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Biomedical subjects

G Baggio

Publications and source records attributed to G Baggio.

At least 55 records · Page 3Linked to original sources
PubMed1986

Imidazole has similar behavioural effects to yohimbine.

A number of animal behavioural models were used to study the activity of imidazole (IMID) on the central nervous system. IMID antagonized in a dose-related fashion penile erections (PE) as well as stretching and yawning (SY) elicited in male rats by B-HT 920, an alpha 2 and dopamine (DA) autoreceptor agonist. Inhibition of B-HT 920-induced PE and SY was also exhibited by haloperidol, a DA receptor blocker, and yohimbine, but not by prazosin, alpha 2 and alpha 1 receptor antagonists respectively. Moreover IMID behaved similarly to yohimbine in: 1) counteracting clonidine-induced hypothermia in mice; 2) antagonizing sedation and sleep induced by clonidine and B-HT 920 in chicks, while haloperidol was ineffective. When administered to sexually active rats before the copulatory test, IMID at low doses, significantly altered some aspects of mating, a result which is interpretable in terms of enhanced sexual arousal and resembling the aphrodisiac effect reported for yohimbine. The neurochemical mechanisms involved in these effects are discussed.

Adrenergic alpha-Agonists↗
PubMed1986

Effect of probucol treatment on lipoprotein cholesterol and drug levels in blood and lipoproteins in familial hypercholesterolemia.

Twelve patients with mild and 3 with severe hypercholesterolemia were stabilized with an isocaloric diet containing less than 300 mg cholesterol daily with a P/S ratio of 1.8, and placebo period of 4 weeks. They were administered 1000 mg probucol daily for 12 weeks, followed by placebo for 6 weeks. In patients with mild disease, a significant cholesterol reduction was achieved in serum, LDL, and HDL (maximum decrease, 17%, 13%, and 31%, respectively). While HDL3 cholesterol was reduced significantly throughout the period (P less than 0.001), HDL2 cholesterol showed a significant decrease only at the 4th week of treatment (P less than 0.001), and returned to basal levels at the 8th and 12th treatment weeks. Serum apo B levels decreased only slightly, but the HDL-apo A-I fall was significant with a reduction in the HDL-CH/HDL-apo A-I ratio throughout the treatment period. In 3 patients with severe disease, cholesterol decrease in serum and in VLDL, LDL and HDL fractions varied, but on the whole was lower than in patients with mild disease. A decrease in VLDL-CH and HDL-CH was present in all 3, but LDL-CH levels were only slightly lowered in 2 patients, and unchanged in the third. Serum probucol levels fell 66% from the 4th to the 12th treatment week, and in parallel, the percentage of lipoprotein-bound drug increased about 2-fold. It is suggested that these changes in pharmacokinetics as well as the cholesterol-lowering effect of the drug may be due to a change in lipoprotein composition or structure.

Adult↗
PubMed1986

Lisuride-induced mounting and its modification by drugs active on adrenergic and dopaminergic receptors.

Imidazole (IMID), (9.37-75 mg/Kg) and yohimbine (YOH), (0.5-2.5 mg/Kg), strongly potentiated lisuride-induced mounting, scored as a percentage of animals affected and mean number of mounts per animal, while clonidine (150 micrograms/Kg) significantly antagonized the phenomenon. A high (2 mg/Kg) but not a low (50 micrograms/Kg) dose of B-HT 920 and DPI (100 and 500 micrograms/Kg) also inhibited lisuride-induce mounting. While, at present, IMID specific activity on monaminergic system is not yet conclusive, it is demonstrated that, at the doses used, YOH and clonidine are selective alpha 2 antagonist and agonist, respectively; B-HT 920 preferentially stimulates D2 receptors at 50 micrograms/Kg and alpha 2 receptors at 2 mg/Kg; finally DPI, proposed as DAI agonist, also activates alpha 2 receptors. Therefore, in view of the dose-related receptorial selectivity of action of the drugs tested, neurochemical mechanisms on specific receptors involved for modulation of this form of sexual behaviour are briefly discussed.

Animals↗
PubMed1986

Long term-effect of fenofibrate on lipoprotein level and composition in different types of genetic hyperlipidemias.

