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Biomedical subjects

M Baraldini

Publications and source records attributed to M Baraldini.

At least 37 records · Page 2Linked to original sources
PubMed1992

The hemodynamic status of preascitic cirrhosis: an evaluation under steady-state conditions and after postural change.

To assess the hemodynamic status of patients with compensated cirrhosis, mean arterial pressure, cardiac index and peripheral vascular resistance and markers of central (plasma concentrations of atrial natriuretic factor) and arterial volemia (plasma norepinephrine concentration, plasma renin activity) were studied in 10 patients and 10 healthy control subjects under steady-state conditions (after 2 hr of standing) and after assumption of the supine position (30, 60, and 120 min). After standing, neither hemodynamics nor markers of effective volemia differed significantly between controls and patients. By evaluating the areas under the curve during the 2 hr of supine posture, the increase in cardiac output and plasma natriuretic factor and the decrease in peripheral vascular resistance were greater in patients (2.59 +/- 0.43 [S.E.M.] L/min/hr; 32.8 +/- 7.2 pg/ml/hr -1,103 +/- 248.4 dyn.sec/cm5/hr, respectively) than in controls (0.53 +/- 0.24 L/min/hr, p = 0.005; 17.4 +/- 4.7 pg/ml/hr, p = 0.005; -265.5 +/- 206.2 dyn.sec/cm5/hr, p = 0.02). The declines in heart rate, plasma norepinephrine concentration and plasma renin activity did not differ significantly. Mean arterial pressure did not significantly change. Our results suggest that during periods of upright posture, cirrhotic patients in the preascitic stage, who are known to have expanded blood volume, compensate for dilatation of the splanchnic vascular bed through total hypervolemia. The latter becomes excessive during recumbency, leading to supernormal increases in venous return, central volemia and cardiac index. The decline in peripheral vascular resistance appears to be a compensatory mechanism to maintain steady arterial blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1992

Bed-rest-induced hypernatriuresis in cirrhotic patients without ascites: does it contribute to maintain 'compensation'?

Renal function, plasma renin activity, plasma aldosterone concentration and urine excretion of free norepinephrine were evaluated in 13 cirrhotics without previous or ongoing ascites and in 13 healthy subjects, after 6 days of controlled electrolyte intake (40 mmol of Na and 70 mmol of K per day) and during 24 h of recumbency. Plasma concentrations of the atrial natriuretic peptide (ANP) were also measured in 8 patients and 8 controls. Despite a low-normal filtered load of sodium (14.6 +/- 1.2 vs. 17.1 +/- 1.2 mmol/min), cirrhotic patients showed supernormal natriuresis (141.5 +/- 14.1 vs. 78.8 +/- 8.6 mmol/day; p < 0.001). Whereas the fractional excretion of sodium in these patients was twice that of controls (0.70 +/- 0.05 vs. 0.36 +/- 0.04%; p < 0.001), potassium excretion (42.5 +/- 2.7 vs. 43.1 +/- 2.7 mmol/day) and urine volume (1270 +/- 98 vs. 1452 +/- 148 ml/day) did not differ. In cirrhotics, plasma renin activity was reduced (0.50 +/- 0.12 vs. 1.39 +/- 0.33 ng/ml/h; p < 0.02), and plasma aldosterone concentration tended to be lower (66 +/- 10 vs. 86 +/- 9 pg/ml; p = 0.09), while urine norepinephrine excretion did not significantly differ from controls (961 +/- 120 vs. 782 +/- 43 ng/h). ANP was higher in patients than in controls (92 +/- 17 vs. 48 +/- 9 pg/ml; p < 0.05). Natriuresis was directly correlated with ANP (r = 0.69, p < 0.005) and ANP/plasma aldosterone ratio (r = 0.63; p < 0.01) in patients and healthy subjects taken together.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Reduced cardiovascular responsiveness to exercise-induced sympathoadrenergic stimulation in patients with cirrhosis.

Cardiovascular responsiveness to sympathoadrenergic activation obtained by muscle exercise in the supine position was evaluated in 22 patients with cirrhosis (11 alcoholic, 11 postnecrotic/cryptogenic; 14 with ascites) and 10 controls of comparable age. Plasma norepinephrine, heart rate, diastolic arterial pressure and cardiac function, as evaluated by systolic time intervals, were monitored. At rest, cirrhotics had higher norepinephrine (154 +/- 19 S.E.M. ng/l) and heart rate (79 +/- 2 beats per min) than controls (71 +/- 3 ng/l, p less than 0.01; 67 +/- 2 beats per min, p less than 0.001), whereas diastolic arterial pressure was similar. Among systolic time intervals, electromechanical systole, pre-ejection period, electromechanical delay and pre-ejection period to left ventricular ejection time ratios were prolonged (p less than 0.05 or less). Exercise led to significant increases in plasma norepinephrine, heart rate and diastolic arterial pressure in both controls and patients. In the latter, however, whereas the increase in norepinephrine was greater (p less than 0.001), those in heart rate and diastolic arterial pressure were less (p less than 0.005). As expected, most systolic time intervals shortened, but the decrease in pre-ejection period (p less than 0.05), isometric contraction time (p less than 0.02) and pre-ejection period to left ventricular ejection time ratio (p = 0.06) was less in patients than in controls. Direct correlations between exercise-induced changes in norepinephrine and both diastolic arterial pressure (r = 0.81; p less than 0.005) and heart rate (r = 0.85; p less than 0.002) were observed in controls, while inverse correlations (r = -0.67, p less than 0.001 and r = -0.44; p less than 0.05) were found in cirrhotics. These results suggest that cardiovascular reactivity to the sympathetic drive is impaired in cirrhotics. The impairment of cardiac contractility may be due to altered electromechanical coupling.

