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PURPOSE: We report the initial French multicenter experience with the Stentor system in the endovascular treatment of AAAs. METHODS: Between May 1994 and March 1996, 79 patients with AAAs were consecutively treated with an endovascular technique using the Stentor system. There were 71 bifurcated grafts and eight straight grafts. The patients were followed-up from 1 to 18 months (mean, 5.7 months). Patient data and events were retrospectively analyzed. RESULTS: No patients was lost to follow-up. There were no surgical conversions. Four patients died after operation (4.8%). Two of them had been considered inoperable by the standard technique. Four patients (4.8%) had pulmonary complications, and three had colonic ischemia (3.7%). Forty-five patients (57%) had postoperative fever, and a transitory thrombocytopenia (10%) developed in eight patients. In 66 patients (83%) the aneurysm was immediately excluded. The exclusion was definitive in 62 (78%). In 17 patients, there were 13 initial and six delayed endoleaks. In two of these patients, the initial endoleak sealed temporarily and resumed after 1 year of follow-up, requiring an additional straight, covered stent. Over all, seven of the leaks were treated successfully by an additional endovascular graft, one leak required a lumbar artery embolization, eight leaks sealed spontaneously, and one leak was untreated. During follow-up, there was no aneurysm rupture. Two patients died of unrelated causes. CONCLUSION: The Stentor system can safely and effectively exclude AAAs in the short term. Careful follow-up is required to detect any delayed endoleak, and long-term results are awaited to confirm the efficacy of the method in preventing AAA rupture.

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PURPOSE: To detail a methodology for evaluation of endovascular abdominal aortic aneurysm (AAA) repair that has been achieved through consensus of an international multidisciplinary team of investigators. METHODS: This schema features an anatomical classification for AAAs, a definition of procedural success, and a procedure for clinical assessment, as well as the necessary data collection forms. Patient data include demographics, procedural and clinical success, complications, and follow-up. Procedural details can be related to anatomic situations, comorbid processes, devices, and effective aneurysmal exclusion. RESULTS: These data would allow assessment of the procedures, physician learning curves, procedural indications, techniques, methodologies, the relationship of indications to success and complications, devices and subsequent graft patency, and aneurysmal exclusion. CONCLUSIONS: The use of this standardized data collection system could enable physicians and industry to better understand endovascular AAA repair and ultimately improve patient care.

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EUROSTAR (EUROpean collaborators on Stent-graft Techniques for abdominal aortic Aneurysm Repair) was established for the purpose of combining and studying data on endovascular abdominal aortic aneurysm (AAA) repair, EUROSTAR is independent of any commercial interest and has as its ultimate goal an independent, scientifically reliable assessment of endovascular AAA grafting. A standardized case record form is used for data collection and transmission, and the database is maintained in a central registry office. A comprehensive set of clinical, imaging, technical, and laboratory data obtained at initial admission and follow-up are recorded; these data are analyzed periodically and reports generated on the collated experience. As a first priority, an observational study without controls was initiated in July 1996 to address the issues of procedural safety, device durability, and long-term effect upon the aneurysms. Several ancillary studies have been initiated, including a "Retrieval and Analysis Study" for the evaluation of explanted devices. While a randomized study does not seem feasible at present, this may be organized at the appropriate time when the devices and techniques become more standardized.

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PURPOSE: To evaluate treatment of infrarenal abdominal aortic aneurysm (AAA) with a new endoluminal stent-graft. MATERIALS AND METHODS: In 26 male patients, straight or bifurcated nitinol stents covered with woven Dacron graft material were implanted to treat eccentric saccular AAA (n = 3) or AAA involving the bifurcation and common iliac arteries (n = 23), with follow-up from 8 days to 8 1/2 months. RESULTS: Implantation was technically successful in all but one of the 26 (96%) patients (leak of the stent-graft for more than 3 months necessitated implantation of an additional covered stent). In seven of the 26 patients, minor residual perfusion persisted immediately after implantation, but complete thrombosis occurred within 7 days. Five procedure-related complications occurred: distal embolization (n = 2); local hematoma, which necessitated surgery (n = 1); acute hepatic failure due to gastric bleeding, in a patient with liver cirrhosis (n = 1); and stent-graft occlusion due to emboli originating from the left atrium (n = 1). CONCLUSION: Exclusion of AAA from circulation was feasible, safe, and clinically effective with the new stent-graft.

