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Biomedical subjects

E Bartoli

Publications and source records attributed to E Bartoli.

At least 145 records · Page 8Linked to original sources
PubMed1993

Intensity of inflammatory damage and serum lipid peroxide concentrations in liver disease.

AIMS: To investigate variations in serum lipid peroxide activities in relation to various clinical entities of liver disease. METHODS: Serum lipid peroxides were measured fluorometrically in eight patients with acute hepatitis, six with liver steatofibrosis, five with chronic persistent hepatitis, 15 with chronic active hepatitis, 28 with liver cirrhosis, 22 with hepatocellular carcinoma; 19 patients with extrahepatic disease (six malignant, 13 benign) were used as controls. RESULTS: Higher serum lipid peroxide concentrations were found in patients with acute hepatitis (4.52 (SEM 0.56)) nmol/ml than in all other groups of patients (p < 0.01). No significant difference was found among the mean values detected in the groups of patients affected by chronic liver disease and extrahepatic diseases. A history of chronic alcohol consumption was not associated with higher lipid peroxide concentrations. A significant correlation (R2 = 0.4538, R = 0.6737, F = 7.617, p = 0.0000) was found between serum lipid peroxides and a set of indices of inflammation (ESR, total leucocyte count, C-reactive protein) and of hepatic function (aspartate aminotransferase (AST) or alkaline phosphatase (ALP) or bilirubin). Of these, bilirubin was the most significant indicator of inflammation. Analysis of covariance showed a significant difference in lipid peroxide values among groups, even when bilirubin was chosen as an independent variable. CONCLUSIONS: Raised serum lipid peroxide concentrations can be found during acute inflammatory liver disease. Acute change in liver function, reflected by high bilirubin concentrations, seems to be more important for intravascular liberation of lipid peroxides than existence of specific aetiological factors or of severe longstanding global liver damage.

Acute Disease↗
PubMed1993

Increased serum phospholipase A2 activity in advanced chronic liver disease as an expression of the acute phase response.

Phospholipase A2 (PLA2) modifications were investigated in patients with acute and chronic liver diseases, PLA2 variations were related to indices of liver function as well as to parameters of the acute phase response. Serum PLA2 activity modifications were fluorimetrically measured in 105 patients affected by acute and chronic liver diseases or extra-hepatic diseases. One-way ANOVA demonstrated a significant difference among groups (F = 4.53, P < 0.001); Bonferroni's test for pairwise comparisons showed that patients with hepatocellular carcinoma had higher mean values than subjects with benign extra-hepatic diseases (P < 0.01) and mild chronic liver disease (P < 0.05). Multiple regression analysis, performed choosing PLA2 as the dependent variable and blood urea nitrogen, C-reactive protein, alkaline phosphatase and alpha 1-fetoprotein as predictor variables was significant (multiple R = 0.7056, multiple R2 = 0.4978, F = 15.36, P = < 0.0001). The standardized regression coefficients found to be significant were those of C-reactive protein, blood urea nitrogen and alpha 1-fetoprotein. In conclusion, in patients with chronic liver disease, serum PLA2 activity increases parallel to disease severity and accompanies the expression of proteins of the acute phase response that, like PLA2 activity, increase in serum while liver synthesis declines.

Acute-Phase Reaction↗
PubMed1993

Acute effects of furosemide on blood pressure in functionally anephric, volume-expanded rats.

