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F Trevisani

Publications and source records attributed to F Trevisani.

At least 73 records · Page 4Linked to original sources
PubMed1989

Circadian variation in renal sodium and potassium handling in cirrhosis. The role of aldosterone, cortisol, sympathoadrenergic tone, and intratubular factors.

Renal sodium and potassium handling, plasma aldosterone and cortisol concentrations, and urine free norepinephrine excretion were determined every 4 h for 24 h in 15 cirrhotics (7 without ascites, group 1; 8 with ascites, group 2) and 7 healthy controls during controlled salt intake and recumbency. Renal sodium excretion was significantly reduced in group 2, whereas it exceeded threefold the salt intake in group 1. Its circadian rhythm was disrupted in both groups of patients. Significant inverse correlations with plasma aldosterone were found erratically in controls, never in group 1, and at every 4-h interval in group 2. In the latter, the indexes of tubular activity and effectiveness of aldosterone were also significantly increased. Urine norepinephrine excretion was never related to sodium excretion in either controls or patients; in group 2 it was directly correlated with glomerular filtration rate in many instances. The cortisol-related circadian rhythm of kaliuresis was retained only in group 1. The 24-h renal potassium excretion of controls and patients was comparable, in spite of the striking hyperaldosteronism, and the more than doubled contribution of aldosterone to kaliuresis shown in group 2. The influence of aldosterone on potassium excretion was also witnessed by the direct correlation between these variables found in group 1 and, when kaliuresis was corrected by the distal sodium delivery, group 2. Renal sodium handling in cirrhosis is altered even before ascites formation and compensated patients can undergo "spontaneous natriuresis." Aldosterone is the main cause of sodium retention in nonazotemic ascitic patients, while sympathoadrenergic hyperactivity may contribute to preserve renal perfusion. The influence of aldosterone on kaliuresis is enhanced, but renal potassium wasting in patients with ascites and hyperaldosteronism is prevented by reduced distal tubular availability of sodium.

Adult↗
PubMed1989

Renal function and effective beta-blockade in cirrhosis with ascites. Relationship with baseline sympathoadrenergic tone.

Renal function, plasma norepinephrine, renin activity (PRA) and aldosterone were determined in 17 cirrhotics with ascites, before and after effective beta-blockade (resting heart rate reduction greater than or equal to 20%) induced by oral propranolol. The drug lowered PRA (from 2.86 +/- 0.96 (S.E.) to 1.86 +/- 0.7 ng/ml/h; P less than 0.005) and plasma aldosterone (from 309.0 +/- 59.2 to 202.6 +/- 26.7 pg/ml; P less than 0.005). As expected, plasma norepinephrine (PNC) increased from 90.7 +/- 12.2 to 176.8 +/- 43 ng/l (P less than 0.01) in the 10 patients with normal basal values ('normal-PNC' group), but it decreased in 6 of the 7 patients with basal sympathoadrenergic hypertone ('high-PNC' group; mean value from 352.6 +/- 37.8 to 273 +/- 39.3 ng/ml (P = 0.06). Glomerular filtration rate and filtered sodium load did not change in the group as a whole and in 'normal-PNC' cirrhotics (from 83.2 +/- 7.1 to 81.4 +/- 7.8 ml/min, and from 11.63 +/- 0.96 to 11.45 +/- 1.14 mmol/min), but rose in 'high-PNC' patients (from 60.7 +/- 9.1 to 109.3 +/- 27.2 ml/min, and from 8.39 +/- 1.31 to 15.47 +/- 3.95 mmol/min; P less than 0.05). Renal sodium excretion increased from 2.45 +/- 0.75 to 3.16 +/- 1.01 mmol/h (P less than 0.01) in the group as a whole. Such an increase, however, was confined to 'high-PNC' cirrhotics. In this group, the tubular rejection fraction did not change and post-beta-blockade sodium excretion was correlated with the filtered sodium load (Rs = 0.83; P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

"Low T3 syndrome" in cirrhosis: effect of beta-blockade.