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The Stentor is a thermal memory Nitinol frame covered by an external permeable polyester fabric. The Mialhe Stentor bifurcation which is matted into the infra renal aorta is designed for the treatment of AAA extended to the bifurcation and the iliac arteries. The bifurcated device is comprised of two separately introduced segments: --the aortic part with a fixed iliac limb loaded into a 18 F delivery system is introduced into the common femoral artery by a cut down approach, --the contralateral iliac leg loaded into a 10 F introducer is inserted percutaneously. This preliminary series involves 84 Stentor procedures: 14 straight, 2 tapered, 21 single bifurcated and 50 bifurcated and extended devices. The per and post operative surgical complications are reported: 4 peripheral emboli, 1 partial left colon ischemia, 2 hematomas and 1 local infection at the access site. Post operative angio and CT scan are necessary to identify the remaining leakages and their origin. In this series two AAA remain injected because of a proximal leakage by mismatch which has to be treated by implanting a cuff. These preliminary results demonstrate the accuracy of the proximal positioning, the adaptability of the device according to the anatomical situation and its ability to be extended. A long term follow-up study is necessary to prove the long term effectiveness of the endovascular exclusion of AAA and to improve the selection criteria.

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Twenty-eight ASA I or ASA II adults undergoing microsurgery were anaesthetized according to a standard protocol using droperidol, phenoperidine and thiopentone followed by enflurane. The patients were randomly assigned to two homogeneous groups: the first group (n = 14) received 0.2 mg.kg-1 alcuronium, whereas the second group (n = 14) received 0.08 mg.kg-1 vecuronium. There was no reinjection of either drug and curarization tapered off spontaneously. Neuromuscular monitoring was begun once anaesthesia was stable and after intentional isovolaemic haemodilution. The type of stimulus used was the train-of-four, delivered by a Relaxograph monitor to the ulnar nerve. Muscle response was measured at the hypothenar eminence. The kinetic study considered the time interval required between the injection of the muscle relaxant and the appearance of the minimal value of the twitch (first response of the train-of-four = T1min). The times to recovery of the twitch height to 25, 75 and 100% of the reference value (T1/T0) and of the fourth response of the train-of-four to 25 and 75% of the ratio (T4/T1) were also recorded. Finally, the recovery indexes represented by the times required for T1/T0 and T4/T1 to rise from 25% to 75% respectively were studied. The maximal twitch height inhibition was significantly greater (p less than 0.001) in the vecuronium group (T1min = 0.36 +/- 1.33%) than in the alcuronium group (T1min = 4.36 +/- 5.08%); it occurred significantly more quickly (p less than 0.001) with vecuronium (139 +/- 48 s) than with alcuronium (316 +/- 133 s).(ABSTRACT TRUNCATED AT 250 WORDS)

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A hitherto undescribed osteo-myocutaneous free flap is presented. It is based on a branch of the superficial branch of the superior gluteal artery and includes the posterior iliac crest, the posterior part of the gluteus maximus and medius muscles and the overlying skin. This type of flap has allowed us to reconstruct a bony defect of up to 8 cm in the tibia.