The hypotensive effect of loop diuretics is primarily mediated by a decrease in extracellular fluid volume that follows the intense diuresis. In the present study we investigated whether furosemide (1.25 mg/kg i.v.) can acutely lower blood pressure independently of its diuretic action. The experiments were performed in four groups of male Wistar rats: (a) rats in which furosemide was administered after bilateral ligation of renal vessels and saline (0.9% NaCl at a rate of 0.25 ml/min to a final volume of 1% of body weight) infusion; (b) rats in which furosemide was injected after bilateral ligation of ureters and saline infusion; (c) rats pretreated with indomethacin (3 mg/kg i.p. for 4 days) in which furosemide was injected after bilateral ligation of ureters and saline infusion; (d) sham-operated rats with intact kidneys. All the groups were compared with appropriate time controls. After furosemide injection, heart rate and blood pressure were serially recorded for 30 min by plethysmography. Hematocrit, plasma 6-keto-prostaglandin F1 alpha levels and plasma renin activity were measured at baseline and 20 min after furosemide injection. No change in blood pressure followed furosemide administration in rats with ligation of the renal vessels. Conversely, furosemide induced a rapid and significant fall in blood pressure associated with a significant increase in heart rate in rats with ligation of the ureters and rats with intact kidneys. Indomethacin pretreatment prevented the furosemide-induced decrease in blood pressure in rats with ligation of the ureters. Hematocrit and plasma 6-keto-prostaglandin F1 alpha levels were not affected by furosemide in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Increase of serum alpha 1-acid glycoprotein despite the decline of liver synthetic function in cirrhotics with hepatocellular carcinoma.

alpha 1-Acid glycoprotein, an acute phase reactant synthesised by the liver, has been reported to be increased in neoplastic conditions and reduced in chronic liver disease. We measured serum alpha 1-acid glycoprotein by a nephelometric method in 186 subjects (112 males, 74 females): 55 had mild chronic liver disease (chronic hepatitis and steatofibrosis), 45 cirrhosis, 38 hepatocellular carcinoma, 15 extra-hepatic malignant disease; 33 healthy subjects were used as controls. Analysis of variance demonstrated a significant variability among groups (F = 17.08, P = 0.0000). Higher concentrations of alpha 1-acid glycoprotein were detected in malignant extra-hepatic disease than in all other groups (P < 0.01); concentrations of alpha 1-acid glycoprotein were higher in hepatocellular carcinoma than in cirrhosis (P < 0.01). Multiple regression analysis by groups (dependent variable = alpha 1-acid glycoprotein; group 1 = mild chronic liver disease + cirrhosis; group 2 = hepatocellular carcinoma) showed a significant correlation for both group 1 (r = 0.6264, F = 8.005, P = 0.0000) and group 2 (r = 0.8947, F = 13.643, P = 0.0000). The significant standardised regression coefficients were: cholinesterase, C-reactive protein, gamma-glutamyltransferase and iron (negative) for regression upon group 1; C-reactive protein, alpha 1-antiproteinase, gamma-glutamyltransferase, iron (negative) for regression upon group 2. A difference between the 2 regression equation coefficients was detected (F = 5.209, P = 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Angiotensin II receptors in the heart conduction tissue].

Angiotensin II exerts a positive chronotropic effect on mammalian heart. This effect can be mediated either by activation of the sympathetic nervous system or binding to specific receptors located in cardiac conduction tissue. Recently, two angiotensin II receptor subtypes have been identified in rat tissues. In the present study, we have investigated tissue distribution of angiotensin II receptor subtypes in conduction tissue obtained from rat hearts, employing an in situ autoradiographic technique. Receptor subtypes were identified by use of the peptide antagonists losartan (AT1) and PD123,177 (AT2). Angiotensin II binding was homogeneously distributed in right and left ventricle, and interventricular septum, with each subtype accounting for approximately 50% of the specific binding. Receptor density in the conduction tissue, identified by acetylcholinesterase histochemistry, was quantitated by counting the silver grains on tissue sections which, following incubation, were dipped in photographic emulsion and developed. In both sinoatrial and atrioventricular node AT1 and AT2 receptors were homogeneously distributed. Receptor density in sinoatrial node was comparable to myocardium, whereas it was significantly higher (p < 0.02) in atrioventricular node. In conclusion, both AT1 and AT2 receptors are homogeneously distributed in cardiac conduction tissue. Binding density is higher in the atrioventricular node than in the other structures examined in our study, suggesting a possible role of angiotensin II in the atrioventricular conduction.

Angiotensin II↗
PubMed1993

[Angiotensin receptors in the rat myocardium during pre- and postnatal development].

