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Biomedical subjects

G Bianchi

Publications and source records attributed to G Bianchi.

At least 325 records · Page 18Linked to original sources
PubMed1990

Double blind study of intrathecal beta-interferon in multiple sclerosis: clinical and laboratory results.

Sixteen patients with clinically definite MS admitted to a double blind randomised controlled trial of intrathecal natural beta-IFN were followed for a mean of 22 months including the six month treatment period. Clinical response, evaluated in terms of relapse frequency and of progression rate, showed an increase in relapse rate in treated patients during the six month treatment period and, overall, no benefit in treated versus placebo patients. Serial evaluations were made of cerebrospinal fluid (CSF) cells, IgG, myelin basic protein and CSF and blood T-cell subsets. A rise in CSF IgG Index, MBP and DR+ cells in IFN-treated patients suggested an activation of intrathecal immune response in treated patients.

Adolescent↗
PubMed1990

Genetic aspects of ion transport systems in hypertension.

Environmental factors, genetic polymorphism and differences in experimental design have been the main impediments to evaluating the evidence for a genetic association between cell membrane cation transport abnormalities and human essential or genetic hypertension. The present paper reviews the results obtained in the Milan hypertensive rat (MHS) and in its corresponding normotensive strain (MNS) in order to illustrate our approach to defining the role of cation transport abnormality in a particular type of genetic hypertension. Kidney cross-transplantation between the strains showed that hypertension is transplanted along with the kidney. Proximal tubular cell volume and sodium content were lower in MHS rats while sodium transport across the brush border membrane vesicles of MHS rats was faster. Erythrocytes of MHS rats have a smaller volume, faster Na,K cotransport and a lower Km for internal sodium compared with MNS rats. The faster cotransport is also present in renal cells of the ascending limb and in vascular muscle cells. Moreover, these erythrocyte abnormalities are genetically associated in F2 hybrids and are primarily determined in the stem cells. These differences in ion transport between MHS and MNS rats are not present when studied in erythrocyte inside-out vesicles, which are deprived of membrane skeletal proteins, suggesting that a molecular abnormality underlies the functional one. We have identified a point mutation of one of these cytoskeletal membrane protein adducin genes in MHS rats. At present we are evaluating the possibility that mutation of the adducin gene in MHS rats might account for the differences in ion transport and, therefore, in blood pressure between the two strains.

Animals↗
PubMed1990

[Parameters of tubulo-glomerular function in anesthetized rabbits with acute kidney insufficiency].

We have induced acute renal failure (ARF) in barbiturate anesthetized rabbits, through warm ischaemia of 30 or 60 min duration caused by transient bilateral occlusion of renal arteries. In this model we have monitored some renal performance parameters, before and 4 hours after reperfusion, aiming to characterize ARF in this animal species. Glomerular filtration rate (determined by the inulin clearance technique) was of 9.74 +/- 0.48 ml min-1 in 4 rabbits before injury and declined by 91% (60 min ischemia) during the first reperfusion hour. In 6 rabbits undergoing 30 min occlusion, pre-ARF values of 10.70 +/- 0.98 ml min-1 declined by 47%. In both groups no recovery was observed in the following hours. Tubular enzymes (alanine-amino-peptidase, AAP and N-acetyl-beta-glucosaminidase, NAG) were released into urines before injury at the rate of 1.11 +/- 0.18 and 1.32 +/- 0.41 mU min-1, respectively, in the 30 min model (3 animals/group). During ARF, maximal AAP output was five-fold increased (5.83 +/- 0.35 mU min-1), whereas NAG was unmodified. On the other hand, renal haemodynamics in 5 rabbits did not change after the ischaemic procedure: total renal blood flow (44 +/- 5 ml min-1) and renal vascular resistances (225 +/- 26 Pa ml-min) displayed less than 10% variations throughout the reperfusion period. We concluded that ARF in rabbits can be reliably and reproducibly monitored and that the pathogenesis of the disease, in our situation, is attributable mainly to tubular cell damage and not to impairment of the vascular component of renal performance.