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The present investigation was conducted in order to get more insight into the mechanism of action of vasopressin (VP) on ACTH secretion and characterize VP interaction with putative receptor sites at the level of the anterior pituitary gland. The experimental procedure consisted of increasing ACTH release from incubated pituitary fragments as induced by VP in the presence or absence of oxytocin (OT) and various releasing factors. Our results show that, whereas OT was able to depress VP-induced release of ACTH (Fig. 2), TRF (Fig. 3), LH-RH (Fig. 4) and crude "CRF" extract (Fig. 1) it did not exhibit any significant inhibitory effect. This provides indirect evidence for the presence of specific pituitary sites for VP and related peptides such as OT. The latter, however, was devoided of corticotrophic releasing properties.

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Incubation of anterior pituitary (AP) fragments of rats was used to determine the specific role played by vasopressin (VP) in the overall effect of crude hypothalamic median eminence (HME) extract on ACTH release. Using the property of an AVP antiserum (AS) to completely abolish the CRF-like effect of hypothalamic VP without apparently affecting the effect of CRF, we show that under specific incubation conditions, the effect of the two secretagogues are additive at the pituitary level. ACTH secretion of pituitaries was enhanced when incubation was carried out in the presence of VP together with a maximum effective dose of VP-free HME extract (from Brattleboro rats). These observations favor the hypothesis that VP and CRF have different receptor sites in the anterior pituitary.

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The effects of adrenalectomy (Adx) and hypercorticism on the ACTH content in the anterior (AH) and the neurointermediate lobe (NIL) of the pituitary in Long Evans (+/+), heterozygous (+/DI) and homozygous (DI/DI) Brattleboro rats were determined using dispersed adrenal cells bioassay. Adx decreased the NIL-ACTH content in +/DI and DI/DI rats and left it unchanged in the +/+ rats. Adx increased the AH-ACTH content in the three groups. Hypercorticism had a delayed decreasing effect both in the AH and in the NIL in all rats, with one exception for the NIL in DI/DI rats. Conversely to what appeared in Wistar rats, in Long Evans and Brattleboro rats the corticosterone administered in drinking water was unable to reduce the increase in AH-ACTH activity. These data suggest that Brattleboro, and, to a lesser extent, Long Evans rats from which the former are derived present some particularities in the regulation of their corticotropic function at the AH and the NIL level. We also observed that NaCl (0.9%) added to drinking water and hypercorticism are two factors able to increase diabetes insipidus in homozygous rats without modifying the water intake in Long Evans and heterozygous rats.

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The effects of K+-enhanced and Ca++-free media on alpha-MSH and adrenocorticotropic hormone (ACTH) release from superfused neurointermediate lobe (NIL) were studied in the same experiments. High K+ caused reversible and repeatable inhibition of alpha-MSH release and stimulation of ACTH release, Removal of Ca++ impaired the effect of K+, irreversibly for alpha-MSH and reversibly for ACTH. The existence of both melanotrophic and corticotrophic cells within the intermediate lobe (IL) of rat hypophysis could account for the different effects of ionic modifications on in vitro alpha-MSH and ACTH release.

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This study reports on the kinetics of glucocorticoid-induced inhibition of ACTH release, together with steroid binding to specific pituitary receptors. It was shown that corticosterone (CORT) inhibited ACTH output provoked by either corticotropin-releasing factor (CRF) extracts or dbcAMP, in a manner which was both dose- and time-dependent. A close correlation appeared to exist between the degree of ACTH blockade and the percentage of filled steroid-binding sites. However, exposure of hypophyses to CORT for a critical period of time was a prerequisite for such a relationship to develop. Furthermore, it was found that dexamethasone (DEX) was more potent than CORT in inhibiting ACTH secretion and, in addition, bound to a greater extent to nuclei of pituitary cells. These data suggest the existence of a close correlation between occupancy of pituitary glucocorticoid receptors and modulation of ACTH secretion.

