase and systolic blood pressure (r = -0.603; p less than 0.01), but not between Na+,K+-ATPase and plasma renin activity or plasma aldosterone levels. These data confirm the findings of a number of previous studies reporting reduced activity of erythrocyte Na+,K+-ATPase possibly related to the presence of a circulatory inhibitor of sodium pump. The method, based on ATP assay by bioluminescence, presents a high degree of specificity as well as simple, rapid execution.

Adult↗
PubMed1987

Reduced excretion of vasodilator prostaglandins in preeclampsia.

The role of prostaglandin (PG) system in preeclampsia (pre-E) was investigated. Urinary excretion of PGE2,6-keto PGF1 alpha,2,3 dinor 6-keto PGF1 alpha, TxB2 and 2,3-dinor-TxB2 and kallikrein were determined in 10 normotensive pregnant women and 14 with pre-E. 6-keto PGF1 alpha and 2,3-dinor 6-keto PGF1 alpha (the main renal and extrarenal metabolites of vasodilator PGI2) and PGE2 excretion was lower in pre-E. TxB2 metabolites in urine were similar in the two groups of women. Our data are consistent with the hypothesis of an imbalance between vasodilator and vasoconstrictor PGs in pre-E.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Increased basal and thrombin-induced free calcium in platelets of essential hypertensive patients.

Intracellular free calcium, [Ca2+]i, was studied in platelets of essential hypertensive subjects and normotensive controls under basal conditions and after stimulation with epinephrine, norepinephrine, angiotensin II, ouabain, and thrombin, using the fluorescent calcium indicator quin 2. Basal [Ca2+]i was significantly higher in hypertensive subjects (n = 32) than in normotensive controls (n = 30; 167.4 +/- 5.0 vs 143.2 +/- 3.1 nmol/L; p less than 0.001). Epinephrine, norepinephrine, angiotensin II, and ouabain had no effect on platelet calcium, whereas thrombin induced a dose-dependent increase in [Ca2+]i in both the presence and absence of extracellular calcium. This [Ca2+]i increase in the presence of extracellular calcium, which depends mainly on calcium influx, was significantly higher (p less than 0.05) in platelets of hypertensive subjects at all thrombin concentrations (ranging from 0.025-0.1 U/ml), while the [Ca2+]i increase in the absence of extracellular calcium, which depends only on release from intracellular stores, was similar in hypertensive subjects and controls. These results suggest that, in essential hypertension, there is not only increased platelet resting [Ca2+]i but also an increase in agonist-mediated calcium influx, which appears to indicate a cell membrane abnormality in the platelets of subjects with essential hypertension.

Adult↗
PubMed1987

Antihypertensive activity of enalapril. Effect of ibuprofen and different salt intakes.

It has been suggested that angiotensin-converting enzyme (ACE) inhibitors may also act through the renal prostaglandin (PG) system; moreover, it has been shown that nonsteroidal antiinflammatory drugs (NSAIDs) are capable of reducing the antihypertensive activity of ACE inhibitors. Sixteen essential hypertensive patients (WHO stages, I-II, eight on a low-sodium diet and eight on a high-sodium diet) were treated with enalapril, 20 mg/day per os, for 4 days. On days 3 and 4, ibuprofen, 1,200 mg/day per os, was also given. Enalapril reduced blood pressure, particularly in the group on the low-sodium diet. Urinary 6-keto-PGF1 alpha, an indicator of renal PGI2 production (determined by HPLC-RIA), increased in the first few hours after enalapril in the low-sodium group. Ibuprofen did not reduce the antihypertensive effect of enalapril, nor did it affect plasma renin activity or plasma aldosterone. Only a slight reduction in 6-keto-PGF1 alpha excretion was observed after enalapril plus ibuprofen. It is suggested that the effect of enalapril on urinary 6-keto-PGF1 alpha excretion is largely dependent on factors such as sodium intake.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Verapamil inhibits platelet aggregation by a calcium-independent mechanism.

We studied the inhibitory effects of the calcium channel blocker verapamil both on platelet aggregation and intracellular calcium [Ca2+]i in platelets loaded with a fluorescent indicator (quin 2). The inhibitory effects of verapamil on the platelet aggregation response to both thrombin and ionomycin were seen to be clearly dissociated from the verapamil-induced inhibition of the [Ca2+]i increase produced by these agonists. Verapamil-induced inhibition of platelet aggregation was also obtained when using the "calcium-independent" agonist phorbol-myristate acetate (PMA). It may be deduced that a calcium-independent mechanism plays a role in verapamil-induced inhibition of platelet aggregation. We postulate that this mechanism may operate via a protein-kinase C pathway.

Calcium↗
PubMed1985

Spectrin extractability from erythrocytes in Duchenne muscular dystrophy patients and carriers and in other myopathies.

