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Biomedical subjects

A Rubino

Publications and source records attributed to A Rubino.

At least 55 records · Page 3Linked to original sources

[Manual obliteration of femoral artery pseudoaneurysm. Report of a case and brief review of the literature].

The authors report a case of non-surgical repair of a femoral artery pseudoaneurysm due to percutaneous catheterization. The procedure was performed by direct manual compression under intermittent color-flow duplex ultrasound control. Some conditions reported in the Literature as unfavorable for a prompt resolution were present (long time interval between invasive procedure and treatment, anticoagulant medication); nevertheless the manoeuvre was successful after only 20'. In comparison with previous experiences (reporting direct compression with the ultrasound transducer or with a mechanical vascular clamp device) the authors underline some observations: a) direct manual compression seems to guarantee a better stability in the optimal position allowing flow interruption in the lesion; b) ultrasound guide is necessary to prove the efficacy of compression, but a continuous monitoring doesn't seem necessary; c) in order to stop the procedure perhaps it is sufficient to interrupt completely the flow in the pseudoaneurysm cavity; a small flow, limited to the neck of the lesion, can be resolved if a pressure bandage is applied and the patient is maintained at bed rest for 12 hours. Manual, ultrasound guided obliteration may be considered a safe and efficacious method for non-surgical treatment of femoral artery pseudoaneurysms.

Adult↗

Prejunctional modulation of sensory-motor nerve-mediated vasodilatation of the rat mesenteric arterial bed by opioid peptides.

In the rat isolated mesenteric arterial bed, perivascular nerve stimulation in the presence of guanethidine (5 microM) and methoxamine (30-50 microM), elicited frequency-dependent vasodilatation due to activation of sensory-motor nerves. The present study examined the modulation of this sensory-motor activity by opioid peptides. The mu-selective opioid agonist [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) inhibited vasodilator responses to sensory-motor nerve stimulation. The native enkephalins [Met5]enkephalin (mENK) and [Leu5]enkephalin (IENK) were less potent, whereas the delta-selective agonist DPDPE was without effect. Naloxone (30 nM) reversed the inhibitory effects of both DAMGO and mENK. The delta opioid antagonist ICI 174864 (0.1 microM) had no effect on the inhibition by mENK. Inhibitory effects of the kappa opioid-selective agonist 3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]-methanesulfonate hydrate (U-50,488H) on sensory-motor nerve-induced vasodilatation were unaffected by naloxone (0.3 microM) or by the kappa opioid receptor-selective antagonist (-)-5,9 alpha-diethyl-2-(3-furylmethyl)-2'-hydroxy-6,7-benzomorphane (MR 2266). Neither DAMGO nor mENK inhibited vasodilator responses to calcitonin gene-related peptide (CGRP), the principle vasodilator transmitter released from sensory-motor nerves in the rat mesenteric arterial bed or to the sensory neurotoxin capsaicin. In mesenteric beds from reserpine-treated rats (to abolish the catecholamine, but not opioid, content of sympathetic nerves) naloxone facilitated sensory-motor nerve-mediated vasodilatation. These results suggest that sensory-motor neurotransmission in the rat mesenteric arterial bed is inhibited by prejunctional mu, but not by delta or kappa opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Oral immunoglobulins for treatment of acute rotaviral gastroenteritis.

OBJECTIVE: Preliminary evidence has been reported on the antirotavirus effect of human serum immunoglobulin administered orally. The aim was to see whether such treatment might be effective in rotavirus acute gastroenteritis. METHODS: A prospective, double-blind, placebo-controlled study was performed. Ninety-eight children admitted with acute gastroenteritis were enrolled and randomly assigned to groups A (treated) and B (control). Children in group A received a single oral dose of 300 mg/kg body weight of human serum immunoglobulin. Parameters of efficacy were clinical condition, frequency and consistency of stools, duration of diarrhea, duration of viral excretion, and length of hospital stay. Antirotaviral activity was determined in the immunoglobulin preparation by a specific neutralization assay. RESULTS: Seventy-one of the 98 children enrolled had rotaviral gastroenteritis; 36 belonged to group A. Children who received immunoglobulin had significantly faster clinical improvement of clinical condition and stool pattern than control children. Mean total duration of rotaviral diarrhea was 76 hours in group A and 131 in group B (P < .01). Viral excretion lasted 114 and 180 hours, respectively (P < .01). Hospital stay was significantly reduced in children in group A. Neutralizing antibodies against rotavirus were detected in the immunoglobulin preparation. CONCLUSION: Oral administration of immunoglobulin is associated with a faster recovery from acute gastroenteritis and should be given to children hospitalized with this illness.

