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N Stella

Publications and source records attributed to N Stella.

29 records · Page 2Linked to original sources
PubMed1996

[Endovascular treatment of abdominal aorta aneurysms using the Stentor device. Preliminary experience].

PURPOSE: The aim of this report is to describe our experience with the Stentor device for endovascular treatment of the abdominal aortic infrarenal aneurysms also extending to the bifurcation and the common iliac arteries. Stentor is a thermal memory (Nitinol) self-expanding graft, covered by an external 0.1 mm Dacron material. METHODS: Between December 1994 and July 1995 endoluminal repair of infrarenal aneurysmal disease was undertaken in 6 patients at high surgical risk. The lesions include 2 infrarenal abdominal aorto-aortic aneurysms, 2 infrarenal abdominal aortic aneurysms extended to the common iliac arteries and 2 false aortic aneurysms in patients with previous aorto-bifemoral graft. Straight grafts were implanted in 4 patients and bifurcated in 2. Repair was done in the operating room using general anesthesia. The endograft was placed through remote arteriotomies and advanced under fluoroscopic guidance to his predetermined site. Three-dimensionally reconstructed spiral CT scan and arteriography were performed before the procedure for a preoperative accurate measurement for endograft preprocedural adaptation in length and diameter. RESULTS: All endografts were successfully deployed. Intraoperative arteriography at the end of the procedure revealed a distal "leak" into an aneurysmal common iliac artery, due to diameter mismatch, in a bifurcated device. There was no instance of embolism or graft migration. No patient required conversion to an open operation. There were no instances of embolism or graft migration. No patient required conversion to an open operation. There were no coagulative disorders. Minor complications were: groin haematoma (1), fever (1), intestinal paralysis (1), pelvic pain (1). Follow-up with spiral CT-scan and echo color-Doppler confirmed normal blood flow through the graft in 5 patients and persistence of distal leak in 1 patient. CONCLUSIONS: These preliminary results demonstrate the accuracy of implantation and device's adaptability to the particular anatomy of the aneurysmal aorta and iliac arteries. Proximal fixation to the aortic wall, secure seal at the proximal and distal fixation point present the critical aspects of this new surgical technique. More detailed preoperative measurements of aneurysmal disease are required rather than for traditional surgery. Presently we prefer to treat the no operable patients with this endovascular technique in relation with shortness of the follow-up.

Aged↗
PubMed1995

Modulation of the glutamate-evoked release of arachidonic acid from mouse cortical neurons: involvement of a pH-sensitive membrane phospholipase A2.

Excitatory synaptic transmission is associated with changes in both extracellular and intracellular pH. Using mouse cortical neurons in primary cultures, we studied the sensitivity of glutamate-evoked release of 3H-arachidonic acid (3H-AA) to changes in extracellular pH (pHo) and related intracellular pH (pHi). As pHo was shifted from 7.2 to 7.8, the glutamate-evoked release of 3H-AA was enhanced by approximately threefold. The effect of alkaline pHo on the glutamate response was rapid, becoming significant within 2 min. 3H-AA release, evoked by both NMDA and kainate, was also enhanced by pHo alkalinization. NMDA- and kainate-induced increase in free intracellular Ca2+ was unaffected by changing pHo from 7.2 to 7.8, indicating that the receptor-induced Ca2+ influx is not responsible for the pHo sensitivity of the glutamate-evoked release of 3H-AA. Alkalinization of pHi obtained by incubating neurons in the presence of HCO3- or NH4 enhanced the glutamate-evoked release of 3H-AA, while pHi acidification obtained by blockade of Na+/H+ and Cl-/HCO3- exchangers decreased the glutamate response. Membrane-bound phospholipase A2 (mPLA2) activity was stimulated by Ca2+ in a pH-dependent manner, increasing its activity as pH was shifted from 7.2 to 7.8. This pH profile corresponds to the pH profile of the glutamate-, NMDA- and kainate-evoked release of 3H-AA. Taken together, these results indicate that the glutamate-evoked release of 3H-AA may be mediated by the pH-sensitive mPLA2. Since excitatory neurotransmission mediated by glutamate results in both pHo and pHi changes and since AA enhances glutamatergic neurotransmission at both pre- and postsynaptic levels, the data reported here reveals a possible molecular mechanism whereby glutamate can modulate its own signalling efficacy in a pH-dependent manner by regulating the release of AA.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Glial receptors and their intervention in astrocyto-astrocytic and astrocyto-neuronal interactions.