Fenofibrate effect on plasma lipids and lipoproteins was studied in 23 patients with primary hyperlipoproteinemias (HLP): 12 with familial hypercholesterolemia (FH), 5 with combined HLP and 6 with Type III HLP. Trial lasted from 8 to 10 months. Cholesterol and triglycerides were significantly reduced in all patients as follows: cholesterol dropped 26% in FH (p less than 0.001), 32% in combined HLP and 48% in type III HLP; triglycerides dropped 29%, 64% and 72% respectively. This drop involved LDL in FH, VLDL and LDL in combined HLP and beta-VLDL in type III HLP patients. In FH and combined HLP patients we observed a +10% (p less than 0.01) and a +9% (n.s.) increase of HDL, respectively. Two patients had a mild SGOT and SGPT increase and three had a vescicular cutaneous erythema.

Cholesterol↗
PubMed1986

Lipoprotein modifications during dietary treatment in patients with primary type V hyperlipoproteinaemia.

Type V hyperlipoproteinaemia is a disorder of lipid transport characterized by the accumulation in serum of chylomicrons and very low density lipoproteins. The purpose of the study was the analysis of serum lipids and lipoproteins by ultracentrifugation in nine patients with primary type V hyperlipoproteinaemia before and during dietary treatment. After 30 days of balanced isocaloric diet mean serum triglycerides fell from 25.4 +/- 15.0 (mean +/- SD) to 2.8 +/- 1.7 mmol l-1. At the same time the chylomicrons and the very low density lipoproteins of flotation rate higher than 100 disappeared from the serum while the remaining very low density lipoproteins maintained unaltered their normal protein-lipid composition. After 30 days the low density lipoproteins increased significantly in concentration (from 1.6 +/- 0.8 to 4.1 +/- 1.1 mmol l-1 cholesterol) and their percentage content of cholesterol and triglyceride was increased and reduced, respectively. The highest concentration of intermediate density lipoprotein cholesterol was observed after 15 days of treatment (1.2 +/- 0.6 mmol l-1. The abnormally low concentrations and the physicochemical properties of the high density lipoproteins remained unchanged throughout the study (from 0.6 +/- 0.2 to 0.8 +/- 0.2 mmol l-1 cholesterol concentration) and no high density lipoproteins two (HDL2) were observed at any time. The effects of this treatment were an increase in low density and marginal change in high density lipoproteins which are considered, respectively, a positive and a negative risk factor for atherosclerosis.

Adult↗
PubMed1986

Apolipoprotein C-II deficiency syndrome. Clinical features, lipoprotein characterization, lipase activity, and correction of hypertriglyceridemia after apolipoprotein C-II administration in two affected patients.

Two patients (brother and sister, 41 and 39 yr of age, respectively) have been shown to have marked elevation of plasma triglycerides and chylomicrons, decreased low density lipoproteins (LDL) and high density lipoproteins (HDL), a type I lipoprotein phenotype, and a deficiency of plasma apolipoprotein C-II (apo C-II). The male patient had a history of recurrent bouts of abdominal pain often accompanied by eruptive xanthomas. The female subject, identified by family screening, was asymptomatic. Hepatosplenomegaly was present in both subjects. Analytical and zonal ultracentrifugation revealed a marked increase in triglyceride-rich lipoproteins including chylomicrons and very low density lipoproteins, a reduction in LDL, and the presence of virtually only the HDL3 subfraction. LDL were heterogeneous with the major subfraction of a higher hydrated density than that observed in plasma lipoproteins of normal subjects. Apo C-II levels, quantitated by radioimmunoassay, were 0.13 mg/dl and 0.12 mg/dl, in the male and female proband, respectively. A variant of apo C-II (apo C-IIPadova) with lower apparent molecular weight and more acidic isoelectric point was identified in both probands by two-dimensional gel electrophoresis. The marked hypertriglyceridemia and elevation of triglyceride-rich lipoproteins were corrected by the infusion of normal plasma or the injection of a biologically active synthesized 44-79 amino acid residue peptide fragment of apo C-II. The reduction in plasma triglycerides after the injection of the synthetic apo C-II peptide persisted for 13-20 d. These results definitively established that the dyslipoproteinemia in this syndrome is due to a deficiency of normal apo C-II. A possible therapeutic role for replacement therapy of apo C-II by synthetic or recombinant apo C-II in those patients with severe hypertriglyceridemia and recurrent pancreatitis may be possible in the future.