Acute Disease↗

Pertussis toxin does not affect the adenosine-induced inhibition of the efferent function of cardiac capsaicin-sensitive nerves.

The negative inotropic effect of adenosine (1-100 microM) was abolished in isolated guinea-pig atria obtained from pertussis toxin-pretreated guinea pigs electrically driven at 4 Hz. However, the inhibitory effect of the same concentrations of adenosine on the cardiac response to stimulation of non-adrenergic non-cholinergic (NANC), capsaicin-sensitive sensory nerves, was not modified by the toxin. These results suggest that, while pertussis toxin-sensitive G proteins are involved in the negative inotropic effect of adenosine, they do not mediate the inhibitory effect of adenosine on cardiac NANC neurotransmission.

Adenosine↗

Non-adrenergic non-cholinergic (NANC) neural control of the atrial myocardium.

1. Current concepts in the regulation of atrial contractility by non-adrenergic non-cholinergic (NANC) sensory nerves are reviewed. 2. There is now evidence that in addition to sympathetic and parasympathetic innervation capsaicin-sensitive sensory nerves contribute to the local control of atrial contractility by releasing NANC transmitters, such as calcitonin gene-related peptide (CGRP). 3. Certain chemical and physical stimuli affect atrial contractility by inducing the release of CGRP from sensory nerves. In addition, as widely recognized for the sympathetic and vagal atrial innervation, NANC neurotransmission is under the inhibitory control of several endogenous modulators. 4. Cardioexcitatory actions of NANC neurotransmission on the atrial myocardium are considered. 5. Pharmacological modulation of NANC neurotransmission and functional evidence for cross-talk between NANC and sympathetic neurones are also discussed.

Animals↗

The P1-purinoceptors that mediate the prejunctional inhibitory effect of adenosine on capsaicin-sensitive nonadrenergic noncholinergic neurotransmission in the rat mesenteric arterial bed are of the A1 subtype.

It has been shown that capsaicin-sensitive sensory-motor nerves contribute to the control of peripheral vascular resistance by releasing the potent vasodilator calcitonin gene-related peptide. The purpose of the present study was to characterize the P1-purinoceptor subtype that modulates capsaicin-sensitive non-adrenergic noncholinergic (NANC) neurotransmission in the rat mesenteric arterial bed. Analogs of adenosine, selective for the adenosine receptor subtypes A1 or A2, were evaluated on the vasodilator response to electrical stimulation of capsaicin-sensitive sensory-motor nerves. The order of potency of adenosine receptor agonists to inhibit the NANC neurotransmission was: the selective adenosine A1 receptor agonist N6cyclopentyl-adenosine > or = R-phenylisopropyladenosine > 5'N-ethylcarboxamide adenosine > or = 2-chloroadenosine > or = S-phenylisopropyladenosine. The A2-selective agonist CGS 21680 was devoid of any effect on NANC neurotransmission. In addition, the selective A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine inhibited the effect of adenosine. None of the agonists tested showed direct action on the tone of the mesenteric vasculature. Neither N6cyclopentyladenosine nor adenosine modified the vasodilator response to exogenous calcitonin gene-related peptide. Moreover, adenosine failed to affect the vasodilator response to capsaicin. In conclusion, these results indicate that adenosine and its analogs inhibit NANC neurotransmission via prejunctional P1-purinoceptors of the A1 subtype. The inhibitory action of adenosine appears to be selective for the release of transmitters during electrical activation of sensory-motor nerve endings, adenosine being inactive on capsaicin-induced vasodilatation.

