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Biomedical subjects

M G Bianchetti

Publications and source records attributed to M G Bianchetti.

144 records · Page 8Linked to original sources
PubMed1983

Effects of indapamide and various diuretics alone or combined with beta-blockers on serum lipoproteins.

A prospective evaluation was started in 1976 to study the influence of diuretics alone or combined with beta-blockers on serum lipoproteins in normal or hypertensive subjects. Compared to placebo conditions, 4 or 6-weeks' monotherapy with various diuretics significantly (p less than 0.05) increased the beta-lipoprotein fraction (furosemide, 80 mg/day or chlorthalidone, 100 mg/day; n = 16) or low-density lipoprotein-cholesterol (LDL-C) (chlorthalidone, 100 mg/day, n = 27 men; tienilic acid, 250 mg/day, n = 16 men, clopamide, 5 mg/day, n = 17 men; or muzolimine, 20 to 40 mg/day, n = 13 men or post-menopausal women). No increase in LDL-C was noted in 43 men (32 normal, 11 with mild hypertension) treated with indapamide, 2.5 mg/day. Serum high-density lipoprotein-cholesterol and apoproteins A1, A2 and B were not consistently changed by any of these agents. In women, chlorthalidone (100 mg/day) significantly increased LDL-C in the (100 mg/day) significantly increased LDL-C in the post-menopausal (n = 18) but not in the pre-menopausal (n = 22) state. Increases in LDL-C caused by chlorthalidone monotherapy were prevented or reversed by the addition of a beta-blocker, usually propranolol or atenolol (n = 18); increases in LDL-C during clopamide monotherapy were reversed after the addition of the beta-blocker pindolol (10 mg/day, n = 17). In all studies, variations in beta-lipoprotein or LDL-C levels could not be explained by changes in blood volume, serum glucose or insulin and did not correlate with alterations in blood pressure, plasma potassium, renin, aldosterone, adrenaline or noradrenaline. These observations indicate that various diuretics may increase serum LDL-C in men or post-menopausal women. Pre-menopausal women may often be protected from this side-effect. Long-term studies are now needed to clarify the pathogenic and prognostic relevance of lipoprotein changes induced by diuretics. In the meantime, it is of clinical interest that indapamide had no significant effect on serum lipoproteins and that certain beta-blockers appear to prevent or reverse increases in LDL-C during diuretic treatment in men and post-menopausal women.

Adrenergic beta-Antagonists↗
PubMed1983

Different blood pressure responses to diuretic treatment in normotensive subjects with and without a family history of hypertension.

The possibility that the familial background for hypertension may influence the blood pressure response to diuretic treatment was evaluated in 14 normotensive subjects with negative and 14 normotensive subjects with positive family history of hypertension. Under control conditions, blood pressure, heart rate, body weight, urinary sodium and potassium, plasma sodium, potassium, creatinine, norepinephrine, epinephrine, renin and aldosterone levels did not differ between the two study groups. Each subject received chlorthalidone, 100 mg/day, or indapamide, 2.5 mg/day for eight weeks. Compared with control values, blood pressure was decreased during diuretic treatment in subjects with positive (P less than 0.05), but not in those with negative family history for hypertension. Diuretic-induced decreases in plasma potassium (P less than 0.005), increases in plasma renin activity and aldosterone (P less than 0.005), and a tendency towards higher plasma norepinephrine levels were not different between the two study groups. These findings suggest that the familial background of hypertension may, at least in part, determine the blood pressure response to diuretic treatment.

Adult↗
PubMed1982

Effects of tyramine on blood pressure and plasma catecholamines in normal and hypertensive subjects.