The so-called "low T3 syndrome" has frequently been reported in patients with cirrhosis. In this study, we aimed to determine whether administration of propranolol to such patients leads to further changes in plasma thyroid hormones, since it can affect their peripheral metabolism. Twenty cirrhotics (11 with ascites) whom we investigated showed no clinical evidence of thyroid dysfunction. The free fractions of plasma T3 and T4 (FT3, FT4) were determined by radioimmunoassay before and after the achievement of an effective beta-blockade by propranolol. The activity of the sympathetic nervous system also was evaluated by measuring plasma norepinephrine concentration. Under basal conditions, cirrhotics showed a reduced FT3 (2.45 +/- 0.11 SEM vs 3.55 +/- 0.16 pg/ml; p less than 0.001) and comparable FT4 (7.62 +/- 0.79 vs 9.2 +/- 0.42 pg/ml) and FT3/FT4 ratio (0.38 +/- 0.04 vs 0.42 +/- 0.013) with respect to healthy controls. When patients with ascites were considered apart, a reduction of FT4 was also found (6.78 +/- 0.74 pg/ml; p less than 0.01). In these patients, many of whom showed an increased plasma norepinephrine concentration, an inverse correlation between log FT3/FT4 and log plasma norepinephrine concentration was found (r = -0.79; p less than 0.01). The effective beta-blockade did not lead to significant changes in either FT3 or FT4 or FT3/FT4, whether the patients were considered as a whole (2.52 +/- 0.19 pg/ml, 9.3 +/- 1.41 pg/ml, and 0.36 +/- 0.04, respectively), or were split into groups according to the presence of ascites. When administered to cirrhotics, propranolol did not worsen thyroid hormone abnormalities, thus appearing to be safe in this respect. This may result from an impaired influence of the sympathoadrenergic system on thyroid hormone metabolism.

Adult↗
PubMed1988

Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis.

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.

Adult↗
PubMed1988

Role of gluconeogenesis from amino acids in determining fasting and absorptive levels of plasma ammonia in cirrhosis.

The aim of this study was to evaluate the contribution of gluconeogenesis from amino acids in the development of fasting and absorptive hyperammonemia in cirrhosis. Somatostatin (SRIF), which is known to inhibit the hepatic disposal of gluconeogenic amino acids, was administered in a continuous infusion (500 micrograms/h) for 90 min before and 5 h after a protein meal (240 g of meat) in 11 overnight fasting patients. Plasma glucagon, insulin, gluconeogenic amino acids (GAA: alanine, serine, glycine, and threonine) and ammonia (NH3) were evaluated before the infusion, immediately before, and at 1, 3, and 5 h after the meal. As control study, the same protocol was randomly repeated in a different day with saline infusion. During the latter, a direct correlation was found between fasting glucagon and ammonia (r = 0.68; p less than 0.05). Fasting glucagon, insulin, and NH3 did not change, whereas alanine (p less than 0.05) and the GAA sum decreased (p less than 0.01). When SRIF was infused, fasting glucagon (p less than 0.05), insulin (p less than 0.05), and NH3 (p less than 0.05) decreased. Alanine did not change, and GAA sum increased (p less than 0.02). No correlations were found by plotting changes in glucagon or GAA sum and NH3. After the meal, SRIF infusion abolished the plasma response of glucagon and markedly reduced that of insulin, so that their area under the curve (AUC0-5) were reduced (p less than 0.005, for both), with respect to control study. Moreover, the AUC0-5 of alanine (p less than 0.005) and GAA sum (p less than 0.005) were increased, suggesting a reduced disposal of these compounds. In spite of this, the meal-induced early increase and the AUC0-5 of plasma NH3 observed during SRIF and saline infusion did not differ. Our results do not confirm the importance of gluconeogenesis from alpha-amino-nitrogens in determining the fasting ammonemia of cirrhosis, and suggest that this metabolic pathway does not significantly influence the protein meal-induced exacerbation of plasma ammonia.

Adult↗
PubMed1987

Chronobiological evaluation of sympathoadrenergic function in cirrhosis. Relationship with arterial pressure and heart rate.

