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Biomedical subjects

A Bertolini

Publications and source records attributed to A Bertolini.

At least 163 records · Page 9Linked to original sources
PubMed1989

[3H]imipramine binding in discrete brain areas is affected by castration in male rats.

In adult male rats, castration induces a progressive decrease in the number of [3H]imipramine binding sites in the cerebral cortex and hypothalamus, and a progressive increase in the hippocampus. Testosterone completely prevents this effect of castration, but has no effect on the characteristics of brain imipramine binding sites in intact, non-castrated animals. These data suggest that threshold levels of testosterone are necessary for the maintenance of a normal number of imipramine binding sites in the rat brain, but that these binding sites are not modified by excess testosterone.

Animals↗
PubMed1989

Bombesin reverses bleeding-induced hypovolemic shock, in rats.

In an experimental model of bleeding-induced hypovolemic shock causing the death of all saline-treated rats within 26 +/- 4 min, the intravenous injection of bombesin (2.5, 5 or 10 micrograms/kg) dose-dependently restored blood pressure, pulse amplitude, heart rate and respiratory function, and improved survival rate as assessed at the end of the experiment (2 h). The effect on cardiovascular and respiratory functions was prompt (within 1-2 min) and sustained. The release of cholecystokinin seems to be the main mechanism of action, because the anti-shock effect of bombesin is largely prevented by the CCK-antagonist, L-364,718.

Animals↗
PubMed1989

ODC-polyamine system is involved in morphine analgesia.

alpha-Difluoromethylornithine (DFMO) directly infused into a brain-lateral ventricle (12.5, 25 and 50 micrograms/rat) dose- and time-dependently inhibited brain ODC activity. While having no influence per se on pain threshold, DFMO significantly inhibited the analgesic activity of morphine (15 mg/kg i.p.), this effect being obtained when brain ODC activity was reduced by at least 80%. On the other hand, DFMO had no influence on number and affinity of brain opiate binding sites. Morphine per se neither modified whole brain ODC activity nor significantly affected the ODC inhibitory effect of DFMO. In more discrete brain areas (midbrain, brainstem) morphine actually increased ODC activity. The present results indicate that brain ODC/polyamines system may play a role in the analgesic activity of opioids, probably at a post-receptorial level or through a non-opiate receptor-linked mechanism.

Analgesia↗
PubMed1989

Influence of ovariectomy, estradiol and progesterone on the behavior of mice in an experimental model of depression.

In the tail suspension test (an animal model of depression) the duration of immobility during the 6 min of observation was 56.84 +/- 6.54 sec in sham-ovariectomized mice and 113.11 +/- 7.86 sec 30-32 days after ovariectomy. Estradiol (10, 100 or 1,000 micrograms/kg) and progesterone (50, 1,000 or 10,000 micrograms/kg), subcutaneously injected daily 4 times before the test, restored the duration of immobility in ovariectomized mice to normal, while having no effect on sham-operated animals. On the other hand, desipramine (20 mg/kg IP 1 hr before testing) significantly reduced the duration of immobility both in ovariectomized and in sham-operated mice. These data indicate that ovarian sex hormones, while having no "antidepressant," desipramine-like, effect on the behavior of intact adult female mice, have such an effect in ovariectomized mice, and enable the animal to cope in a "normal" way with adverse environmental situations.

Animals↗
PubMed1989

The adrenocorticotropic hormone (ACTH)-induced reversal of hemorrhagic shock.

Adrenocorticotropic hormone (ACTH), while having negligible effects on cardiovascular function in the intact animal, induces a potent and sustained reversal of an otherwise invariably, rapidly fatal condition of hemorrhage-induced hypovolemic shock, in rats and dogs. The main site(s) of action are at the peripheral level; however, subsidiary site(s) of action in the CNS cannot be excluded. The studies on the mechanism of action indicate that the ACTH-induced reversal of hemorrhagic shock (a) is an extra-hormonal, adrenal-independent effect, because it is not affected by adrenalectomy and is shared by many ACTH-fragments practically devoid of corticotropic activity; (b) is antagonized by morphine in a surmontable way; (c) needs the functional integrity of the sympathetic nervous system (it is prevented by guanethidine, reserpine, and clonidine) and the availability of peripheral alpha-adrenoceptors (it is antagonized by dibenamine, prazosin and yohimbine, but not by practolol); (d) requires the integrity of afferent vagal fibers (it is almost completely abolished by vagotomy); (e) involves central cholinergic networks (it is antagonized by atropine sulphate, but not by atropine methyl bromide; and it is prevented by the intracerebroventricular injection of hemicholinium-3); (f) is associated with a massive increase in the volume of circulating blood, likely due to a mobilization from peripheral pooling sites (it is largely prevented by splenectomy or by suprahepatic veins ligature, and is associated with a restoration of the venous blood flow in peripheral vascular beds and with a normalization of venous PO2); (g) is associated with a restoration of heart and spleen adrenoceptors, whose number is significantly decreased during hemorrhagic shock. The survival time of hemorrhage-shocked animals, which is 26 +/- 3 min in controls, is greatly prolonged (44 +/- 18 h) by ACTH, provided that the treatment is made within 5-10 min after bleeding. Finally, in animals treated with ACTH within 5-10 min after bleeding, blood reinfusion retains its effectiveness and reverse shock even if performed 2-5 h later.