Acetylglucosaminidase↗
PubMed1990

Predicting interindividual variations in antihypertensive therapy: the role of sodium transport systems and renin.

The efficacy of captopril at 75 mg/day, atenolol at 100 mg/day and canrenoate potassium at 200 mg/day was compared in 42 essential hypertensive patients in randomly assigned sequences. All the drugs lowered blood pressure significantly but variations were found in the individual response. Patients who were more responsive to captopril also seemed to be more responsive to atenolol and vice versa (r = 0.75; P less than 0.0001), while the relationship between mean blood pressure reached after canrenoate potassium and that reached after atenolol or captopril was much weaker. The patients who were responsive to atenolol and captopril were considered as one group (n = 22) and compared with the 12 patients more responsive to canrenoate potassium. Before treatment, the former group had higher plasma renin activity (PRA) and lower Na,K cotransport activity across the erythrocyte membrane than the latter. These two variables, considered together as a discriminant function, correctly classified 92% of cases in the canrenoate potassium responder group and 73% of cases in the atenolol-captopril responders. These results raise the problem of individual assessment to obtain the most effective antihypertensive therapy and suggest that PRA and Na,K cotransport may be useful in predicting the individual response to antihypertensive drugs.

Adolescent↗
PubMed1990

[Treatment of renal cysts by percutaneous drainage and alcoholization. Our experience].

Since many years renal cysts have been treated by percutaneous puncture and successive aspiration. The introduction of various sclerosing substances has been associated with this manoeuvre. In our study we examined 44 patients with renal cysts submitted to percutaneous puncture, aspiration and injection with 95% ethanol. We thought right to leave a small pig tail catheter so that the sclerosing substance could be easily and completely eliminated allowing the adhesion of the cystic walls in the following days, without any accumulation of cystic and/or exudative liquid. The follow up (12-24 months) has shown no relapsing in 40/44 cases. Only in 4 patients a cyst was present, but with dimensions lower than 30% of the original volume.

Administration, Cutaneous↗
PubMed1990

Genetic polymorphism of Na-K cotransport in essential hypertension.

Erythrocyte Na-K cotransport is high and genetically correlated to hypertension in Milan hypertensive strain (MHS) rats. In man there is a substantial overlap of individual values between essential hypertensives and controls. However, the findings in rat strains with different types of genetic hypertension suggest that Na-K cotransport studies may throw light on the different pathogenetic mechanisms of the human disease. In 28 normotensive and 22 hypertensive families the midparent-offspring correlation of Na-K cotransport values was significant only in hypertensive families (r = 0.48) and not significant in normotensive ones (r = 0.06), indicating genetic polymorphism for its phenotypic expression only in the hypertensives. In 189 essential hypertensives and 109 normotensives carefully selected from a population-based screening in order to exclude uneven sampling bias, analysis for the bimodality of the distribution of Na-K cotransport clearly showed that normotensives are distributed unimodally and hypertensives bimodally, with nadir of the distributions at about 450 mumols (1 RBC/h). Dividing the hypertensives according to Na-K cotransport value, the high Na-K cotransport subgroup has lower fractional percent excretion of uric acid and plasma renin activity. These data suggest that the high Na-K cotransport subgroup has peculiar characteristics of greater proximal tubular reabsorption (lower fractional excretion of uric acid) that may cause body volume expansion (lower plasma renin activity).

Biological Transport, Active↗
PubMed1989

Immunoblotting techniques with picogram sensitivity in cerebrospinal fluid protein detection.

Agarose isoelectric focusing followed by blotting with nitrocellulose, nylon or polyvinylidene difluoride membranes, and immunochemical detection of cerebrospinal fluid IgG with various combinations of antisera, was evaluated. Polyvinylidene difluoride proved to be an easy-to-handle and reliable membrane for protein blotting. Among immunochemical visualization reactions, the most sensitive employed biotinylated goat anti-human IgG followed by streptavidin colloidal gold conjugate and silver enhancement in 20% w/v urea, allowing a sensitivity of less then 1 picogram IgG/band.