Adenosine↗

[Determinants of body fat in prepubertal age].

In order to evaluate the factors affecting body fat excess and distribution, we have studied children attending the 4th grade of a primary school randomly selected in Naples. 52 girls, 58 boys; mean age = 9.6 years (SE +/- 0.1) were examined. Among the familial factors assessed, a correlation between parental BMI and child's anthropometry was found. Among congenital factors, sex correlates with the children's waist/hip ratio ("t" = -2.07; p = 0.05). Moreover the girl's percent body fat was higher. These two findings suggest the expression of sexual characters in prepubertal age. Systolic blood pressure showed a positive correlation with children's percent body fat ("t" = 2.43; p = 0.016) and subscapular skinfold thickness ("t" = 1.19; p = 0.05), suggesting an influence of these factors on blood pressure level since this age. No correlation was found between children's BMI and weight at birth, family history of diabetes, hypertension or hyperlipidemia. Among environmental factors, only the mothers weight gain during pregnancy ("t" = -2.21; p = 0.03) and breast feeding ("t" = -2.07; p = 0.05) correlated with the children's BMI. The correlation between children's BMI and waist/hip ratio ("t" = 4.64; p = 0.0001), was not confirmed in children who exercise, suggesting a beneficial action of physical activity on body fat distribution. The identification in different populations of factors associated with childhood obesity is important for prevention planning.

Animals↗

Cardiovascular effects of capsaicin-sensitive neurons.

Calcitonin gene-related peptide, the main transmitter released from capsaicin-sensitive sensory-motor fibers, has positive inotropic and chronotropic effects on the heart and causes vasodilatation in the coronary arteries and elsewhere in the peripheral vasculature. We review some aspects of the cardiovascular actions induced by exogenous calcitonin gene-related peptide and by release of the peptide following activation of capsaicin-sensitive nerves. The efferent function of cardiac sensory-motor neurones is modulated by a number of endogenous substances of physiopathological interest, including opioid peptides, norepinephrine and adenosine. The receptors involved in the prejunctional regulation due to these substances have been characterized. Studies on the mesenteric bed of the rat have shown that, at least in such a resistance vascular bed, the relaxing effect of calcitonin gene-related peptide is mediated by a direct mechanism independent of endothelium-derived nitric oxide release. In cultured human endothelial cells from the umbilical cord vein, calcitonin gene-related peptide, at nM concentrations, stimulates cell growth in a dose-dependent manner. The possible implications of calcitonin gene-related peptide in the physio-pathological regulation of the cardiovascular system and in the trophism of vascular tissues are discussed.

Animals↗

Prejunctional modulation of sensory-motor nerve mediated vasodilation of the rat mesenteric arterial bed by adenosine.

The effect of adenosine on the vasodilator response of the rat mesenteric arterial bed to electrical field stimulation of perivascular sensory-motor nerves was examined. Adenosine (0.3-10 microM) produced a concentration-dependent attenuation of the vasodilator response to electrical stimulation of sensory-motor nerves, which is mediated by the sensory neuropeptide calcitonin gene-related peptide (CGRP). The adenosine receptor antagonist, 8-phenyltheophylline (1 microM) competitively antagonized the inhibitory effect of adenosine. Adenosine did not affect the vasodilator response to exogenous CGRP, thus indicating that the inhibitory action of adenosine on the vasodilator response to perivascular sensory-motor nerve stimulation was prejunctional.

Adenosine↗

The inhibitory effect of opioid and alpha 2-adrenoceptor agonists on cardiac sensory neurones is pertussis toxin-insensitive.