Adrenocorticotropic Hormone↗
PubMed1989

Adrenocorticotropic hormone (ACTH) and centrally-acting cholinomimetic drugs improve survival of rats with severe hemorrhagic shock through distinct central cholinergic mechanisms.

Pharmacological doses (40-160 micrograms/kg) of adrenocorticotropic hormone (ACTH) intravenously injected to urethane-anesthetized rats subjected to otherwise lethal hemorrhagic shock (mean arterial pressure stabilized at 20-25 mmHg) promptly restore blood pressure to about the pre-bleeding values, and prevent death (anti-shock effect). Hemicholinium-3 (i.c.v. injected) and atropine sulphate, but not atropine methylbromide, antagonize these ACTH effects. Moreover, since pirenzepine, injected i.v. or i.c.v., does not affect the anti-shock activity of ACTH, the central cholinergic mechanism participating in this ACTH action must involve M2, but not M1 brain muscarinic receptors. Intravenous physostigmine, too (but not neostigmine) and oxotremorine have an ACTH-like anti-shock effect, which however is neither affected by hemicholinium-3, nor by atropine methylbromide, nor by atropine sulphate, but only by high i.c.v. doses of gallamine or pancuronium. On the other hand, reserpine, guanethidine, and alpha-adrenoceptor blocking drugs inhibit the anti-shock effect of ACTH as well as that of oxotremorine and physostigmine. It is suggested that, in rats, both ACTH and cholinergic drugs must activate a central cholinergic mechanism(s) in order to exert a sympathetic nerve-mediated anti-shock effect. However, receptors involved are of the muscarinic M2 subtype in the case of ACTH, and probably nicotinic in the case of cholinergic drugs. That ACTH and cholinergic drugs activate different central cholinergic mechanisms is also suggested by the fact that cholinergic drugs have a centrally-mediated hypertensive action in normal animals, which is not shared by ACTH.

Adrenocorticotropic Hormone↗
PubMed1989

Effect of castration and testosterone in experimental models of depression in mice.

In the behavioral despair (forced swimming) test and in the tail-suspension test, long-term (30-32 days) castration significantly increased the duration of immobility in mice. Testosterone propionate (1 or 10 mg.kg-1.day sc for 4 days), although not affecting the duration of immobility in sham-operated mice, reduced the duration of immobility in castrated mice to within normal limits. Desipramine (20 mg/kg ip) decreased the duration of immobility both in sham-operated and in castrated animals. These results indicate that castration favors an inactive behavior and that testosterone, although having no "antidepressant" effect per se, is necessary for the male animal to cope normally with adverse environmental situations.

Affect↗
PubMed1989

Reversal of haemorrhagic shock in rats by cholinomimetic drugs.

1. In an experimental model of haemorrhagic shock resulting in the death of all rats within 20-30 min, the intravenous (i.v.) injection of the tertiary amine cholinesterase inhibitor physostigmine (17-70 micrograms kg-1) induced a prompt, sustained and dose-dependent improvement of cardiovascular and respiratory function, with marked increase in the volume of circulating blood and survival of all treated animals, at least for the 2 h of observation. 2. Similar results were obtained with the i.v. injection of the cholinoceptor agonist oxotremorine (5-25 micrograms kg-1), while neostigmine (54 or 70 micrograms kg-1), a quaternary cholinesterase inhibitor which cannot cross the blood-brain barrier, had negligible effects. 3. The anti-shock activities of oxotremorine and physostigmine were blocked by the intracerebroventricular injection of either of the combined nicotinic and M2-muscarinic receptor antagonists gallamine and pancuronium, or of the nicotinic antagonist mecamylamine. They were also blocked by intraperitoneal injection of the adrenergic neurone blocking agent guanethidine, but they were not antagonized by either the combined M1- and M2-muscarinic receptor antagonist atropine, the M1-muscarinic receptor antagonist pirenzepine, or the M2-muscarinic receptor 4-diphenylacetoxy-N-methylpiperidine methobromide. 4. It is concluded that cholinomimetic drugs can reverse hypovolaemic shock through central activation (seemingly mediated by nicotinic receptors) of sympathetic tone, with mobilization and redistribution of the residual blood.

Animals↗
PubMed1989

Putrescine reverses aconitine-induced arrhythmia in rats.