Responses of blood pressure and plasma catecholamines to intravenous injection of tyramine at increasing dosage (30, 45, and 60 microgram/kg, respectively) were evaluated in 25 normal subjects and 20 patients with mild essential hypertension. Basal plasma norepinephrine and epinephrine concentrations before tyramine injections were similar in the two groups. Following tyramine injection, plasma epinephrine was unchanged. Responses of plasma catecholamines and blood pressure to tyramine were similar in the two groups. Plasma norepinephrine increased significantly 2 min after a dose of 30 microgram/kg, but higher tyramine doses failed to produce a further increase in plasma norepinephrine. In contrast, pressor responses to tyramine were dose-dependent. Maximal pressor responses were observed within 23 min after injection. These findings reveal a dissociation between changes in blood pressure and plasma norepinephrine following injection of tyramine. Lack of steady state may limit the value of tyramine bolus injections as a tool for the quantitation of pressor responsiveness to variations in endogenous sympathetic output. Alternatively, it is possible that the pressor effect of tyramine may be mediated at least in part by a norepinephrine independent mechanism.

Adult↗
PubMed1982

Acute effects of prizidilol on blood pressure, heart rate, catecholamines, renin and aldosterone in essential hypertension.

Prizidilol is a new antihypertensive agent reported to possess combined precapillary vasodilator and betareceptor-blocking properties. To clarify the profile of the acute effects of prizidilol in man, a variable dose study was performed in 8 patients with benign essential hypertension. Blood pressure, heart rate, plasma renin activity, aldosterone, plasma and urinary catecholamines and electrolytes were determined at short intervals before and up to 23 h after oral administration of placebo and prizidilol 150, 300 and 600 mg. The 4 studies were performed at weekly intervals according to a Latin square design. Prizidilol produced dose-dependent decreases in supine and upright blood pressure, with an initial change after about 2 h and maximal effects from 4 to 8 h after drug ingestion. Following a high dose of prizidilol, supine mean blood pressure (average 128 mmHg prior to treatment) was normalised (less than 107 mmHg) from 3 to 7 h and was still below predose level 23 h after ingestion. The only reported side effects were postural dizziness in 2 cases (corresponding to a fall in systolic upright blood pressure to less than 95 mmHg) and headache in one case. A biphasic variation in heart rate and plasma renin activity, with an early drop and a subsequent tendency to a slight rise, was observed after an intermediate or high dose of prizidilol. Plasma norepinephrine levels were increased by a high dose of prizidilol, while plasma epinephrine, aldosterone and plasma and urinary electrolytes were not consistently changed. Prizidilol in a a single oral dose appeared to be a potent antihypertensive agent. The profile of heart rate and plasma renin point to early dominance of beta-blockade followed by appearance of the concomitant vasodilator properties of prizidiol.

Adrenergic beta-Antagonists↗
PubMed1982

Comparative evaluation of the new vasodilator carprazidil and minoxidil in the treatment of moderate to severe hypertension.

The efficacy and side effects of the new vasodilator carprazidil and the established vasodilator minoxidil were compared in 18 hypertensive patients inadequately controlled by 2 to 4 conventional drugs; the latter included diuretics, beta-blockers and/or sympatholytics and, in half the cases, vasodilators, such as hydralazine, diazoxide or the postsynaptic alpha-blocker prazosin. The vasodilators were withdrawn and, using a crossover design all patients received carprazidil (mean final dose 88 mg) and minoxidil (20 mg) for an average period of 5 to 6 months. The effects of the 2 agents appeared to be qualitatively and quantitatively similar. Both tended to cause sodium retention and an increase in heart rate, which required an increased dose of diuretic in one third of the cases or of a beta-blocker in a quarter. With this approach mean body weight and blood volume were not altered in the established phase of carprazidil or minoxidil treatment; heart rate and plasma norepinephrine tended to be only minimally increased, plasma renin was slightly increased, and plasma aldosterone and epinephrine were largely unchanged. Supine and upright blood pressure were reduced from initial values of 189/113 and 167/ 113 mm Hg, to 149/95 and 138/95 mm Hg (-18 and - 17%), respectively, during carprazidil, and to 154/95 and 141/96 mm Hg (-17 and - 15%) during minoxidil therapy. Hypertrichosis occurred with both agents in almost all patients, and limits their more prolonged use in females. No adverse side effects on haematological parameters, liver or renal function were observed, nor was antinuclear antibody detected. It is concluded that carprazidil and minoxidil are equivalent vasodilator agents in the treatment of severe hypertension, particularly in males.