Spectrin extractability was measured in the erythrocyte membranes from patients with Duchenne Muscular Dystrophy (DMD), from DMD definite carriers (in whom serum creatine kinase (CK) was also measured) and patients affected by other myopathies. After the extraction of spectrin from ghosts with EDTA, membrane proteins were examined using sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Spectrin extractability was also investigated in the presence of an excess of calcium. Spectrin extraction from erythrocyte ghosts was significantly reduced with respect to controls in DMD patients, in DMD definite carriers and in patients affected by limb-girdle dystrophy, but not in patients suffering from other non-dystrophic myopathies. Fifty percent of DMD definite carriers showed a reduced extraction of spectrin and some of them had normal serum CK. Reduced extractability was also observed in red blood cells incubated in media containing excess calcium. Our results could suggest that reduced spectrin extractability is connected with a modification of intracellular calcium levels.

Adolescent↗
PubMed1984

Increased leukocyte aggregation in patients with hypercholesterolaemia.

Leukocyte aggregation induced by N-formylmethionyl-leucyl-phenylalanine (FMLP) has been measured in a group of patients with hypercholesterolaemia (n = 22) and in a group of control subjects (n = 26), age- and sex-matched. When hypercholesterolaemic patients were divided into two groups, with a discriminatory level of 7.7 mmol/l of plasma cholesterol, FMLP-induced leukocyte aggregation of patients with greater than 7.7 mmol/l of plasma cholesterol was significantly higher compared both with control subjects and patients with plasma cholesterol levels less than 7.7 mmol/l. A positive significant correlation was found between leukocyte aggregation and plasma cholesterol, whereas no correlation was observed between leukocyte aggregation and plasma triglycerides or APO-B levels. These findings provide further support for the hypothesis that elevated plasma cholesterol levels may induce a cellular membrane abnormality responsible for the increased leukocyte aggregation and, subsequently, endothelial damage.

Adolescent↗
PubMed1984

Increased sodium-lithium countertransport in red cells of patients with Bartter's syndrome.

Erythrocyte sodium-lithium countertransport was evaluated in three adult patients with Bartter's syndrome, diagnosed on clinical and histopathological basis and on laboratory tests. As compared with age-matched control subjects, lithium effluxes to both sodium medium and to sodium-free medium were high in two patients and Na+-Li+ countertransport was significantly greater in all three patients. The relationship between increased Na+-Li+ countertransport and the proposed primary disorder of Bartter's syndrome (i.e., a primary tubular defect of chloride reabsorption) is not apparent. However, this finding favours the hypothesis of a generalized cellular membrane dysfunction of ion transport in Bartter's syndrome.

Adult↗
PubMed1984

Reduction of the antihypertensive effect of captopril induced by prostaglandin synthetase inhibition.

The effects of prostaglandin synthetase inhibition by indomethacin on blood pressure and hormonal variations induced by captopril were studied in eight patients with essential hypertension and in six nonhypertensive subjects. Captopril antihypertensive effect and captopril-induced plasma renin increase were almost totally abolished by a short-term administration of indomethacin (50 mg t.i.d.). These results support the hypothesis that prostaglandins contribute to the antihypertensive effects of ACE inhibitors. It may be of clinical importance that anti-inflammatory drugs that inhibit PG-synthetase can also blunt the antihypertensive action of ACE inhibitors.

Adult↗
PubMed1983

[The effect of dopaminergic stimulation and inhibition on the urinary excretion of aldosterone and kallikrein in spontaneously hypertensive rats].

The effect on the electrolyte balance of a dopaminergic agonist (bromocriptine) and an antagonist (metoclopramide) and their effect on renal aldosterone and kallikrein excretion were investigated. Ten normotensive Wistar rats and ten spontaneously hypertensive rats (SHR-Wistar Kioto) were treated with BCR (4 mg/Kg weight b.i.d.) for 4 days; after a week of pharmacological wash-out they received MCP (0,5 mg/Kg weight b.i.d.) for 4 days. Before and after treatment and at the 2nd and 4th day of each treatment diuresis, urinary excretion of aldosterone, kallikrein, sodium, potassium and proteins were measured. During the 24-hour urine collections the rats were kept in separate metabolic cages with free access to food and water. Kallikrein urinary excretion was lower in SHR than in normotensive rats under basal conditions (p 0.05); urinary sodium, potassium, proteins and sodium/potassium rate were also reduced in SHR. After treatment with bromocriptine a further reduction in urinary kallikrein excretion was observed in SHR. After MCP all the parameters were unchanged both in normotensive rats and in SHR, but SHR showed a significant correlation between aldosterone and kallikrein excretion (p less than 0,001); in this condition it seems that in SHR the control exerted by aldosterone on kallikrein excretion is greater than the one exerted by dopamine. It may indicate a defect of the natriuretic and vasodilator dopaminergic system in spontaneously hypertensive rats.

Aldosterone↗