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Biomedical subjects

G Bianchi

Publications and source records attributed to G Bianchi.

At least 433 records · Page 24Linked to original sources
PubMed1984

Sodium balance and peripheral resistance in arterial hypertension.

In this brief review, some aspects of the relation between sodium balance and peripheral resistance in four types of arterial hypertension are discussed. Renal hypertension, hypertension caused by reduced kidney mass and sodium load, mineralocorticoid hypertension, and spontaneous or "genetic" hypertension in rats are considered. In all these forms of hypertension, the increase in peripheral resistance is preceded by changes in body sodium and fluids. However, the precise role of these changes in the development of the subsequent rise of peripheral resistance is not yet clear. Changes in ion transport across the cell membranes have been demonstrated even before the development of hypertension, especially the forms caused by mineralocorticoids or genetic factors. Even though we do not know the underlying mechanisms, it is very likely that these cell-membrane changes are involved in the rise of peripheral resistance and blood pressure.

Animals↗
PubMed1984

The peripheral narcotic antagonist N-allyl levallorphan-bromide (CM 32191) selectively prevents morphine antipropulsive action and buprenorphine in-vivo binding in the rat intestine.

The assumed low ability of the quaternary narcotic antagonist N-allyl levallorphan-bromide (CM 32191) to cross the blood-brain barrier and its selectivity in relieving the peripherally-elicited antipropulsive action of morphine while preserving analgesia has been tested. To ascertain the extent of penetration of CM 32191 into the cns, its relative potency in preventing the in-vivo binding of high specific activity [3H]buprenorphine in the rat cns and small intestine was compared. Pretreatment was with CM 32191 at 16, 30 or 60 mg kg-1 s.c., 20, 60 or 120 min before buprenorphine, the concentrations of which in cerebrum and spinal cord were comparable with control values, but were consistently reduced in the intestine (longitudinal muscle with attached myenteric plexus). Pretreatment with naloxone (20 min, 0.5 or 1 mg kg-1 s.c.) lowered buprenorphine binding in intestine and cns. Neither narcotic antagonist produced significant changes in buprenorphine plasma concentrations. The peripheral selectivity of CM 32191, methyl naloxone and naloxone was examined by investigating in the same rats nociception in the hot plate (central opiate-sensitive mechanism) and the transit of a charcoal meal along the small intestine (local opiate-sensitive mechanism). Both effects were inhibited by morphine (5 mg kg-1 i.v.). Naloxone (10 min pretreatment, 0.5 or 1 mg kg-1 s.c.) did not selectively antagonize intestinal action of the morphine since the relief of charcoal transit inhibition was consistently associated with complete loss of analgesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Central and peripheral inhibition of gastrointestinal transit in rats: narcotics differ substantially by acting at either or both levels.

The roles of local intestinal and centrally mediated opiate-specific mechanisms underlying gastrointestinal transit inhibiton by five typical narcotic analgesics were assessed by the rat charcoal meal test. The doses (mg kg-1 s.c.) reducing the progression of charcoal to 50% of drug-free controls in 5 min (ID50) were approximately 1 for morphine and methadone, 0.5 and 40 for diamorphine and pethidine (all given 25 min before charcoal) and 0.001 for etorphine (10 min before charcoal). The delay in test meal travel caused by these ID50 doses was completely prevented by i.p. naloxone. Intracerebroventricular (i.c.v.) naloxone fully antagonized pethidine and etorphine but had no effect on morphine. Morphine, but either pethidine nor etorphine, was antagonized by i.p. N-methyl naloxone (a peripheral antagonist). Diamorphine and methadone were partially antagonized by i.c.v. naloxone or i.p. N-methyl naloxone.

Analgesics, Opioid↗
PubMed1984

Blood pressure in patients with four different primary glomerulopathies.

It is well known that patients with different kidney diseases have different prevalence of hypertension, independent of renal function. To investigate whether a lesion of some portion of the glomerular tuft, without renal insufficiency, is associated more frequently with high blood pressure, we undertook a retrospective study on 189 patients analyzing by means of multiple regression analysis as independent variables : type of glomerulopathy (IgA Nephropathy, Acute Glomerulonephritis, Membranous Glomerulonephritis and Focal Glomerulosclerosis), sex, age, body weight, plasma creatinine, plasma and urinary proteins, plasma urate, time interval first symptom-renal biopsy and steroid therapy. The dependent variable was a Principal Component formed by Mean Blood Pressure and an Antihypertensive Therapy score, calculated with a computer program. Focal Glomerulosclerosis patients had a higher prevalence of hypertension and a higher Principal Component value than patients of the other 3 groups. Plasma urate was correlated and time interval first symptom-renal biopsy was inversely correlated to Principal Component. These observations suggest that sclerosis of the glomeruli is the lesion most often associated with hypertension. On the other hand, since plasma urate is correlated with blood pressure also in "essential" hypertensives, it seems likely that hyperuricemia is a phenomenon secondary to hypertension.