Adult↗
PubMed1982

Studies on aldosterone responsiveness to angiotensin II during clinical variations in calcium metabolism in normal man.

1. Angiotensin II was infused at stepwise increasing dose rates (2, 4 and 10 pmol min-1 kg-1) in 12 normal subjects. Infusions were performed in the presence of normocalcaemia, mild hypercalcemia induced by concomitant calcium gluconate infusion, and after 2 weeks of treatment with nifedipine. 2. Pre-infusion plasma levels of angiotensin II, renin or aldosterone were not altered by acute mild hypercalcaemia or administration of nifedipine. The angiotensin II-induced increases in plasma aldosterone were also similar under the three study conditions. 3. Variations in calcium metabolism occurring under clinical conditions appear to play a minor role in modulating the angiotensin II-dependent pathway of aldosterone regulation in normal man.

Adult↗
PubMed1982

Effect of oral glucose loading on plasma insulin, potassium, renin and aldosterone in normal subjects and patients with primary hyperaldosteronism.

The effects of standard oral glucose loading (100 g) on plasma aldosterone and some regulatory factors were assessed in patients with primary hyperaldosteronism and normal subjects. Following overnight fast, mean plasma glucose was identical (10 patients and normal subjects approximately matched per age and sex); plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in the patients. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups; plasma renin activity was significantly increased only in normal subjects. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Relationships among glucose-induced changes in plasma aldosterone and other factors were assessed by multiple regression analysis in these patients and normal subjects as well as an additional group of 21 normal subjects; in the latter, plasma cortisol was also measured and found to decrease significantly after glucose loading. Changes in plasma aldosterone correlated (P less than 0.025) more closely with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that complex metabolic changes occur following glucose ingestion which are capable of modifying aldosterone secretion in normal subjects and primary hyperaldosteronism. The aldosterone-inhibitory effect of glucose tends to be blunted in the latter disorder. This could be related at least in part to an impaired insulin response in primary hyperaldosteronism.

Administration, Oral↗
PubMed1982

Effects of acute mild hypercalcemia or of the calcium antagonist nifedipine on cardiovascular responsiveness to norepinephrine or angiotensin II in normal humans.

Pressor doses of infused norepinephrine (NE) (mean pressure, +20 mm Hg) or angiotensin II (AII) (diastolic pressure, +20 mm Hg) and corresponding blood levels of NE or AII were assessed in 12 young normal subjects under basal conditions (study A), during slow calcium infusion (0.034 mg/kg/min) started 60 min previously (study C), and following 2 weeks of treatment with the Ca antagonist nifedipine, 50 mg/day (study D). Control values of blood pressure, 24-h urinary sodium, plasma NE, epinephrine, AII, and renin activity did not differ among the three studies. Plasma Ca was higher during study C than during studies A and D [10.7 +/- 0.8 (+/- SD) versus 9.1 +/- 0.3 mg/dl; p less than 0.01]. Plasma NE or AII levels obtained during NE or AII infusion as well as the pressor doses of AII were not modified by concomitant Ca infusion or following nifedipine. However, compared with basal conditions, the NE pressor dose tended to be decreased slightly during Ca infusion (106 +/- 71 versus 77 +/- 38 ng/kg/min; difference not significant) and was increased markedly following nifedipine (178 +/- 87 ng/kg/min; p less than 0.05). A control infusion of Ca alone (study B) during 120 min did not modify blood pressure or plasma renin and NE levels. Our observations suggest that in normal humans, inhibition of cellular Ca transport may predominantly affect the noradrenergic control mechanism, whereas angiotensinogenic cardiovascular regulation may be less dependent.

Adult↗
PubMedDate not supplied

[Simplified determination of proteinuria in children using a single urine sample].