The role of pertussis toxin-sensitive G proteins on the alpha 2-adrenoceptor and mu-opioid receptor-mediated inhibition of the efferent function of capsaicin-sensitive neurones was investigated in guinea-pig atria pretreated with guanethidine. In the presence of atropine, CGP 20712A (2-hydroxy-5-(2-[hydroxy-3-(4-[(1-methyl- 4-trifluormethyl)1H-imidazol-2-yl]-phenoxy)propyl]aminoethoxyl+ ++)-benzamide) and prazosin, [D-Ala2,NMe-Phe4,Gly5-ol]enkephalin (DAGO, 0.1-3 microM) and 2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo(4,5-d)azepine (BHT 920, 0.01-1 microM) reduced the positive inotropic effect induced by transmural stimulation of preparations obtained from control and from pertussis toxin-treated animals. These results suggest that pertussis toxin-sensitive G proteins are not involved in the inhibitory regulation of the efferent function of capsaicin-sensitive nerve terminals in cardiac tissue induced by alpha 2 and opioid receptor stimulation.

Adrenergic alpha-Agonists↗

Effects of thromboxane agonists on cardiac adrenergic neurotransmission.

The effects of thromboxane B2 (TxB2) and of two thromboxane mimetics, dl-(9,11), (11,12)-dimethano-TxA2 (ONO 11006) and 9,11-dideoxy-11,9-epoxymethano prostaglandin F2 alpha (U46619) on the cardiac response to adrenergic nerve stimulation in isolated guinea-pig atria were evaluated. All the agonists dose dependently reduced the positive inotropic effect induced by field stimulation, U46619 being the most active. The inhibitory effect of U46619 was reduced by the thromboxane receptor antagonists, sulotroban and AH 23848B. U46619 did not significantly reduce the positive inotropic effect induced by exogenous noradrenaline. However U46619 was unable to modify the tritium overflow induced by field stimulation in preparations preloaded with [3H]noradrenaline. In addition to this influence on adrenergic neurotransmission, U46619 also had a direct positive inotropic effect on cardiac contractility, which was antagonized by AH 23848B. These results indicate that U46619 reduces the cardiac response to sympathetic nerve stimulation and that is also has a direct stimulatory effect on cardiac muscle.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Endothelium-dependent relaxant effect of neurokinins on rabbit aorta is mediated by the NK1 receptor.

Several neurokinins, namely substance P, neurokinin A, neurokinin B, [beta-Ala8]neurokinin A-(4-10) and senktide, were tested on noradrenaline-precontracted rabbit aortic rings to characterize the receptor mediating their endothelium-dependent relaxant effect in this preparation. CP-96,345, the new nonpeptide antagonist selective for the NK1 receptor, was also studied. Substance P, neurokinin A and neurokinin B, in that order of potency, were effective in relaxing precontracted rings, indicating the involvement of the NK1 receptor; [beta-Ala8]neurokinin A-(4-10) and senktide, which are selective agonists for NK2 and NK3 receptors, respectively, had no significant relaxant effect. The relaxant effects of substance P, neurokinin A and neurokinin B were competitively antagonized by nanomolar concentrations of CP-96,345. These findings support the view that the NK1 receptor mediates the endothelium-dependent relaxant effect of the neurokinins in rabbit aorta.

Animals↗

Reference values of the steatocrit and its modifications in diarrheal diseases.

Conflicting results have been reported on the use of the steatocrit to measure fecal fat excretion. Aiming to assess the reliability of this method and its usefulness in the diagnosis of intestinal enteropathies, we measured the steatocrit in 747 healthy children and 442 children with diarrhea grouped according to diagnosis. The steatocrit was found to correlate strictly (r = 0.93) with the chemical measurement of fecal fat. Reference values and ranges were established. The maximal steatocrit was observed in neonates; afterwards, it progressively decreased to an undetectable level in children older than 2 years of age. A steatocrit abnormally high for age was found in 20% of patients with acute diarrhea and in 53% of those with chronic diarrhea. All celiac patients with a gluten-containing diet showed a marked increase of steatocrit. We conclude that the steatocrit is a reliable and easy-to-perform test, which quickly provides valuable information in the diagnostic workup of the child with diarrhea.

Adolescent↗