As shown on cultured astrocytes from the mouse, in the presence of adenosine deaminase, 2-chloroadenosine by acting on A1-adenosine receptors potentiated the activation of phospholipase C induced by the alpha 1-adrenergic agonist, methoxamine. This potentiation required the presence of external calcium and was blocked by pertussis toxin. Moreover, this potentiation resulted from a cascade of events: activation (by calcium and protein kinase C) of a phospholipase A2 coupled to A1-adenosine receptors, release of arachidonic acid, which inhibited the reuptake of glutamate into astrocytes and finally additional activation of phospholipase C by externally accumulated glutamate through metabotropic receptors. The effects of 2-chloroadenosine and methoxamine were respectively mimicked by somatostatin and substance P while endothelins reproduced the combined effects of 2-chloroadenosine and methoxamine. Conditioned media from treated astrocytes enriched in glutamate stimulated phospholipase C in cultured striatal neurones. In addition, glutamate alone was also found to stimulate phospholipase A2 in astrocytes through receptors exhibiting a pharmacological profile distinct from metabotropic receptors coupled to phospholipase C and the glutamate response was potentiated by ATP. Moreover, the neuronal arachidonic acid production evoked by glutamate was potentiated by acetylcholine. Finally, the combined application of 2-chloroadenosine and methoxamine on striatal astrocytes reduced the permeability of gap junctions between astrocytes and this response was mimicked by arachidonic acid. Together, these results emphasized the contribution of astrocytes in the regulation of glutamatergic transmission.

2-Chloroadenosine↗
PubMed1994

Glutamate-evoked release of arachidonic acid from mouse brain astrocytes.

Brain astrocytes in primary culture from the rat or the mouse have been shown to possess ionotropic and metabotropic glutamatergic receptors. The activation of both types of receptors is responsible for a rise in the cytosolic concentration of calcium, while the stimulation of metabotropic receptors induces the accumulation of inositol phosphates. In the present study, it is demonstrated that in striatal astrocytes from mouse embryos, glutamate evokes a release of arachidonic acid. The nonionotropic receptors involved in this effect appeared to be pharmacologically distinct from those coupled to phospholipase C: (1) glutamate displayed different dose-response curves for the production of inositol phosphates (biphasic: EC50 = 25 and 300 microM) and the release of arachidonic acid (monophasic: EC50 = 200 microM); (2) L(+)-2-amino-4-phosphonobutyric acid (AP4) only antagonized the glutamate-evoked release of arachidonic acid without altering the production of inositol phosphates; (3) when used at a concentration of 0.1 mM, quisqualate induced a higher formation of inositol phosphates than glutamate (2 mM) while, in contrast to glutamate, it only weakly stimulated arachidonic acid release when used either at 0.1 mM or 1 mM. L(+)-2-amino-3-phosphonopropionic acid (AP3) suppressed both responses. The glutamate-evoked release of arachidonic acid seems to be oppositely regulated by protein kinases A and C. Indeed, the stimulation of adenylate cyclase by the beta-adrenergic agonist isoproterenol, vasoactive intestinal peptide, or pretreatment of striatal astrocytes with cholera toxin decreased the glutamate-evoked release of arachidonic acid. In contrast, ATP, which markedly stimulated inositol phosphate production, strongly potentiated the glutamate-evoked release of arachidonic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Renal artery stenosis and aorto-iliac restoration: is it necessary to do extensive evaluation?].

In patients with aortoiliac disease and a stenosis of one or two renal artery, renal hypertension is rarely the sole mechanism of the elevated blood pressure. The preservation of nephron mass being the aim of the renal revascularization, we firmly believe that only three tests are required for the operative decision: renal ultrasonography, nephroscintigraphy and global and selective aortography.