In children and adolescents the evaluation of proteinuria is cumbersome because of the need to obtain timed urine collections. The protein/creatinine ratio (using a Coomassie blue binding technique and a kinetic Jaffe reaction, respectively) measured in 134 pediatric patients with renal disease aged 2 months to 16 years correlated closely with the overnight urine protein excretion rates using the statistical approach suggested by Bland and Altman to compare methods of measuring some quantity. The upper limit of urinary protein/creatinine ratio measured in 252 healthy children and adolescents aged 4 to 19 years was shown to be 19 mg/mmol. No age-related differences in urinary protein excretion were noted in healthy subjects. The random urine protein/creatinine ratio provides an accurate assessment of quantitative protein excretion and avoids errors and difficulties associated with timed urine collection.

Adolescent↗
PubMedDate not supplied

Use of salivary levels to predict clearance of caffeine in patients with cystic fibrosis.

The quantification of liver function is possible using the approach of salivary caffeine clearance. Hepatopathy sometimes complicates cystic fibrosis (CF), thus suggesting the use of this diagnostic tool in CF as well. Since in CF some compounds are poorly absorbed or abnormally metabolized, and the function of salivary glands or renal tubuli partly impaired, caffeine was measured in urine, blood, and saliva after a single oral dose of 3 mg/kg in CF patients. The urinary excretion rate of caffeine was normal in five CF patients. The caffeine levels in plasma or saliva, measured 4 to 5 h and 16 to 17 h after caffeine intake, were normal in 34 nonhepatopatic CF patients. The calculated salivary caffeine clearance was comparable in the 34 nonhepatopatic CF patients (1.88 +/- 0.46 ml/min/kg) and in the control group (1.88 +/- 0.44 ml/min/kg). In CF patients, no correlation was found between caffeine clearance and body weight, height, relative underweight, dosage of pancreatic enzymes, or Chrispin-Norman x-ray score. The salivary caffeine clearance was reduced in seven hepatopathic CF patients (1.32 +/- 0.63 ml/min/kg, p less than 0.01); nevertheless, the salivary caffeine clearance was reduced (boundary line at 1.1 ml/min/kg) in three CF patients with proven liver cirrhosis but not in four with hepatosplenomegaly and altered liver tests. These data indicate an unaltered caffeine metabolism in CF and open the way for the use of this diagnostic procedure in CF as well. This test might be valuable in CF patients with clinical or laboratory findings suggesting liver involvement.

Adolescent↗
PubMedDate not supplied

Circulating sodium in acute meningitis.

BACKGROUND: In acute meningitis hyponatremia is common and traditionally attributed exclusively to inappropriate water retention. However, the exact mechanisms underlying hyponatremia are unknown. METHODS: The files of 300 pediatric patients with acute bacterial (n = 190) or aseptic (n = 110) meningitides were retrospectively analyzed. RESULTS: The plasma sodium level ranged from 122 to 148 mmol/l and was low (<133 mmol/l) in 97 patients. Fluid volume contraction was significantly more pronounced in hyponatremia (median 6.0. 10(-2)) than in normonatremia (median 2.0. 10(-2)). The fractional sodium excretion was less than 1.00. 10(-2) in the 26 hyponatremic children with this measurement. CONCLUSION: In acute meningitis hyponatremia is not exclusively brought about by inappropriate water retention.

Acute Disease↗
PubMedDate not supplied

Calcium and blood pressure regulation in normal and hypertensive subjects.

