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Biomedical subjects

S Tagliavini

Publications and source records attributed to S Tagliavini.

At least 19 recordsLinked to original sources
PubMed1992

Capsaicin prevents the adrenocorticotropin-induced improvement of cardiovascular function and survival in hemorrhage-shocked rats.

A volume-controlled hemorrhagic shock was produced in anesthetized rats by intermittent bleeding from an iliac vein over a period of 20-30 min, until the carotid mean arterial pressure (MAP) stabilized around 20-24 mmHg. In this condition, which caused the death of all saline-treated animals within 25-30 min, the intravenous (i.v.) bolus injection of the adrenocorticotropin fragment 1-24 (ACTH(1-24)) at a dose of 160 micrograms/kg promptly restored MAP, as well as pulse pressure, heart rate and respiratory function, and greatly prolonged the survival time. Capsaicin (125 mg/kg cumulatively, s.c., 1 week before) completely prevented the anti-shock effect of ACTH(1-24), which, on the other hand, was shared by i.v. [Nle11]-substance P (SP) (200-300 micrograms/kg). Finally the SP-antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]-SP prevented the effect of ACTH(1-24). These results suggest that SP-containing nerve fibers are required for the effect of ACTH in hemorrhagic shock.

Adrenocorticotropic Hormone↗
PubMed1992

Reversal of experimental hemorrhagic shock by dimethylphenylpiperazinium (DMPP).

In a rat model of hemorrhagic shock which caused the death of all control rats within 30 min, i.v. injection of the ganglion-stimulating drug dimethylphenylpiperazinium (DMPP) caused a dose-dependent reversal of the shock condition--without the need for reinfusion of the shed blood--starting from the dose of 4 ng/kg i.v. Shock reversal was associated with the mobilization of residual blood and improvement in blood flow, particularly at the carotid level. These results could influence our thinking on pathophysiology and first-aid management of shock.

Animals↗
PubMed1991

Ischemia- and reperfusion-induced arrhythmias are prevented by putrescine.

The influence of putrescine on cardiac arrhythmias induced by either permanent ligature of the left anterior coronary artery or heart reperfusion following a 5-min coronary occlusion was studied in anesthetized rats. Reperfusion-induced arrhythmias were significantly prevented by the i.v. injection of 150-200 mg/kg of putrescine, the survival rate being 100% in treated animals and 40% in controls. At a dose level of 200-300 mg/kg i.v., putrescine also significantly reduced the duration of ventricular tachycardia induced by permanent coronary occlusion. These findings show that putrescine significantly reduces the consequences of cardiac ischemia and reperfusion, probably as a consequence of its multiple stabilizing effects at the membrane level.

Anesthesia↗
PubMed1991

Nicotine reverses hemorrhagic shock in rats.

Cholinergic mechanisms are currently thought to play an essential role in blood pressure homeostasis. Here we show that, in urethane-anaesthetized rats bled to severe hemorrhagic shock, the i.v. administration of nicotine 0.2-50 micrograms/kg causes a prompt, sustained and dose-dependent improvement in cardiovascular and respiratory functions, the animals' survival rate being significantly higher than that of animals treated with saline. These effects are prevented by bilateral cervical vagotomy and by concurrent local anaesthesia of the carotid bodies, which suggests that stimulation of visceral afferents is the main mechanism of action of nicotine in hemorrhagic shock.

Animals↗
PubMed1991

TRH reverses the ECG and EEG ischemic changes induced by massive hemorrhage in rats.

In a rat model of volume-controlled hemorrhagic shock causing the death of all saline-treated animals within 30 min of treatment, the intravenous bolus injection of thyrotropin- releasing hormone tartrate (TRH-T) at the dose of 4 mg/kg induced the prompt and sustained disappearance of the ECG and EEG signs of heart and brain ischemia, along with the reversal of hypotension and respiratory depression and with 100% survival rate at the end of the 2 h observation period. These data confirm that, in a pre-terminal condition induced by massive hemorrhage, timely treatment with TRH-T will restore heart and brain perfusion to levels compatible with survival and with functional recovery from ischemia and maintain it at those levels for some hours.