Adult↗
PubMed1986

Studies on epinephrine-induced lung edema in the rat. I. Selective alpha 1-adrenoceptor involvement.

Phentolamine (Phe) prevents the induction by epinephrine (E: 1800 nmol/kg, i.v.) of lung edema (LE) in urethane-anesthetized and bivagotomized rats in a dose-related manner (from 246 to 3933 nmol/kg, i.v.). Since Phe blocks and E activates both alpha 1- and alpha 2-adrenoceptors, the evidence does not allow us to link LE to selective (alpha 1 or alpha 2) or non-selective (alpha 1 + alpha 2) alpha-adrenoceptor activation. Accordingly, we tried to find out whether: phenylephrine (PE), a selective alpha 1-adrenoceptor agonist, and B-HT 920, a selective alpha 2-adrenoceptor agonist, would cause LE; prazosin (Praz), a selective alpha 1-adrenoceptor antagonist, and yohimbine (Yoh), a selective alpha 2-adrenoceptor antagonist, would protect rats against LE caused by E or PE. We found that: 1) PE (from 736 to 5892 nmol/kg, i.v.), but not B-HT 920 (from 190 to 12200 nmol/kg, i.v.), caused LE, while both drugs increased arterial blood pressure; 2) Praz prevented induction of LE, whether by E (1800 nmol/kg, i.v.) or by PE (5892 nmol/kg, i.v.), in a dose-related manner (from 15 to 119 nmol/kg, i.v.). In contrast, Yoh was ineffective at doses up to 7675 nmol/kg, i.v. We conclude, therefore, that E-induced LE in urethane-anesthetized and bivagotomized rats strictly depends on alpha 1-adrenoceptor activation. The outcome of E-induced LE is usually rat death, the incidence of which depends on the dose. Since alpha 1-adrenoceptor agonists rank in the same order of potency for the induction of death as for that of LE, and since Phe and Praz protect from death at LE-preventing doses, there seems to be some link between LE and death, even though protection against death is obtained with doses of antagonists lower than those abolishing induction of LE. Finally, alpha 1-agonists cause maximum arterial hypertension at all doses used, irrespective of induction of LE and of protective pretreatment against LE.

Animals↗
PubMed1986

Modifications of plasma lipoproteins after lipase activation in patients with chylomicronemia.

Lipoprotein lipase (LPL) and hepatic lipase (HL) are enzymatic activities involved in lipoprotein metabolism. The purpose of this study was to analyze the physicochemical modifications of plasma lipoproteins produced by LPL activation in two patients with apoC-II deficiency syndrome and by HL activation in two patients with LPL deficiency. LPL activation was achieved by the infusion of normal plasma containing apoC-II and HL was released by the injection of heparin. Lipoproteins were analyzed by ultracentrifugation in a zonal rotor under rate flotation conditions before and after lipase activation. The LPL activation resulted in: a reduction of plasma triglycerides; a reduction of fast-floating very low density lipoprotein (VLDL) concentration; an increase of intermediate density lipoprotein (IDL), which maintained unaltered flotation properties; an increase of low density lipoproteins (LDL) accompanied by modifications of their flotation rates and composition; no significant variations of high density lipoprotein (HDL) levels; and an increase of the HDL flotation rate. The HL activation resulted in: a slight reduction of plasma triglycerides; a reduction of the relative triglyceride content of slow-floating VLDL, IDL, LDL2, and HDL3 accompanied by an increase of phospholipid in VLDL and by an increase of cholesteryl ester in IDL; and a reduction of the HDL flotation rate. These experiments in chylomicronemic patients provide in vivo evidence that LPL and HL are responsible for plasma triglyceride hydrolysis of different lipoproteins, and that LPL is particularly involved in determining the levels and physicochemical properties of LDL. Moreover, in these patients, the LPL activation does not directly change the HDL levels, and LPL or HL does not produce a step-wise conversion of HDL3 to HDL2 (or vice versa) but rather modifies the flotation rates of all the HDL molecules present in plasma.

Adult↗
PubMed1986

Studies on epinephrine-induced lung edema in the rat. II. Hemodynamic changes.