Adult↗
PubMed1990

Antacids in gastric ulcer treatment: evidence of cytoprotection.

Antacids are more effective than placebo, and their efficacy is comparable to that of H2-blockers in gastric ulcer healing even though the healing time is about 2 weeks longer than with H2-blockers. Some observations in animals and healthy subjects may indicate that antacids (particularly those containing aluminium hydroxide) have a protective effect on the gastroduodenal mucosa in that they increase the production of prostanoids and sulphydryl-containing compounds. We showed that 10 days' treatment with high-dose antacids (Maalox TC) is able to increase 6-keto-PGF1 alpha production from cultured biopsy specimens of patients with gastric ulcer. These data could constitute a further indication in the treatment of peptic disease.

Aluminum Hydroxide↗
PubMed1990

Protection of the upper gastrointestinal mucosa: the role of antacids.

Experiments performed in animals and in healthy human subjects suggest that antacids increase prostaglandin synthesis and have a cytoprotective effect on gastroduodenal mucosa. To investigate this hypothesis, the ability was evaluated of an antacid containing an aluminium/magnesium hydroxide combination (Maalox TC) to modify prostanoid production at the gastric level in 28 patients with gastric antral ulcer of various sizes in different stages of activity with or without erosive gastritis. After the antacid treatment, a significant prostaglandin E2 reduction was observed, together with a significant 6-keto-prostaglandin F1 alpha increase, but there was no thromboxane B2 variation at antrum level, nor any significant modification of prostanoid production at body level. The decreased prostaglandin E2 levels, detected after treatment with the antacid combination, may be due to lesion improvement, decreased synthesis or increased catabolism by mucosal cells, to a drop in this prostaglandin production by inflammatory cells. As far as 6-keto-prostaglandin F1 alpha is concerned, the obtained data confirm the results reported by other authors in healthy human subjects. The increase of this prostaglandin could enhance blood flow, resulting in a protective effect.

6-Ketoprostaglandin F1 alpha↗
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

Lymphocyte membrane alpha-1-acid glycoprotein: a cellular synthesis during lymphocyte activation.

Soluble alpha 1 acid-glycoprotein is considered an "acute phase protein" with an inhibitory effect on lymphocyte activity; it has recently been shown that a lymphocyte modulatory variant of alpha 1 acid-glycoprotein has a positive role on T cell activation. It is not clear whether the presence of this glycoprotein on lymphocyte membranes is due to an endogenous production or to a passive uptake of soluble alpha 1 acid-glycoprotein by its carbohydrate moiety. Our data show an increase of membrane alpha 1 acid-glycoprotein both in peripheral blood lymphocyte and T-enriched lymphocytes after phytohemagglutinin stimulation. Peripheral blood lymphocyte enzymatic treatment by neuraminidase does not affect alpha 1 acid-glycoprotein expression while pronase digestion induces a strong decrease of alpha 1 acid-glycoprotein positive lymphocytes and a resynthesis after phytohemagglutinin stimulation. Furthermore, the presence of alpha 1 acid-glycoprotein was prevalently, found on helper/inducer lymphocytes. These data support the hypothesis of a synthesis of alpha 1 acid-glycoprotein by T lymphocytes during their activation process.

Cell Membrane↗
PubMed1989

Influence of cimetidine in low doses (less than ED50) on prostanoid production by human gastric mucosa in vitro.

Cimetidine has been defined as a cytoprotective agent and numerous studies have reported that it is able to influence prostaglandin production as well as mechanisms which protect the surface epithelium of the gastric mucosa. However, results have been contradictory and high drug concentrations contrasting the cytoprotection concept have been utilized. The present study tried to evaluate whether low concentrations (less than ED50) of cimetidine in vitro are able to modify prostanoids produced by gastric mucosa fragments. Thirteen patients without histological lesions were examined. Five mucosal biopsy specimens were obtained from the antrum in seven patients and from the body in another six patients. One biopsy was utilized for histological examination, while the remaining four specimens were incubated in the absence or in the presence of 5, 50 and 500 ng/ml of cimetidine, respectively. Concentrations of PGE2, 6-oxo-PGF1 alpha, PGF2 alpha and TXB2 in the incubate were determined by radioimmunoassay. Cimetidine at 50 ng/ml increased PGE2 production at the antrum level while 500 ng/ml of cimetidine increased PGF 2 alpha and TXB2 production at the body level. Furthermore, the drug dose was directly related to PGE2 production (at the antrum level) and TXB2 (at the body level). The differences in prostanoid production between the antrum and body could be due to the different cell composition of the two anatomical areas, and suggest that the effects of cimetidine are mediated through binding to H2-receptors. The authors conclude that cimetidine in low doses stimulates the net production of some but not all prostanoids, the observed effects varying with anatomical site.