Animals↗
PubMed1991

Influence of TRH on regional blood flow and metabolic acidosis in a model of volume-controlled hemorrhagic shock in rats.

In anesthetized rats, massive bleeding to a severe condition of hemorrhagic shock (invariably leading to death within 30 min) was obviously associated with a dramatic decrease in tissue blood flow and with profound modifications of several blood parameters leading to metabolic acidosis: decrease in arterial and venous pH, bicarbonate and BE, decrease in arterial pCO2 and in venous pO2 and SO2, increase in arterial pO2, venous pCO2 and venous lactate. The i.v. bolus injection of protirelin tartrate (TRH-T, 4 mg/kg), which produces a prompt and sustained reversal of the shock condition, caused a rapid increase in venous pO2, pCO2 and SO2; on the other hand, arterial and venous pH, bicarbonate and BE continued to decrease--and venous lactate to increase during the first few minutes after treatment. However venous pCO2 and lactate, as well as arterial and venous pH, returned to the pre-bleeding values within 60 min after treatment. The data are in keeping with the TRH-T-induced improvement of circulatory and respiratory functions, with mobilization of the residual blood from its capillary pooling and consequent immission of acid metabolites into the blood stream.

Acidosis↗
PubMed1991

Afferent vagal fibres and central cholinergic mechanisms are involved in the TRH-induced reversal of haemorrhagic shock.

In a model of haemorrhagic shock causing the death of all saline-treated rats within 25.8 +/- 2.7 min after treatment, the intravenous injection of thyrotropin-releasing hormone tartrate (TRH-T) at the dose of 4 mg/kg induces a prompt and sustained increase of arterial pressure and pulse amplitude, with survival of all rats. Bilateral vagotomy, atropine sulphate (2 mg/kg intraperitoneally) and hemicholinium-3 (20 micrograms/rat intracerebroventricularly) partially prevent the TRH-T-induced shock reversal, whereas atropine methylbromide has no effect. These data indicate that afferent vagal fibres, brain cholinergic neurons and central muscarinic receptors play a role in the mechanism of the anti-shock effect of TRH-T.

Animals↗
PubMed1991

Antidiuretic and nephrotoxic effects of putrescine in rats.

Putrescine, intraperitoneally injected either into intact or into hypophysectomized rats, caused a reduction in urine volume at doses of 200-300 mg/kg. At doses of 100 mg/kg or more, there was also a significant loss of potassium. The highest dose (300 mg/kg) caused haemoglobinuria, proteinuria, increased natriuresis, increased urinary osmolarity, reduced aldosteronaemia, ectasis of glomerular capillaries and tubular damage. The underlying mechanism(s) are probably mostly linked to the strong cationic charge of putrescine and to its binding to fixed anions of tubular-cell membrane.

Animals↗
PubMed1990

Influence of gonadotropin-releasing hormone on castration-induced 'depression' in mice: a behavioral and binding study.

Long-term (33-35 days) castration caused a significant increase in the duration of immobility of male and female mice in the tail suspension test (an animal model of depression), and a significant decrease in the maximum number (Bmax) of [3H]imipramine binding sites in the cerebral cortex of male mice. In the tail suspension test, gonadotropin-releasing hormone (GnRH), s.c. injected 3 times at 3-h intervals at doses of 0.2, 2 or 20 micrograms/kg, did not significantly modify the duration of immobility of castrated animals and did not reduce that of sham-operated ones, while desipramine (20 mg/kg s.c. 1 h before testing) restored immobility to normal in castrated animals and reduced it significantly in sham-operated ones. The same treatment schedule with GnRH produced an increase in the number of [3H]imipramine Bmax in cortical membranes that was statistically significant at the dose of 2 micrograms/kg. It is concluded that the castration-induced depression-like behavior in mice seems not to be due to the decreased levels and release of GnRH, and that GnRH has no antidepressant-like effect in mice, at least at our dose levels; however, GnRH seems to increase the number of cortical [3H]imipramine binding sites.