Angiotensin II exerts positive inotropic and chronotropic effects on mammalian heart by binding to specific membrane receptors. Recently, 2 subtypes of angiotensin II receptors (AT1 and AT2) have been distinguished using the nonpeptide antagonists losartan and PD123177. Because angiotensin II has been reported to have growth potentiating effects in several tissues, we examined angiotensin II receptors in fetal (embryonic day 16 and 19), neonatal (1, 2, 3 and 10 days), and adult (10 and 16 weeks) rats. We performed an 125I-[Sar1,Ile8]-angiotensin II in situ binding assay on tissue sections obtained from Sprague-Dawley rats. Binding specificity was verified by competition with unlabeled [Sar1]-angiotensin II. Distribution of AT1 and AT2 receptors was determined by competition with losartan and PD123177, respectively, and the density of receptors quantitated by emulsion autoradiography. Angiotensin II receptors were widely distributed throughout the heart, with each receptor subtype accounting for approximately 50% of the specific binding. Binding density was comparable in right and left ventricles, and interventricular septum. Throughout cardiac development a significant increase (p < 0.005) in the density of both receptor subtypes was found immediately after birth, reaching a maximum on day 2, and decreasing toward prenatal values thereafter. No variation in the proportion of the 2 receptor subtypes was observed during development. Thus, in rat heart, AT1 and AT2 receptors are equally distributed over the myocardium. The density of these angiotensin II receptors is developmentally regulated, suggesting a possible role of the cardiac renin-angiotensin system in heart growth and in the adaptation of the heart to postnatal circulatory conditions.

Analysis of Variance↗
PubMed1993

[The role of G-regulatory proteins in the intracellular mechanism of cardiac angiotensin-II receptors].

High-affinity angiotensin II receptors have been identified in cardiac tissue of many animal species. In the heart, angiotensin II exerts positive inotropic and chronotropic effects, constricts coronary vessels, and stimulates cell growth. In vascular smooth muscle and adrenal cortex angiotensin II interacts with guanidine nucleotide regulatory proteins because GTP-gamma-S causes dissociation of the radioligand from its receptor. To investigate whether angiotensin II interacts with guanidine nucleotide regulatory proteins also in cardiac tissue, we studied the effects of GTP-gamma-S on [Sar1, Ile8]-angiotensin II binding to angiotensin II receptor subtypes (AT1 and AT2) in hearts obtained from 16- to 20-week-old Sprague-Dawley rats. We employed an in situ technique performed on frozen tissue sections. Competition experiments performed with the nonpeptide inhibitors losartan and PD123177 allowed identification of both AT1 and AT2 angiotensin II receptors in rat heart. These receptors were present in comparable amounts. In a different set of experiments the effects of GTP-gamma-S (100 microM) on radioligand displacement from AT1 and AT2 receptors were studied. GTP-gamma-S caused a progressive dissociation of the radioligand from the AT1 receptor indicating that this receptor interacts with guanidine nucleotide regulatory proteins. In contrast, the AT2 receptor does not appear to directly interact with guanidine nucleotide regulatory proteins. In summary, the study shows that both angiotensin II receptor subtypes are present in rat heart and that guanidine nucleotide regulatory proteins are implicated in the signal transduction mechanism of the cardiac AT1 receptor.

Angiotensin II↗
PubMed1992

Relief of pruritus and decreases in plasma histamine concentrations during erythropoietin therapy in patients with uremia.