In order to elucidate the pathogenesis of epinephrine (E)-induced lung edema (LE) as well as the mechanism of protection afforded by alpha-adrenoceptor blockade in urethane-anesthetized and bivagotomized rats, we investigated the influence of phentolamine (Phe) and prazosin (Praz) on arterial hypertension and LE provoked by continuous intravenous infusion of E and on blood pressure changes in left (LHV) and right (RHV) heart ventricles caused by a bolus injection of E at a LE-producing dose (1800 nmol/kg). Our results show that neither LE nor death are related to E-induced hypertension and also that LE-induction is accompanied by significant increases in LHV (telediastolic and systolic) as well as in RHV (systolic) pressures, of which the LHV telediastolic and the RHV systolic pressure increases are prevented by Phe and Praz at a dose capable of counteracting E-induced LE. The significance of this finding is briefly discussed.

Animals↗
PubMed1986

Antagonism of imidazole-induced shaking in the rat: a behavioural tool predictive of antidyskinetic activity?

In rats the intraperitoneal injection of imidazole (IMID) induced shaking behaviour, the effect appearing to be age- and sex-linked; younger animals responded less vigorously than older animals, while females always exhibited a significantly weaker response than males of the same age. After ovariectomy, however, the number of shakes of the two sexes was very similar. A number of drugs were examined for their antagonism of this highly reproducible syndrome. IMID-shakes were antagonized by reserpine, clonidine, high doses of B-HT 920, propranolol, haloperidol, morphine and diazepam, were not affected by apomorphine, (+)3-PPP, physostigmine, naloxone or methysergide, and were potentiated by sulpiride and scopolamine. The results are considered in the light of the possible neurochemical mechanisms underlying the IMID-syndrome; the suggested usefulness of this test for the study of human dyskinetic movements is disputed.

Aging↗
PubMed1985

The dopamine autoreceptor agonist B-HT 920 markedly stimulates sexual behavior in male rats.

B-HT 920, a selective agonist at dopamine (DA) autoreceptors, strongly increased the incidence of penile erections (PE) in male rats, an effect which was dose-related and antagonized by haloperidol. B-HT 920 at 100 and 200 micrograms/kg i.p. significantly altered the copulatory pattern of sexually active male rats, reducing the number of mounts and intromissions as well as the latency to the first ejaculation, a stimulant effect which was confirmed in sluggish males at a dose of 100 micrograms/kg.

Animals↗
PubMed1985

Influence of imidazole on behavioral effects induced by dopaminergic agonists in rats.

Imidazole (IMI) (from 18.7 to 300 mg/Kg) i.p. injected in adult rats induced shaking, which was antagonized by both morphine (MOR) and haloperidol (HALO) but not by methysergide (MET). I.p. IMI pretreatment inhibited the penile erections (PE) and stretching and yawning (SY) typically elicited by N-n-propylnorapomorphine (NPA), a well-known CNS dopamine (DA) receptor stimulant, injected either i.p. or i.c.v., whereas it enhanced stereotyped behavior (SB). IMI had similar effects on the same parameters considered when injected before lisuride, an ergot derivative also active as a central DA receptor agonist. In this case not only SB but also and above all aggressiveness were markedly potentiated, both the signs appearing at doses of lisuride which were "per se" ineffective. Aggressiveness, like SB, was not sex linked and was antagonized by HALO and MOR, but not by MET. IMI alone potentiated the fighting induced by electrical shock, an effect which was abolished by HALO pretreatment. Considering the results obtained as a whole it is submitted that IMI antagonizes PE and SY through a selective blockade of a class of DA receptors, presumably DA presynaptic autoinhibitors, thus potentiating SB and aggressiveness, which involve stimulation of DA postsynaptic receptors.

Adrenergic Agonists↗
PubMed1985

Influence of cimetidine, ranitidine and imidazole on the behavioral effects of (+/-) N-n-propylnorapomorphine in male rats.