Animals↗
PubMed1990

Circulatory and respiratory consequences of massive hemorrhage are reversed by protoveratrines.

In a rat model of severe hypotension and respiratory depression induced by step-wise bleeding, protoveratrines cause a prompt and sustained improvement of cardiovascular and respiratory functions, both in anesthetized and in conscious animals, seemingly through a magnification of the reflex response originated by the chemoreceptors of aortic and carotid bodies. The restoration of cardiovascular function is attributable to an increase both in total peripheral resistance and cardiac output. The finding could provide the basis for a new approach to the first-aid management of massive blood losses.

Animals↗
PubMed1990

Brain M3 muscarinic receptors are involved in the ACTH-induced reversal of hemorrhagic shock.

In an experimental model of bleeding-induced hemorrhagic shock causing the death of all saline-treated rats within 30 min, the intravenous injection of ACTH-(1-24) at the dose of 160 micrograms/kg induced a sustained reversal of the shock condition, with almost complete recovery of blood pressure, pulse amplitude, respiratory rate, heart rate, and 100% survival, at least for the 2 h of observation. This effect of ACTH-(1-24) was prevented by the intracerebroventricular injection of 4-DAMP (a highly selective antagonist for M1 and M3 muscarinic receptors), but unaffected by the intracerebroventricular injection of pirenzepine (a highly selective antagonist for M1 muscarinic receptors). These data indicate that an essential step in the complex mechanism of the ACTH-induced shock reversal may be the activation of brain M3 muscarinic receptors.

Adrenocorticotropic Hormone↗
PubMed1990

Early treatment with ACTH-(1-24) in a rat model of hemorrhagic shock prolongs survival and extends the time-limit for blood reinfusion to be effective.

The ability of ACTH-(1-24) to prolong survival and to extend the deadline for effective blood reinfusion has been studied in a model of lethal hypovolemic shock in the rat. Anesthetized rats were bled to a mean arterial pressure of 18 to 25 mm Hg and then subjected to one of the following iv treatments: a) saline; b) ACTH-(1-24), 160 micrograms/kg; c) blood reinfusion; d) ACTH-(1-24), 160 micrograms/kg; c) blood reinfusion; d) ACTH-(1-24), with saline 5 min after bleeding died within 0.05 h. On the other hand, the treatment with ACTH-(1-24) induced an almost complete and sustained recovery of cardiovascular and respiratory functions associated with a survival time of 44 +/- 18 h, while four of six rats reinfused with the withdrawn blood were still alive 15 days later. The time-lapse between bleeding and treatment was of crucial importance, and neither ACTH-(1-24) injection nor blood reinfusion had any effect if performed 25 min after bleeding. However, treatment with ACTH-(1-24) shortly after bleeding (5 min) greatly improved the effect of a later blood reinfusion. These data indicate that ACTH-(1-24) can prolong survival and permit the time-lapse between blood loss and blood reinfusion to be extended.

Animals↗
PubMed1990

Intracerebroventricular injection of hemicholinium-3 prevents the ACTH-induced, but not the physostigmine-induced, reversal of hemorrhagic shock in rats.

In rats bled to hypovolemic shock, the intracerebroventricular injection of hemicholinium-3 (20 micrograms/rat) completely prevented the shock reversal induced by the intravenous injection of ACTH (1-24) (160 micrograms/kg), but had no influence on the shock reversal induced by the intravenous injection of physostigmine (70 micrograms/kg). These data indicate that brain cholinergic neurons are involved in the anti-shock effect of ACTH-peptides, but not in that of centrally acting cholinergic drugs.

Adrenocorticotropic Hormone↗
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↗