BACKGROUND: The pathophysiologic aspects of pruritus in patients with chronic renal insufficiency are poorly understood, and there is no universally effective treatment. The improvement of pruritus in several patients receiving erythropoietin therapy raised the possibility that erythropoietin affects uremic pruritus directly. METHODS: We undertook a 10-week placebo-controlled, double-blind, crossover study in a group of patients receiving hemodialysis who had severe pruritus, to investigate the effects of recombinant human erythropoietin on their pruritus and plasma histamine levels. Twenty patients with uremia, of whom 10 had severe pruritus and 10 did not, received erythropoietin (36 units per kilogram of body weight three times weekly) and placebo in random order, each for five weeks. The severity of pruritus was scored weekly, and plasma histamine levels were measured at the beginning and end of each five-week period. RESULTS: Eight of the 10 patients with pruritus had marked reductions in their pruritus scores during erythropoietin therapy. The mean (+/- SE) pruritus score decreased from 25 +/- 3 to 6 +/- 1 in these patients. The pruritus returned within one week after the discontinuation of therapy. The improvement was not related to the change in hemoglobin level. These eight patients were successfully treated again with low doses of erythropoietin (18 units per kilogram three times weekly), and the effect has persisted for six months. The patients with pruritus had elevated plasma histamine concentrations (20.7 +/- 2.7 nmol per liter), as compared with the patients without pruritus (4.2 +/- 0.6 nmol per liter; P less than 0.001) and normal subjects (2.1 +/- 0.2 nmol per liter; P less than 0.001). Therapy with erythropoietin induced a decrease in plasma histamine concentrations in both groups of patients with uremia, and recurrences of pruritus after the discontinuation of erythropoietin were accompanied by increases in plasma histamine concentrations. CONCLUSIONS: Erythropoietin therapy lowers plasma histamine concentrations in patients with uremia and can result in marked improvement of pruritus.

Double-Blind Method↗
PubMed1992

Abnormalities of erythrocyte sodium transport systems in Bartter's syndrome.

The basic tubular alteration present in Bartter's syndrome is still a subject of controversy. The possibility that a generalized defect in the transmembrane ion transport underlies the disease has been extensively investigated. Previous evaluations of cellular sodium metabolism in Bartter patients showed extremely variable findings. We have examined in the red blood cells of two patients with Bartter's syndrome the intracellular Na+ and K+ concentrations, the activity of the ouabain-sensitive Na+/K+ pump, furosemide-sensitive Na+/K+ cotransport, Na+/Li+ countertransport and the rate constant of Na+ and K+ passive permeability. We have compared these values with those of healthy subjects and patients with chronic hypokalemia produced by conditions other than Bartter's syndrome. Ouabain-sensitive Na+/K+ pump activity was decreased in both patients, whereas Na+/Li+ countertransport was activated. One of the patients also exhibited markedly decreased intraerythrocyte K+ concentration and decreased furosemide-sensitive Na+/K+ cotransport. The other had increased Na+/K+ cotransport activity and Na+ passive permeability. Intracellular Na+ and passive permeability to K+ were normal in both subjects. Neither oral potassium supplementation (100 mEq/day) nor indomethacin treatment (150 mg/day) could correct these abnormalities. Our results are partially consistent with previous observations and indicate the existence of heterogenous abnormalities of erythrocyte sodium transport systems in patients with Bartter's syndrome which are not a consequence of chronic hypokalemia.

Adult↗
PubMed1992

Bardet-Biedl syndrome and cystinuria.

An unusual association of Bardet-Biedl syndrome with cystinuria was described in one patient. A 21-year-old male was admitted to hospital because of renal failure, severe deterioration of visual acuity, polydactyly, brachydactyly, and mental retardation. Laboratory investigations revealed a serum creatinine of 292 mumol/L (3.3 mg/dL) and a GFR of 25 mL/min per 1.73 m2. Quantitative ion exchange chromatography demonstrated an increased urinary excretion rate of cystine, lysine, arginine, and ornithine. The ophthalmologic examination showed a severe atypical retinal dystrophy. Visual acuity was severely deteriorated and the patient could only count the examining physician's fingers. The patient had been previously evaluated at the age of 7 years for polyuria, polydipsia, and growth failure. His workup at that time demonstrated nephrogenic diabetes insipidus, normal GFR, and a urinary amino acid pattern consistent with the cystinuric phenotype. There was mental retardation notwithstanding the normal ophthalmologic examination. Intravenous pyelography showed calyceal clubbing, calyceal cysts, and lobulated renal outlines of the fetal type. The patient was evaluated again at the age of 13 years for deterioration of visual acuity and the ophthalmologic examination showed an atypical retinal dystrophy, with sparse pigmentation, central and peripheral atrophy, attenuated vessels, and marked optic disk pallor. To our knowledge the association of Bardet-Biedl syndrome with cystinuria has never been reported. It is unlikely that cystinuria may have contributed to the kidney damage. The possibility that mental retardation has been induced or aggravated by cystinuria cannot be excluded.