6-Ketoprostaglandin F1 alpha↗
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↗
PubMed1987

Sonographic evaluation of the portal venous system after elective endoscopic sclerotherapy of esophageal varices.

In order to evaluate possible changes in the portal venous system after endoscopic sclerosis of esophageal varices, 25 cirrhotic patients underwent abdominal ultrasonography before the first session of sclerotherapy and after eradication of esophageal varices had been achieved. The caliber of the portal, splenic, and superior mesenteric veins was measured sonographically in each case. Sonographic results were compared statistically before and after sclerotherapy. Neither evidence of significant variations in the caliber of the portal veins nor thrombotic obliteration was seen. These results support the view that sclerotherapy has no significant negative side effects on the portal venous system.

Endoscopy↗
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↗
PubMed1987

A possible cytotoxicity inducer role of 5/9 positive lymphocytes infiltrating the liver in CAH patients.

The presence, in chronic active hepatitis (CAH) patients, of an inflammatory infiltrate basically composed of T lymphocytes suggested the hypothesis that these lymphocytes could play a role in the pathogenesis of the disease. The aim of this study has been to characterize, in a group of carefully selected CAH patients, the liver-infiltrating T lymphocyte, utilizing commercial monoclonal antibody (anti-Leu 1, anti-Leu 2a, anti-Leu 3a) and 5/9 monoclonal antibody that recognizes a further lymphocyte subset within T4 cells. Our data show that both T4 positive subpopulation and T8 positive subpopulation are represented in the infiltrate in the same ratio; furthermore the distribution of 5/9 positive lymphocytes is prevalent where the infiltrate is mainly composed of T8 positive lymphocytes. Moreover, there is a positive correlation between 5/9 positive cells in the liver and GPT and the patients with high percentages of infiltrating 5/9 positive lymphocytes show a low T4/T8 ratio with respect to patients with low percentages of 5/9 positive cells. These data support the hypothesis that 5/9 positive lymphocytes may present an inducer role on cytotoxic cells.

Adult↗
PubMed1987

Expression of major histocompatibility complex class II antigens on bile duct epithelium in patients with hepatic graft-versus-host disease after bone marrow transplantation.

We studied the expression of major histocompatibility complex (MHC) class II antigens in liver biopsies taken from ten patients with clinical and biochemical evidence of liver damage after bone marrow transplantation. In all six patients who had histologically confirmed graft-versus-host disease, MHC class II antigens were detected on intrahepatic bile ducts. In four patients with no histological features of graft-versus-host disease, MHC class II antigens were not detected. In controls, a positive reaction for bile duct MHC class II antigens was only detected in the patients with primary biliary cirrhosis. Characterisation of the lymphocytes surrounding the bile ducts showed a prevalence of Leu 3+ cells in graft-versus-host disease and primary biliary cirrhosis. We propose that the aberrant expression of class II antigens on bile duct epithelium cells may play a role in the pathogenesis of graft-versus-host disease. A similar pattern in primary biliary cirrhosis may suggest a common pathogenetic mechanism.

Adult↗
PubMed1987

Alterations in helper-specific circulating T lymphocytes and in the autologous mixed lymphocyte reaction in chronic hepatitis B.

Defects in T lymphocyte subpopulations and in the functional characteristics of such cells have been thought to play a role in the evolution of chronic hepatitis B, but the precise nature of the alterations and their significance remains unresolved. We studied lymphocyte subsets in 27 patients with chronic hepatitis B utilizing standard monoclonal antibodies including Leu 1,2a,3a,7 and D1/12 (against the common determinant of the Dr molecule), as well as a newly described monoclonal antibody, "5/9," which is thought to characterize a unique subpopulation of T4 cells with specific helper/inducer function. These results were compared with those obtained using the autologous mixed lymphocyte reaction assay for the same patients in order to further delineate the lymphocyte alterations in chronic hepatitis B. A significant reduction in the mean number of Leu 3a (T4) positive cells was observed as well as a reduction in the number of 5/9 positive cells. These changes were most evident in those positive for HBeAg in serum. Reduction in Leu 3a cells was associated with a reduced autologous mixed lymphocyte reaction assay response, and was most marked in the HBeAg-positive individuals. These findings suggest that HBeAg-positive patients in whom active viral replication is occurring have a defect in T lymphocyte number and function, which may be due in part to reduced 5/9 positive cells. These alterations may be related to the persistence of virus in chronic active hepatitis B patients.

Antibodies, Monoclonal↗
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↗