Intraday activity of the adrenergic system was investigated in 7 healthy controls and in cirrhotic patients without ascites (group 1, 7 cases) and with ascites (group 2, 9 cases) by determining the urinary norepinephrine and vanillylmandelic acid excretions at 4-h intervals for 24 h. Mean arterial pressure and heart rate were also recorded. In controls, the statistical evaluation by the cosinor method showed a circadian rhythm of such variables, with zenith in the morning and nadir at night. Intraday changes of urinary excretion of norepinephrine were closely related to arterial pressure and heart rate in most subjects. The most important change in cirrhotic patients was the achronia [no detection of a statistically significant (p greater than 0.05) rhythm] in urinary excretion of norepinephrine and arterial pressure. This occurred not only in group 2 patients, who had lower arterial pressure and higher NE mesors than controls (p less than 0.05), but also in group 1 patients, whose mesors were comparable to controls. The statistical significance of heart rate rhythmicity was preserved in patients, but its zenith was progressively displaced toward evening (group 1) and night hours (group 2, whose mesor was increased). Changes in urinary excretion of vanillylmandelic acid roughly paralleled those of norepinephrine both in controls and patients, but they did not significantly increase even in the group with ascites. In both groups of cirrhotic patients, the correlation between urinary excretion of norepinephrine, arterial pressure, and heart rate within the same subject was lost in most cases. This chronobiological study showed that the sympathoadrenergic activity can be deranged also in the early stages of cirrhosis, and suggested that an altered control of cardiovascular homeostasis is present even under steady state conditions. This alteration might blunt adrenergic responses to stress conditions.

Adrenergic Fibers↗
PubMed1986

Chronobiological study of factors affecting plasma aldosterone concentration in cirrhosis.

We studied the mechanisms leading to derangement of aldosterone secretion in cirrhosis. The circadian patterns of plasma renin activity (PRA), aldosterone, cortisol, sodium, and potassium were studied in 16 nonazotemic cirrhotics (group 1 without ascites, 7 cases; group 2 with ascites, 9 cases) and 7 healthy controls. Group 1 did not differ from controls in aldosterone, sodium, and potassium mean daily levels (mesors), but had reduced PRA mesor (p less than 0.05). Moreover, minor derangements in circadian patterns of PRA, aldosterone, and potassium were also found. Group 2 not only showed an increased mesor of PRA (p less than 0.05), aldosterone (p less than 0.001), and reduced sodium (p less than 0.005), but also achronia in daily fluctuations of PRA, aldosterone, and potassium. In all groups the mesors of PRA and aldosterone were correlated (r greater than or equal to 0.82; p less than 0.01 or less), but the regression line slopes of patients were steeper than those of controls (group 1, p less than 0.05; group 2, p less than 0.01). Moreover, although in controls and some group 1 patients aldosterone paralleled cortisol rhythmicity, most group 2 patients had aldosterone daily patterns correlated with those of PRA. Finally, no relationships between plasma potassium and aldosterone concentrations were found in patients, whereas they were strictly related in controls. These results suggest that the renin-angiotensin system is the prevalent determinant of aldosterone secretion in cirrhosis.

Adult↗
PubMed1986

Effects of somatostatin on plasma ammonia and amino acid profile during fasting and after protein feeding in cirrhotic patients.

The effects of somatostatin on fasting and absorptive plasma ammonia and amino acids were studied in 12 cirrhotic patients. They received a 6 h intravenous infusion of somatostatin (500 micrograms/h) or saline, starting 90 min before protein feeding. During the fasting period somatostatin significantly reduced plasma ammonia (-18%) and total tryptophan (-39%), increased plasma leucine (+19%), isoleucine (+17%), glutamine (+22%), glycine (+13%), arginine (+14%) and lysine (+12%), and prevented the significant fall of phenylalanine (-8%), tyrosine (-6%), alanine (-8%) and threonine (-9%) seen with saline. The percent changes in ammonia and glutamine concentrations were inversely correlated (r = -80; p less than 0.001) After protein ingestion, somatostatin slowed the maximal plasma increase in ammonia and alpha-nitrogens by at least two hours, but their total 5 h plasma response was not reduced, and even, in some instances, significantly increased (valine, leucine, glutamine, alanine and serine) with respect to saline. The results suggest that in fasting cirrhotics somatostatin reduces plasma ammonia, probably through an impaired intestinal ammoniogenesis from circulating precursors, and inhibits the disposal of branched chain, aromatic (except tryptophan) and gluconeogenic amino acids. Furthermore, it delays, but does not reduce, the plasma increase in nitrogen after protein ingestion.

Adult↗
PubMed1985

Renal function impairment induced by change in posture in patients with cirrhosis and ascites.