Adult↗
PubMed1989

Volume receptors in guinea pig labyrinth: relevance with respect to ADH and Na control.

We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +/- 2.4 to 29.1 +/- 6.9 pg/ml, in urine osmolality (Uosmol) from 470 +/- 48 to 712 +/- 46 mosmol/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +/- 47 to 71 +/- 11 microliters/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +/- 3.9 to 18.4 +/- 3.1, Uosmol from 829 +/- 58 to 627 +/- 43 (P less than 0.001), and V rose from 51 +/- 11 to 130 +/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[The role of echography in the diagnosis of neonatal clavicular fractures].

The authors' aim was to investigate the utility of US in the diagnosis of clavicular fractures in neonates. The technique, which is quite simple, consists in obtaining longitudinal scans of the bone by directing the probe along its axis. Ten cases of clavicular fracture were demonstrated in 11 neonates. Some patients were reexamined after 15 days to investigate fracture healing. After US examination, plain X-rays were always performed and the results compared: perfect correspondence was demonstrated between US and X-ray findings. Since clavicular fractures have a very good prognosis, this affection only needs documenting, for which purpose US can fully replace conventional X-rays, being quite simple to perform and avoiding the use of ionizing radiations, though yielding the same diagnostic results.

Clavicle↗
PubMed1988

Importance of liver interstitial pressure on sodium retention.

Experiments were performed on 23 dogs to assess the effect of splanchnic pooling on renal hemodynamics and Na retention. When the thoracic duct pressure was raised to 40 cm H2O (HTDP), liver interstitial pressure rose from 9.0 +/- 0.4 to 19.8 +/- 1.1 cm H2O. Simultaneously, glomerular filtration rate (GFR) and renal plasma flow fell in the left kidney from 16.3 +/- 1.7 to 9.6 +/- 1.3 and from 73.7 +/- 12.2 to 44.3 +/- 9.8 ml.min-1, respectively (p less than 0.01). UNa.V fell to 59 +/- 9% of control value (p less than 0.01). Plasma antidiuretic hormone (ADH) rose from 29.5 +/- 7.7 to 46.9 +/- 9.2 pg.ml-1 (p less than 0.05). When a portocaval shunt (PCS) was opened in 10 dogs during HTDP after the first set of experimental measurements, splanchnic pressure fell from 17.2 +/- 1.1 to 11.5 +/- 1.2 cm H2O, attended by a return towards control of GFR. ADH fell significantly to 16.5 +/- 8.1 during PCS, and to 9.7 +/- 1.5 pg.ml-1 during a last, postexperimental control period. Instead, UNa.V remained unchanged at the low levels measured during HTDP alone. When the HTDP was released in the 17 dogs without, and the 10 dogs with PCS, all variables became indistinguishable from control, except for UNa.V, which remained reduced, even in 4 aldosterone-escaped animals. No significant change in any of these variables occurred in 6 sham-operated control animals. These data demonstrate that it is possible to increase interstitial liver pressure through the lymph duct.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Echographic aspect of the diaphragm].

The authors investigated the sonographic patterns of the right hemidiaphragm, with high-resolution real-time equipments. Sixty healthy subjects and two patients were examined; the patients suffered from ascites and pleural effusion, and ascites and pulmonary emphysema, respectively. Even though the muscle is generally described as a thin, highly echogenic line surrounding the liver, in a large number of cases the diaphragm could be demonstrated as a hypoechoic layer, bordered by thin echogenic lines (pleural and peritoneal membranes). This pattern was observed in the lateral part of the muscle in 81% of cases, and along the whole border of the liver in 37% of cases. Such findings were detected in pathological cases too. Thus, the patterns described in previous experimental works on specimens of human diaphragm were confirmed in vivo. As the perfect knowledge of normal appearance is the first step towards diagnosis, the above peculiarities of the normal diaphragm should become more widely known.

Ascites↗