Cerebrospinal Fluid Proteins↗
PubMed1989

CSF T-cell subsets in multiple sclerosis: relationship to cerebrospinal fluid myelin basic protein and clinical activity.

Cerebrospinal fluid myelin basic protein and cerebrospinal fluid and peripheral blood T-cell subsets have been studied in patients with multiple sclerosis and other inflammatory and non-inflammatory nervous system diseases. These biological parameters have been correlated with clinical disease activity. No changes in peripheral blood T-cell subsets were seen in multiple sclerosis patients. Low cerebrospinal fluid T8+ cells occurred only in multiple sclerosis, while high cerebrospinal fluid T4+ cells were detected both in clinically active multiple sclerosis and in inflammatory nervous system diseases. A close relationship was found between cerebrospinal fluid T4/T8 ratio and myelin basic protein in relapsing multiple sclerosis patients.

Adolescent↗
PubMed1989

Pathogenetic aspects of involutional osteoporosis.

The pathogenetic factors of postmenopausal and senile osteoporosis are reviewed. Both postmenopausal and senile osteoporosis occur as a result of a defective regulation of bone remodelling which leads to a negative uncoupling between bone resorption and bone formation. Systemic and local factors contribute to the development of the phenomenon. While studies of the systemic factors involved in age-related bone loss are well advanced, although still incomplete, the study of the local factors responsible at a tissue level for the negative skeletal balance has barely begun.

Adult↗
PubMed1989

Pathogenetic mechanisms in essential hypertension. Analogies between a rat model and the human disease.

Essential hypertension is a genetic disease. Its phenotypic expression depends on the interaction between genetic and environmental factors. In prehypertensive rats of the Milan hypertensive strain (MHS) a genetically inherited increase of tubular reabsorption was found, which causes the increase of blood pressure. Studies of ion transport systems in these rats have shown that the Na-K cotransport activity is increased both in erythrocytes and in tubular cells of MHS rats compared with their normotensive controls (MNS) and that this alteration is genetically linked to the transmission of high blood pressure levels. Also, in young human normotensives prone to develop essential hypertension there is an abnormal pattern of renal function which could be in agreement with a primitive increase in tubular reabsorption. Studies of erythrocyte ion transport systems in these subjects suggest that at least in a subgroup of humans predisposed to develop essential hypertension a pathogenetic mechanism similar to the one proposed for the MHS rat can be at work.

Animals↗
PubMed1989

Effects of gonadotrophin-releasing hormone agonist on uterine fibroids and bone density.

Bone density (BD) was evaluated by single photon absorptiometry (SPA) in 18 women treated with Buserelin a gonadotrophin-releasing hormone (LHRH) analogue, for uterine fibroids. Buserelin was administered for a period of 6 mth. Amenorrhoea and oestradiol levels in the follicular-phase range were recorded in all patients during treatment. Fibroid volume was evaluated by means of ultrasound. SPA was performed at the 1/3 proximal radius and at the 1/10 distal radius sites before starting therapy and every 2 mth subsequently for 12 mth. BD was also measured in a control group of 18 normally-menstruating premenopausal women, matched for age and body mass index. No significant changes in BD at the proximal or distal radius sites were observed in either the cases or the controls during the study. Moreover, comparison of the data on the cases and the controls revealed no differences in BD at 0, 6 or 12 mth. Thus, although LHRH analogue treatment proved effective in reducing fibroids, it did not cause any significant changes in BD.

Adult↗
PubMed1989

A possible primary role for the kidney in essential hypertension.