Adult↗
PubMed1984

Renal function of isolated perfused kidneys from hypertensive (MHS) and normotensive (MNS) rats of the Milan strain at different ages.

Young pre-hypertensive rats of the Milan strain (MHS) have a faster glomerular filtration rate (GFR) and a higher urine flow in vivo than matched normotensive controls (MNS). Kidneys from both MHS and MNS at different ages were perfused in vitro with cell-free artificial medium, in order to further clarify the nature of these differences, in the absence of extrarenal uncontrolled factors. Isolated kidneys from young MHS showed a faster GFR, a larger tubular Na+ reabsorption and urine flow as compared to matched MNS: such differences endured throughout the 2 h of perfusion. These results support an intrinsic kidney abnormality as causing the above described differences between young rats of the two strains. Isolated kidneys from adult MHS showed faster GFR, higher renal perfusion flow and urine flow, yet similar tubular Na+ reabsorption when compared to MNS. Moreover a faster decay in kidney function was observed in the experiments with MHS. The existence of an extrarenal factor(s) correcting the intrinsic MHS kidney abnormality in vivo is suggested, as no differences were reported in kidney function of intact adult animals.

Absorption↗
PubMed1983

Venous imprint on the superior infundibulum. An unusual pyelographic appearance.

Venous imprints on the upper urinary tract are common urographic findings but are rarely documented by renal angiography. The authors describe an unusual urographic appearance of a vascular imprint on the superior infundibulum due to a normal venous trunk. In this case retrograde phlebography was performed for a complete diagnosis.

Adult↗
PubMed1983

Relative ability of N-methyl nalorphine and N-methyl levallorphan to prevent antinociception and intestinal transit inhibition in morphine treated rats.

Nalorphine, levallorphan and their quaternary analogs, N-(eq)allyl derivatives of the two diastereoisomers at the nitrogen atom (N-methyl nalorphine and N-methyl levallorphan) were tested for their peripheral selectivity. We compared their relative ability to prevent morphine-induced (5 mg/kg i.v.) antinociception (central antagonism) and constipation (peripheral antagonism) in the same rats. Nalorphine and levallorphan reduced morphine-induced antinociception to half maximal response at doses of 5.1 and 0.89 mg/kg s.c. and restored the intestinal transit to 50% of controls (AD50) respectively at doses of 0.25 and 0.12 mg/kg. N-methyl nalorphine up to 24 and N-methyl levallorphan up to 30 mg/kg given s.c. 10 min before morphine did not antagonize narcotic-induced antinociception, fully preventing constipation (AD50 0.65 and 0.32 mg/kg respectively), but when injected 50 min before morphine they partially lost their antagonist potency (AD50 2.3 and 2.6 mg/kg respectively) and peripheral selectivity. N-methyl nalorphine and N-methyl levallorphan thus seem more peripherally selective than their tertiary analogs and more potent than quaternary narcotic antagonists tested to date.

Analgesia↗
PubMed1983

Renal dysfunction as a possible cause of essential hypertension in predisposed subjects.

In 65 young normotensive subjects with two hypertensive parents (HP), and in 55 matched subjects with two normotensive parents (NP), the following factors were measured: renal plasma flow (RPF), glomerular filtration rate (GFR) both as Inutest and creatinine clearances; 24-hr urinary output; plasma renin activity (PRA); Na and K in plasma and in 24-hr urine and 24-hr urinary excretion of aldosterone. In 30 HP and in 34 NP, the cardiac output and plasma concentrations of noradrenaline, adrenaline, and dopamine were also measured in the supine position and after 10 min of standing. The HP have greater RPF (P less than 0.01), faster GFR (P less than 0.02), greater 24-hr urinary output (P less than 0.05), and lower PRA (P less than 0.01) than the NP. All the other factors were similar in the two groups of patients. It is proposed that the differences in renal function in the HP and the NP may be due to an abnormality in tubular handling of ions and water in the HP, which may be responsible for the increase in blood pressure in a proportion of patients with essential hypertension.

Adolescent↗
PubMed1983

Morphine tissue levels and reduction of gastrointestinal transit in rats. Correlation supports primary action site in the gut.