Aorta↗
PubMed1993

Arachidonic acid stimulates glucose uptake in cerebral cortical astrocytes.

Arachidonic acid (AA) has recently been shown to influence various cellular functions in the central nervous system. Here we report that AA increases, in a time- and concentration-dependent manner, 2-deoxy-D-[1-3H]glucose ([3H]2DG) uptake in primary cultures of astrocytes prepared from the cerebral cortex of neonatal mice. This effect is mimicked by an unsaturated fatty acid such as linolenic acid, while palmitic and arachidic acids, two saturated fatty acids, are inactive. Pharmacological agents that increase the endogenous levels of AA by stimulating AA release (melittin) or by inhibiting its reacylation (thimerosal) also promote [3H]2DG uptake by astrocytes. We also report that norepinephrine (NE) stimulates the release of [3H]AA from membrane phospholipids, with an EC50 of 3 microM; this effect is accompanied, with a temporal delay of approximately 4 min, by the stimulation of [3H]2DG uptake, for which the EC50 of NE is 1 microM. Since the cerebral cortex, the brain region from which astrocytes used in this study were prepared, receives a massive noradrenergic innervation, originating from the locus coeruleus, the effects of NE reported here further stress the notion that certain neurotransmitters may play a role in the regulation of energy metabolism in the cerebral cortex and point at astrocytes as the likely targets of such metabolic effects.

Animals↗
PubMed1993

Role of arachidonic acid and glutamate in the formation of inositol phosphates induced by noradrenalin in striatal astrocytes.

The noradrenalin-evoked production of [3H]inositol phosphates in mouse striatal astrocytes in primary culture appeared to be the result of the combined stimulation of alpha 1- and alpha 2-adrenergic receptors. Indeed, the noradrenalin (100 microM) response was only partially reproduced by a maximally effective concentration of methoxamine (100 microM), a selective agonist of alpha 1-adrenergic receptors. In addition, the noradrenalin (100 microM)-induced production of [3H]inositol phosphates, which was completely suppressed by the alpha 1-adrenergic antagonist prazosin (1 microM), was also partially inhibited by yohimbine, a selective antagonist of alpha 2-adrenoceptors (maximum inhibition = -57 +/- 11%, measured in the presence of 10 microM yohimbine; six experiments). Finally, UK14.304, a selective alpha 2-adrenergic agonist that was ineffective alone, enhanced the methoxamine-evoked production of [3H] inositol phosphates (EC50 = 86 +/- 21 nM; three experiments). These results suggest that the stimulation of alpha 1-adrenergic receptors is required for the alpha 2-adrenergic receptor-mediated enhancement of phospholipase C activity. The increased production of [3H]inositol phosphates resulting from the stimulation of alpha 2-adrenergic receptors involved pertussis toxin-sensitive G proteins (Gi/o) and depended on extracellular calcium. As shown using the fluorescent dye indo-1, noradrenalin (100 microM) induced a long-lasting increase in cytosolic calcium in striatal astrocytes. Moreover, noradrenalin (100 microM) stimulated [3H]arachidonic acid release from these cells. These two latter responses may result from synergistic effects due to the combined stimulation of alpha 1- and alpha 2-adrenergic receptors, because they were inhibited by either prazosin (1 microM) or yohimbine (10 microM). Finally, the noradrenalin-evoked production of [3H]inositol phosphates seems to result partly from an inhibition by arachidonic acid of glutamate uptake into astrocytes, leading to the stimulation of glutamate metabotropic receptors coupled to phospholipase C. Indeed, the alpha 2-adrenergic component of the noradrenalin response was suppressed by either enzymatic removal of external glutamate or addition of 2-amino-3-phosphonopropionic acid (1 mM), an antagonist of glutamate metabotropic receptors that blocked the glutamate-evoked production of [3H]inositol phosphates in striatal astrocytes, and was reproduced by the direct application of either glutamate or an inhibitor of glutamate uptake, beta-methyl-DL-aspartic acid.