The role of the kidney in "essential" or "genetic" types of hypertension has been evaluated both in a rat model such as the Milan hypertensive strain (MHS) or in humans. In both species, abnormalities of renal function have been demonstrated before the development of hypertension. Moreover hypertension could be "transplanted" with the kidney when kidney cross-transplantation was carried out between MHS and the Milan normotensive strain (MNS). Also in humans, the familiality for hypertension of the donor affected the requirement of antihypertensive therapy of the recipient. Further studies furnished results that were consistent with the hypothesis that a primary increase in Na transport across the tubular cell could be responsible for the pressor effect of the kidney in MHS or in humans. Because many similarities were found between the function of the tubular cell and the red blood cell in MHS, red blood cells were used to gain information about the molecular genetic mechanisms underlying these cellular changes. The results so far obtained showed that red blood cell abnormalities in MHS were genetically determined within the stem cells and genetically associated with the development of hypertension in F2 hybrids obtained by crossing the F1 (MHS X MNS). Moreover, the abnormal Na transport across the cell membrane may be due to an abnormal function of the membrane skeleton proteins. Studies are in progress to evaluate a possible cause-effect relationship between: membrane skeleton protein-ion transport across the cell membrane and the development of hypertension.

Animals↗
PubMed1989

Mechanism of the antihypertensive effect of FCE 22716, a new ergoline derivative, in the spontaneously hypertensive rat.

Both acute and chronic oral administration (1-20 mg/kg) of FCE 22716, a new ergoline derivative, resulted in a dose-related fall of arterial blood pressure lasting for more than 6 h. Tachycardia was observed only at high dosages. Yohimbine, propranolol and indometacin did not modify its antihypertensive effect; on the other hand pretreatment with prazosin, a selective alpha 1-adrenoceptor antagonist and pithing, almost completely neutralized its antihypertensive effect. Haloperidol, a dopamine antagonist that crosses the blood-brain barrier, also antagonized FCE 22716 activity. The lack of effects of domperidone (DA2-receptor antagonist selectively acting on the periphery) together with the finding that norepinephrine and epinephrine levels were unchanged after treatment with FCE 22716, seem to rule out an involvement of peripheral DA2-receptors. Both in vitro (isolated organs) and in vivo the compound antagonized responses mediated by stimulation of alpha 1-adrenoceptors and S2-receptors. Radioligand binding studies in different cerebral regions are in line with the above reported in vitro and in vivo results. These data suggest that FCE 22716 is endowed with a multitarget mechanism of action, mainly involving blockade of alpha 1-adrenoceptors and S2-receptors.

Animals↗
PubMed1989

[Physiologic role of the sodium pump. Implications for the study of arterial hypertension].

Mammalian cells have the same hydroelectrolytic composition (high K, low Na), highly different from that of their surrounding. Constancy of cellular composition is insured by the balance between ionic leaks and (Na, K)-pump activity. Ionic leaks, specially sodium, are fundamental. They allow cells to perform a majority of their general and special functions (import of aminoacids, glucose, phosphates; export of acids; nerve influx; muscular contraction; glandular secretion; intestinal and renal reabsorption and secretion). (Na, K)-pump is essential to life. It is a kind of general motor that creates and maintains ionic concentrations differences whose potential energy is dissipated by leaks to perform cellular functions. Constancy of hydroelectrolytic intracellular composition hides that leak and pump rates, equivalent between them, are extremely variable among cell types (more than 200 times), and can increase 4 times in less than one minute within a cell type with cellular activity. In a cell, (Na, K)-pump rate is far from maximum velocity. This rate is adjusted nearly instantaneously to balance variations in leak rates; it may undergo short term modulation by endo or exocellular factors; it may undergo long term changes through synthesis of new enzyme molecules. Studies on whole cells of the balance between leaks and pump rates is necessary to understand these cells physiology and pathology. Balance between leaks and (Na, K)-pump activity is altered in renal cells from hypertensive rats, spontaneously (SHR) or genetically selected (Milan Hypertensive Strain: MHS). Strikingly, sodium activation of (Na, K)-pump of inner medullary collecting duct cells of MHS rats is greatly blunted compared to controls.

Adenosine Triphosphatases↗