Overnight-fasted male rats given a single dose of tritium-labeled morphine either intraperitoneally or intravenously were fed a charcoal test meal by stomach tube. The drug remaining in tissues was assayed by liquid scintillation counting of thin-layer chromatograms from homogenates, and gastrointestinal transit was tested by measuring the portion of the small intestine traversed by charcoal in 5 min. Morphine, 0.15 mg/kg, given intraperitoneally either 10 min or 30 min before testing substantially reduced gastrointestinal transit (to 23% and 55% of drug-free controls, respectively), and produced maximum drug levels 5 min after administration in small intestine longitudinal muscle with attached myenteric plexus (500 +/- 42 ng/g, mean +/- SE, n = 4). Intact small intestine, plasma, and brain, respectively, contained decreasing drug concentrations that, in the latter, never exceeded 2%-3% of that in longitudinal muscle. Rats receiving 0.15 mg/kg morphine intravenously presented only minor and short-lived inhibition of gastrointestinal transit that was significantly below (approximately 35%) that of drug-free controls at 10 min, but not 30 min, after drug administration. Morphine levels in the brain and plasma of these rats were up to five times higher, and in the intact small intestine longitudinal muscle were up to 20 times lower than in intraperitoneally treated rats. Morphine concentration in the tissues assayed was plotted against the effect on gastrointestinal transit at the same interval for individual rats regardless of dose, administration route, and observation time: data analysis, in small intestine longitudinal muscle, but not in the brain or plasma, indicated a highly significant correlation and fitting of computer-generated curves described by a currently accepted equation according to the receptor occupation theory of drug response. In view of these findings, and of the complete prevention by the "peripherally selective" narcotic antagonist N-methyl naloxone of gastrointestinal transit inhibition after an intravenous analgesic dose of morphine (1 mg/kg), the investigated animal model is consistent with the primary role of a gut-located action site in opiate-induced constipation.

Animals↗
PubMed1983

Plasma amino acid response to protein ingestion in patients with liver cirrhosis.

The metabolic effects of a protein-rich meal were studied for 3 h in 10 controls and in 20 cirrhotic patients. After protein ingestion, blood glucose did not vary significantly. Insulin and glucagon levels rose in controls and, more markedly, in cirrhotics. Aromatic amino acids and tryptophan increased more in cirrhotics as a result of their decreased liver function. Similarly, branched-chain amino acids increased by 153 +/- 14 nmol/ml X min (mean +/- SE) in controls and by 259 +/- 27 nmol/ml X min in cirrhotics (p less than 0.02), in the presence of a markedly increased insulin response. Branched-chain amino acid metabolism mainly occurs in skeletal muscle under insulin control; in cirrhosis, it might be reduced as a consequence of insulin resistance. To support this hypothesis, the effects of the protein meal were compared with those of an oral glucose load in 15 cirrhotic patients. Branched-chain amino acid response to protein ingestion significantly correlated with blood glucose response to oral glucose (r = 0.714), and with insulin resistance during the glucose tolerance test, when assessed by the insulinogenic index (r = 0.628). Similarly, in 8 patients, increased branched-chain amino acid response also correlated with the index of tissue sensitivity to insulin obtained by means of the glucose clamp technique during continuous insulin infusion (r = -0.809). We conclude that liver cirrhosis is characterized by an abnormal branched-chain amino acid response to protein ingestion, which matches the well-known intolerance to oral glucose. Both alterations are possibly due to decreased peripheral insulin activity on substrates.

Amino Acids↗
PubMed1983

Expression at the haemopoietic stem cell level of the genetically determined erythrocyte membrane defects in the Milan hypertensive rat strain (MHS).

Both humans and rats with essential or genetic arterial hypertension show many alterations of erythrocyte membrane ion transport. The Milan hypertensive rat strain (MHS) has smaller red cells and faster Na+/K+ cotransport across erythrocyte membrane when compared with the control strain (MNS). In order to distinguish if these alterations are due to some inherited cell membrane characteristics or are secondary to some extrinsic factor responsible for hypertension, we have transplanted bone marrow (BM) cells from MHS or MNS rats to two groups of F1 hybrids, lethally irradiated (850 R). Three months after BM transplantation the F1 recipients were killed and their erythrocytes studied. The differences between erythrocytes of F1 MHS BM recipients and F1 MNS BM recipients follow the same pattern described for the donor parental strains. These results indicate that the MHS red cell abnormalities are present in the haemopoietic stem cell and therefore the MHS erythrocyte defects are not due to some extrinsic factors.

Animals↗