To elucidate the mechanisms involved in calcium-mediated blood pressure (BP) control, plasma norepinephrine (NE), epinephrine, renin activity, and angiotensin II (AII) levels and the cardiovascular pressor responsiveness to NE and AII were assessed before and during acute mild hypercalcemia or short-term calcium (Ca) inhibition with nifedipine in 20 normal and five borderline hypertensive subjects. In normal subjects, systolic BP and plasma NE and epinephrine concentrations were increased significantly (p less than 0.05) during an acute rise in serum Ca of 3.1 mg/dl (intermediate rate Ca infusion, 0.05 mg/kg/min for 3 hours), but not following an increase of 1 mg/dl (low rate Ca infusion, 0.034 mg/kg/min for 2 hours). In the borderline hypertensive group, low-rate Ca infusion elevating serum Ca by 1 mg/dl was associated with a slight increase in systolic BP (p less than 0.05) and plasma catecholamines. In both groups, the pressor responses to infused NE and AII, and plasma renin and AII levels, were unchanged during mild to moderate hypercalcemia. Nifedipine given for 2 weeks (average dose, 48 mg/d) reduced BP significantly (p less than 0.05) in the borderline hypertensive subjects only and NE pressor responses in both groups (p less than 0.025), but had no significant effect on plasma catecholamines, renin, or AII levels. These findings suggest that the adrenergic BP control mechanism may be more dependent on clinical variations in calcium metabolism than the angiotensin BP regulatory mechanism. Acute hypercalcemia may increase BP at least in part by causing an increase in adrenergic activity without an equivalent decrease in cardiovascular reactivity. Calcium inhibition with nifedipine may modify noradrenergic BP control by lowering the NE pressor reactivity without causing an equivalent increase in adrenergic activity.

Adult↗
PubMedDate not supplied

Cardiovascular counterregulation during sympathetic inhibition in normal subjects and patients with mild hypertension.

The influence of agents that inhibit sympathetic nerve activity on cardiovascular responsiveness as related to major pressor factors has been unclear. Therefore, these components were evaluated in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of sympathetic neuron blockade with the agent debrisoquine. In these normal and mildly hypertensive subjects, sympathetic neuron blockade caused approximately similar decreases in urinary and supine or upright plasma norepinephrine (NE) levels (average changes in the two groups, -41% and -45%, respectively; p less than 0.05 to less than 0.005), the chronotropic dose of isoproterenol (-45% and -38%), and the NE pressor dose (-47% and -51%, p less than 0.01), while the relationship between NE-induced changes in blood pressure and concomitant plasma NE concentrations was displaced to the left (p less than 0.01). Supine heart rate was also lowered (-10% and -8%, p less than 0.05). Compared to the orthostatic variations during placebo conditions, mild postural decreases in blood pressure were apparent in both the normal and hypertensive groups (-8% and -7.5%). However, supine blood pressure was unchanged following debrisoquine treatment. Other parameters were also not consistently changed, such as total blood volume, exchangeable body sodium, urinary electrolytes, plasma epinephrine, renin, and angiotensin II (AII) levels, the pressor dose of infused AII, and the relationship between AII-induced changes in blood pressure and plasma AII measured before and during AII infusion. These findings demonstrate that the reduction in sympathetic outflow during sympathetic neuron blockade may elicit a hyperresponsiveness of alpha- and beta-adrenergic receptors that is equal in normal subjects and patients with mild essential hypertension.

Adult↗
PubMedDate not supplied

Serum lipoproteins during treatment with the antihypertensive agent indapamide.

Considering the documented, potentially undesirable influence of various thiazide-type or loop diuretics on serum lipoproteins, we prospectively investigated in 69 men (mean age +/- SEM, 32 +/- 1 years) the metabolic effects of the new diuretic-antihypertensive compound indapamide. Compared to placebo, indapamide (2.5 mg/day) given for 6 to 8 weeks lowered (p less than 0.02 to less than 0.001) blood pressure (supine values from 148/98 +/- 3/2 to 137/93 +/- 3/2) in 29 men with mild to moderate essential hypertension, but not in 40 healthy men. In both groups, significant (p less than 0.05 to less than 0.001) decreases in body weight (-0.8 kg) and plasma potassium (-0.6 mmol/L), and increases in plasma uric acid (+20%), renin activity (+200%), and aldosterone documented good compliance. There were no significant changes in total cholesterol (in all subjects, from 208 +/- 6 to 213 +/- 6 mg/dl), low- or very low-density lipoprotein (VLDL) cholesterol (127 +/- 6 to 129 +/- 6 and 21 +/- 1 to 21 +/- 2 respectively), high-density lipoprotein cholesterol (50 +/- 1 to 51 +/- 1 mg/dl), total triglycerides (Tg) (108 +/- 5 to 112 +/- 6 mg/dl), VLDL-Tg, apoproteins A1 and A2, plasma glucose, epinephrine, norepinephrine, sodium, calcium, magnesium, and creatinine; apoprotein B (84 +/- 2 to 88 +/- 3 mg/dl) and plasma insulin after glucose loading dose tended to be increased minimally. The absence of distinct lipoprotein alterations after short-term indapamide treatment may be of clinical and epidemiological interest.