The assumption of upright posture by patients with liver cirrhosis leads to striking activation of adrenergic and renin-angiotensin systems. The tilting-induced modifications in renal function of eight healthy controls and 14 untreated patients with liver cirrhosis and ascites were related to plasma concentrations of noradrenaline, renin activity and aldosterone. All patients had preserved renal blood perfusion. All parameters were evaluated during bed rest for two hours and in the sitting posture for one hour. Basal plasma renin activity (0.1 greater than p greater than 0.05), aldosterone and noradrenaline concentrations (p less than or equal to 0.01) were raised in cirrhotics. The renal function tests (creatinine clearance, filtered sodium, tubular rejection fraction, urinary sodium excretion) were significantly reduced in cirrhosis. Under basal conditions, in cirrhotic patients tubular rejection fraction and urinary sodium excretion were inversely related to both noradrenaline and aldosterone concentrations. After tilting, the noradrenaline and aldosterone integrated outputs (sigma delta) were significantly greater in cirrhosis. All renal function tests significantly decreased in cirrhotics, whereas creatinine clearance only significantly decreased in controls. Patient's tubular rejection fraction of sodium and sodium excretion were related to sigma delta aldosteronaemia (r = -0.72; p less than 0.01), but no longer to sigma delta plasma noradrenaline.

Adult↗
PubMed1985

Importance of plasma aldosterone concentration on the natriuretic effect of spironolactone in patients with liver cirrhosis and ascites.

23 cirrhotics with ascites and sodium retention, whose aldosteronemia had been evaluated after an equilibration period at controlled sodium intake at the occasion of previous studies, were retrospectively investigated. The dosage of spironolactone needed to induce a negative sodium balance correlated significantly with plasma aldosterone concentration: r = 0.64; p less than 0.001. However, in cases with plasma albumin concentration less than 3 g/dl, glomerular filtration rate less than 80 ml/min, and plasma sodium concentration less than 136 mmol/l such a relationship was no longer significant. The diuretic response to spironolactone is mainly linked to plasma aldosterone concentration. Factors affecting the removal of ascites from the peritoneal cavity and renal sodium handling can influence the expected diuretic response to the drug.

Aldosterone↗
PubMed1985

Comparative pharmacodynamics of furosemide and muzolimine in cirrhosis. Study on renal sodium and potassium handling and renin-aldosterone axis.

Ten male cirrhotic patients with ascites and reduced renal function were randomly given equivalent doses of furosemide and muzolimine by the oral route, through a single blind cross-over protocol. Renal function, electrolyte plasma concentrations and urinary excretions and renin-angiotensin-aldosterone system components were evaluated under basal conditions and after drug administration. The diuretic and saluretic effects being equal, the response to muzolimine was initially weaker but more prolonged than to furosemide, without rebound phenomena. The furosemide-induced natriuresis was in part related to the filtered sodium load, whereas muzolimine natriuresis was only correlated to the inhibition of tubular sodium reabsorption. No potassium wasting effect was seen after muzolimine administration. Transient plasma potassium concentration reduction observed during muzolimine suggests an ion shift within the intracellular compartment. Therefore, a possible interaction of the drug with cellular sodium active transport systems can be hypothesized. A significant increase of plasma renin activity was observed after furosemide. No significant changes were seen after muzolimine administration.

Angiotensin II↗
PubMed1983

Aldosterone related blood volume expansion in cirrhosis before and during the early phase of ascites formation.

Thirty-seven patients with liver cirrhosis (16 without ascites: group 1; 21 with untreated ascites at the first onset: group 2) were studied during controlled sodium intake (40 mmol/day). Renal plasma flow, glomerular filtration rate, urinary sodium excretion, plasma sodium and potassium, plasma renin activity, plasma aldosterone concentration, blood volume, and arterial pressure were evaluated. All the patients had normal renal perfusion, plasma sodium and potassium, and arterial pressure. Mean plasma renin activity and plasma aldosterone concentration were significantly depressed in group 1 (p less than 0.001, p less than 0.005 respectively) compared with 21 normal controls in identical experimental conditions. This was possibly a consequence of expanded blood volume (p less than 0.001 compared with controls) which was directly correlated with plasma aldosterone concentration (p less than 0.001). In group 2 plasma renin activity and plasma aldosterone concentration were normal in over 50% of cases. Blood volume was lower than in group 1 (p less than 0.002), but again related to plasma aldosterone concentration (p less than 0.01). In both groups plasma aldosterone concentration was hyperbolically and inversely correlated with urinary sodium excretion, but the two curves were progressively shifted to the left in respect to controls suggesting an enhanced renal tubular sensitivity to the hormone. The results suggest that aldosterone related renal sodium retention, with consequent blood volume expansion, occurs before ascites formation. The mineralocorticoid activity of aldosterone is amplified by an enhanced sensitivity of renal tubules which appears to increase as the disease progresses.

Adult↗