Putrescine, (150-300 mg kg-1 i.v.) injected into anaesthetized rats reversed aconitine-induced arrhythmia and restored sinus rhythm. In the same experimental model, quinidine and lignocaine had a transient therapeutic effect, procainamide was practically ineffective and verapamil worsened the aconitine arrhythmia, causing the death of all treated animals. These data demonstrate that putrescine has an antiarrhythmic effect in an experimental model particularly resistant to usual antiarrhythmic treatments.

Aconitine↗
PubMed1989

[Comparison of high-resolution arterial echography and angiography in the diagnosis of atheromatous lesions of the external carotid].

Personal experience about a correlative study on ultrasonographic and angiographic methods executed on carotid artery is reported. Usual techniques are described and result discordances are considered. Stenosis level is subdivided in four different types: normal, less than 45, 45-75%, greater than 75%. Authors examine in which stenosis range one technique can be superimposed on the other one and show limits and possibilities. Moreover complementary and interdependence position of these two techniques are stressed with respect to atherosclerotic disease study.

Arteriosclerosis↗
PubMed1989

[Clinical assessment of syncopes].

Syncope is a relatively common clinical problem and causes 1% of hospitalizations. The clinical syndrome is characterized by a sudden reduction of the cerebral flow secondary to a number of conditions that includes benign, self-limited causes and life-threatening arrhythmias. A high percentage of these patients is discharged from hospital without an etiological diagnosis. The purpose of this short review is to present the classification of syncope and suggest the methodological approach to detect the underlying cause. The importance of patient's age and of a cardiovascular etiology as a negative prognostic index is stressed. The most valuable diagnostic tool remains a thoroughly taken clinical history.

Humans↗
PubMed1988

[Nle4,D-Phe7]alpha-MSH improves functional recovery in rats subjected to diencephalic hemisection.

Rats subjected to diencephalic hemisection were s.c. treated with alpha-MSH (20 micrograms/rat daily) or with [Nle4,D-Phe7]alpha-MSH (10 micrograms/rat every other day) for two weeks starting on day 3 after lesion. Apomorphine-induced (1 mg/kg s.c.) rotational behavior was studied on days 7, 14 and 21 after lesion, and a sensorimotor test battery was carried out on days 3, 10, 17 and 24 after lesion. [Nle4,D-Phe7]alpha-MSH greatly reduced rotational behavior and significantly improved sensorimotor performance. Histological studies showed that treatment with alpha-MSH and, even more markedly, with [Nle4,D-Phe7]alpha-MSH reduced the size of the lesion and the pseudoinflammatory reaction, and caused a marked proliferation and hypertrophy of astroglia. Binding studies showed that no supersensitivity of striatal dopamine receptors developed on the lesioned side of alpha-MSH- and [Nle4,D-Phe7]alpha-MSH-treated rats. The present results seem to further support the trophic role of MSH peptides on nerve tissue.

Animals↗
PubMed1988

In utero ultrasound diagnosis of congenital heart disease.

Two hundred and one pregnancies considered at high risk for congenital heart disease (CHD) underwent fetal cross-sectional echocardiographic (CSE) examination. In 190 cases a structurally normal heart was correctly predicted; seven cases of CHD were identified, but in two of them the specific diagnosis was inaccurate. One false positive diagnosis of a small ventricular septal defect was made. There were three false negative diagnoses: two of ventricular septal defects and one of aortic coarctation. We conclude that severe heart malformations can be reliably identified or excluded by CSE in utero, but important anatomical details may be missed. Therefore, prognosis should be based only on the structures identified to multiple-scan planes.

Echocardiography↗
PubMed1988

Involvement of the sympathetic nervous system in the cardiovascular effects of ACTH-(1-24) during hemorrhagic shock in rats.

In urethane-anesthetized rats, removal of about 50% of the total blood volume over a period of 25-30 min caused hypovolemic shock, with extreme hypotension (MAP = 18-25 mm Hg and death of all animals within 22 +/- 5 min. The i.v. injection of ACTH-(1-24) in the dose range of 40-160 micrograms/kg induced a sustained, dose-dependent, and, at the highest dose used, an almost complete recovery of blood pressure, and 100% survival, at least for 2 h after treatment. The effect of ACTH-(1-24) was completely prevented by reserpine (5 mg/kg) and clonidine (0.1 mg/kg), significantly reduced by prazosin (0.1 mg/kg), dibenamine (15 mg/kg) and i.v. yohimbine (1 mg/kg) and unaffected by i.c.v. yohimbine (0.2 mg/kg) and i.v. practolol (15 mg/kg). These data suggest that the effect of ACTH-(1-24) in hypovolemic shock depends on the functional integrity of the sympathetic nervous system and is mediated through an activation of peripheral alpha-adrenoceptors.

Animals↗