Adult↗
PubMedDate not supplied

[Diagnostic and therapeutic criteria of arterial hypertension in childhood].

Arterial hypertension (AH), either primary or secondary, is an important issue in childhood for its short- and long-term cardiovascular morbidity. Renal diseases are the most frequent causes of AH in children, but essential hypertension can also be detected early in life. It is important for blood pressure (BP) to be checked regularly (at least once every 5 years) in healthy children and adolescents and every year in those belonging to at-risk categories (family history of AH, low birth weight, obesity, etc). In children, AH is defined as BP recorded in three non-consecutive measurements with an appropriate device and cuff size > or = 95th centile for age, gender and height. Ambulatory BP monitoring is a valuable diagnostic tool and once AH is confirmed, a specific primary cause should always be ruled out (renovascular, cardiac, vascular, endocrine, pharmacologic, other). In case of border-line or significant AH (between 90th and 99th centile) a non-pharmacological treatment should be considered, whereas severe hypertension (>99th centile for height and age) will require pharmacological treatment (Diuretics, Angiotensin Converting Enzyme Inhibitors, Angiotensin Receptor Blockers, beta - and Calcium blockers).

Child↗
PubMedDate not supplied

Genotype-phenotype correlations in normotensive patients with primary renal tubular hypokalemic metabolic alkalosis.

Among the different forms of hereditary renal tubulopathies associated with hypokalemia, metabolic alkalosis and normotension, two main types of disorders have been identified: Gitelman disease, which appears to be a homogeneous post-Henle's loop disorder, and Bartter syndrome, a heterogeneous Henle loop disorder. A specific gene has been found responsible for Gitelman disease, encoding the thiazide-sensitive Na-Cl cotransporter (TSC) of the distal convoluted tubule. From a phenotypic point of view the characteristic findings of this disease are hypocalciuria, hypomagnesemia and tetanic crises appearing during childhood or later. Many subjects are asymptomatic. At least three different genes have been shown to be responsible for Bartter syndrome, characterized by mutations in the proteins encoding respectively the bumetanide-sensitive Na-K-2Cl cotransporter, the inwardly-rectifying renal potassium channel and a renal chloride channel, all protein transports located in the ascending limb of Henle's loop. Mutations in the first two transport proteins have been demonstrated in patients with the hypercalciuric forms of Bartter syndrome associated with nephrocalcinosis (respectively Bartter syndrome type I and II), who were often born after pregnancies complicated by polyhydramnios and premature delivery. Mutations in the gene encoding a renal chloride channel were recently recognized in patients with a Henle tubular defect not associated with nephrocalcinosis (Bartter syndrome type III). Most of the latter group of patients were normo-hypercalciuric and presented dehydration and life-threatening hypotension in the first year of life. However, these three genes do not explain all the patients with Bartter syndrome which unlike Gitelman disease, appears to be a very heterogeneous disorder. Clearance studies, especially if done during furosemide and/or hydrochlorothiazide administration, have been helpful in identifying the site of tubular involvement. Considering both phenotypic and genotypic data, we propose a clinical-pathophysiological and molecular approach to diagnose the different tubulopathies associated with hypokalemic metabolic alkalosis.

Alkalosis↗