Adrenergic alpha-Agonists↗
PubMed1993

Blood magnesium, potassium, sodium, calcium and cortisol in drug-free depressed patients.

Many biochemical variables, including plasma and erythrocyte magnesium, were simultaneously measured in drug-free depressed patients (n = 34), compared to healthy controls (n = 35). Higher plasma and erythrocyte magnesium concentrations were observed in patients than in controls (+12 per cent, P < 0.0001 and 14 per cent, P < 0.0001, respectively). In contrast, patients showed a lower plasma potassium level (-10 per cent; P < 0.007). Cortisol secretion was much higher in patients (+35 per cent; P < 0.02), particularly in females, showing overactivity of the hypothalamo-hypophyseo-adrenal axis in the patients. Except in a few cases, plasma sodium and calcium in patients did not differ from control values. Significant differences in magnesium and cortisol levels were observed between patients classified in diagnostic groups and by sex, whereas little variation in the other biochemical indices was noted. The increase in blood magnesaemia and its possible association with central hypocatecholaminergic deficiency in affective disorders are discussed.

Calcium↗
PubMedDate not supplied

Lecithin: cholesterol-acyltransferase (LCAT) activity in alcoholic liver disease.

The activity of LCAT (the controlling enzyme for cholesterol esterification in plasma) is known to be reduced in alcoholic cirrhosis, while little is known about early stage (liver steatosis) alcoholics. In this study, LCAT activity was assayed by Stokke and Norum's method, before and after a 15-day sobriety period, in liver steatosis and in cirrhosis alcoholics. Before alcohol withdrawal, LCAT activity was depressed in both groups. After the sobriety period, LCAT activity was significantly raised in liver steatosis patients, but was still lower than in controls; in cirrhosis patients, it was increased, but not significantly. According to our results, LCAT activity impairment in alcoholic liver disease is sustained by both the hypothesized mechanisms, alcohol-related metabolic disorders and lowered LCAT-enzyme production, but to different degrees, depending on the stage of the disease. In liver steatosis, metabolic disorders play a major role, as a liver-impairment-induced decrease in LCAT production seems rather unlikely, and increased LCAT activity is more likely to be sustained by metabolic normalisation than by any recovery of the damaged liver. However, the lack of improvement in about 20% of patients, and the fairly wide scattering of individual data, suggest a minor LCAT production impairment in liver steatosis too. In cirrhosis, the major role seems to be played by a permanent decrease in LCAT production, as no significant rise in LCAT activity was observed after alcohol withdrawal. However the restored LCAT activity observed in some patients could be related to improvement in the metabolic disorder, thus confirming the effectiveness of this mechnism in cirrhosis too.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Late results of reconstructive surgery for renovascular hypertension.

In order to evaluate the late results of reconstructive surgery for renovascular hypertension, a review was made on a series of 120 consecutive patients who underwent operations over a 11 year period. There were 82 males (68.3%) and 38 females (31.7%) with a mean age of 48.4 years. Renal artery by-pass grafts were used in 90% (120/133), a thromboendarterectomy in 5.2% (7/133), and other surgical procedures were performed in 4.8% (6/133). Associated vascular procedures were performed in 38.3% (46/120) of patients. Operative mortality was 2.5% (3/120) overall; there was no mortality in the isolated renal artery reconstructions. There was a clinical success (after a mean follow-up of 48 months) in 80.4% of patients. The most important factors influencing clinical result after renal revascularization were: a generalized atherosclerosis (p less than 0.05), duration of hypertension (p less than 0.01) and the early post-operative response of the blood pressure (p less than 0.01). The overall five- and ten-year actuarial survival probabilities were 85 and 68%, respectively. The most common causes of death were myocardial infarction, stroke and cancer. Cox regression analysis for variables influencing survival indicated that persistence of severe hypertension was the major determinant of late survival (p less than 0.05). Hypertension in females is better tolerated, while younger patients appear to have better results and late survival after surgical treatment.

Adolescent↗