Cimetidine injected IP 15 min before (+/-) N-n-propylnorapomorphine (NPA) antagonized in dose-dependent fashion the penile erections (PE) and stretching and yawning (SY) induced by this typical dopaminergic agonist in male rats. Ranitidine, which acts on H2 histamine receptors in much the same way as cimetidine despite its lack of an imidazole ring, failed to produce the same effect. On the other hand, imidazole itself was similar to cimetidine in antagonizing PE and SY induced by (+/-) NPA, whether injected IP or ICV. Neither imidazole nor cimetidine antagonized the stereotyped behaviour (SB) induced by (+/-) NPA. Indeed, imidazole reduced the latency of this response. A mechanism which may underly these effects is discussed, as well as the possible preclinical use of this test in animals.

Animals↗
PubMed1985

Characterization of the contractile activity of dopamine on the rat isolated seminal vesicle.

The mechanism of the contractile effect of dopamine (DA) on the rat isolated seminal vesicle was studied. Cocaine (10 microM/1 in the organ bath, 30 min before DA) and 6-OHDA (50 mg/kg i.v. 24 hr before removal of the seminal vesicle) almost completely prevented the contractile effect of DA. Drugs known to have an affinity for DA receptors or for alpha-adrenoceptors antagonized the contractile effect of DA, the rank order of potency being: prazosin greater than phentolamine greater than yohimbine greater than clonidine greater than sulpiride greater than apomorphine greater than haloperidol. The antagonism was in each case greater against DA than against noradrenaline (NA), used for comparison; selectivity for DA being highest in the case of prazosin and sulpiride. Taken together, these findings indicate that DA makes the rat seminal vesicle contract mostly by means of an indirect mechanism, binding presynaptic DA-receptors and, in part, presynaptic alpha-adrenoceptors as well; or, alternatively, binding presynaptic DA-receptors which have some links with alpha 2-adrenoceptors; the consequence being in either case the release of NA from sympathetic nerve endings.

Animals↗
PubMed1985

Lipoprotein metabolism in patients with elevated lipoprotein-lipase activity in adipose tissue.

We have evaluated the relationships between adipose tissue lipoprotein-lipase activity (AT-LPL) or post-heparin plasma lipolytic activity (PHLA) and the composition of circulating lipoproteins in 7 patients with multiple symmetric lipomatosis (MSL). In addition we have investigated the behaviour of serum triglycerides after an oral fat load (1 g triglycerides/kg body weight) in 5 MSL patients and in 5 age and sex matched controls. We found significantly higher values of HDL, HDL2 and HDL3 cholesterol in MSL patients than in controls. Moreover, HDL2/HDL3 cholesterol ratio was higher in MSL patients than in controls, which indicate a predominant increase in HDL2 subfraction. The mean values of AT-LPL in lipomatous tissue was significantly higher than in control tissue. A positive statistically significant correlation was found between AT-LPL activity and HDL, HDL2 and HDL3 cholesterol values. After the fat load the maximal increments of serum triglyceride levels and the triglyceride areas over 8 and 12 h are lower in MSL patients than in controls; there was an inverse, statistically significant correlation between the total PHLA or the extrahepatic PHLA values and the triglyceride areas after lipid load. We conclude that MSL represents a useful naturally occurring model for the study of the role of AT-LPL in the metabolism of triglyceride-rich lipoproteins and in the clearance of lipoproteins in the post-prandial phase.

Adipose Tissue↗
PubMed1984

Analysis of the apoC-II gene in apoC-II deficient patients.

Apolipoprotein C-II (apoC-II), a 79 amino acid protein, is a cofactor for lipoprotein lipase, the enzyme which catalyzes the lipolysis of triglycerides on plasma chylomicrons and VLDL. Patients with apoC-II deficiency have marked elevations in plasma triglycerides, chylomicrons, VLDL, and a type I hyperlipoproteinemia. In order to evaluate the molecular defect in apoC-II deficiency, genomic DNA was analyzed using Southern Blot from 2 independent apoC-II deficient patients and compared to normal controls. Restriction digests of genomic DNA were performed with five different enzymes and the restriction fragments analyzed utilizing a 354 base pair nick-translated apoC-II probe for hybridization following Southern blotting. The restriction fragments varied from 0.8 to 21 Kb, and the pattern with normal DNA was identical to that of the two apoC-II deficient patients. The present study reveals that the apoC-II gene is present in patients with apoC-II deficiency. In addition, no insertional or deletional polymorphism was detected in the apoC-II gene of apoC-II deficient patients.

Adult↗