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The effect of various neurotransmitters on adrenocorticitropic hormone (ACTH) release from superfused neurointermediate lobes of rat hypophysis (NIL) was investigated. Acetylcholine, serotonin, and histamine were shown to have no significant effect on the spontaneous release of ACTH. In contrast, dopamine (DA) and noradrenaline (NA) stimulated NIL ACTH release in a dose-dependent manner. The stimulating effect of DA was mimicked by apomorphine and inhibited by haloperidol, whereas that of NA was abolished by phentolamine. In a comparative study, none of these neurotransmitters is shown to have any significant stimulating effect on ACTH release from superfused anterior lobes. It is concluded that the ACTH release from NIL might be controlled, at least in part, by catecholaminergic innervation.

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Subcellular fractionation of the mediobasal hypothalamus (MBH) and frontal cerebral cortex was performed by differential and discontinuous sucrose gradient centrifugation. Corticotropin-releasing factor (CRF) activity of the different fractions was evaluated by bioassay. Significant CRF activity was found in acidic extracts of the MBH but not of the cerebral cortex. About 80% of the MBH effect on adrenocorticotropic hormone release was recovered in the crude mitochondrial pellet (P2) which contains synaptosomes. After further fractionation, distribution of CRF activity paralleled that of lactate dehydrogenase activity, a marker of the soluble cytoplasm. It is concluded that most CRF in the MBH is located in nerve endings as already shown for several other neurohormones.

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The binding of glucocorticoids to a crude fraction of rat pituitary plasma membranes and to solubilized membrane proteins was measured. The binding characteristics were similar to those exhibited by transcortin: radioactive corticosterone was bound to a greater extent than radioactive dexamethasone and labelled corticosterone, but not labelled dexamethasone, was displaced by unlabelled corticosterone, deoxycorticosterone and progesterone. A Scatchard plot of the binding data revealed the presence of a binding material with a dissociation constant of about 3.2 nmol/l, which sedimented at 4S after sucrose density-gradient centrifugation. It was found that the number of binding sites was inversely related to the concentration of corticosterone in the circulation and was increased after long-term adrenalectomy. These data suggest that a material similar to transcortin is complexed to the plasma membrane of rat pituitary cells.

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The aim of this study was to determine whether pituitary glucocorticoid binding sites are under hormonal control. It was shown that corticosterone and thyroxine exerted antagonistic effects on both the transcortin-like component and true receptor present in the hypophysis: thyroid hormones, in contrast to glucocorticoids which exhibited opposite influence, increased maximum binding without affecting significantly the apparent association constant. Thus, it seems that the concentration of glucocorticoid binding sites is regulated by the glucocorticoid ligands, as well as by a different hormone. Moreover, a striking parallelism was found between plasma transcortin and pituitary transcotin-like capacity, argueing in favour of a plasma origin for this pituitary binder.

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Using incubated glands, we showed that cerebral cortex and liver extracts (CCE and LE) stimulated ACTH release from neurointermediate lobe (NIL) of hypophysis as well as hypothalmus extract (HE) did. Moreover, the HE-induced ACTH release was much smaller for the NIL (1.9 X basal level) than for the anterior lobe (AL; 13.7 x basal level). Thus, under these conditions, HE seemed to have no specific effect on NIL ACTH release. Using superfused glands, we showed: (a) that both spontaneous and HE-induced ACTH release decreased during superfusion; (b) that using this system, a specific stimulatory effect on HE on NIL was observed. In contrast to HE, CCE and LE had only a small effect on NIL ACTH release (always less than 20% of that caused by HE) which could be considered as a nonspecific response; (c) that trypsin suppressed the stimulating effect on HE as well on NIL as on AL; and (d) that arginine antidiuretic hormone (ADH) was not responsible for the stimulating effect of HE on NIL ACTH release, because synthetic ADH had no effect and HE containing ADH (from normal rats) or HE containing no ADH (from Brattleboro rats or from immunoneutralization of ADH in normal HE) had the same effect. From these results, we can conclude that HE contain a peptidic factor different from ADH which is able to stimulate in vitro release of ACTH from the NIL.

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