Persistent primitive lateral vertebrobasilar anastomosis.
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Aged↗
Biomedical subjects
A Parenti
Publications and source records attributed to A Parenti.
Effect of the non-peptide blocker (+/-) CP 96,345 on the cellular mechanism involved in the response to NK1 receptor stimulation in human skin fibroblasts.
The effect of the selective non-peptide antagonist for NK1 receptors (+/-)CP 96,345 on cellular transduction mechanisms elicited by the NK1 selective agonist [Sar9]-substance P-sulfone ([Sar9]-SP) was investigated in a stabilized culture of human skin fibroblasts (HF) and compared to the effects of two peptide antagonists, FK 888 and GR 82, 334. The exposure of the cells to [Sar9]-SP (100 nM) produced an early increase in inositol 1,4,5-trisphosphate (IP3) level, which peaked after 6 s, and a later rise in cellular inositol 1-phosphate (IP1) content which reached the maximum level in 15 min. The cAMP level was not significantly modified. The increase in IP1 was greatly reduced, at approximately the same extent by the 10 min pretreatment with a concentration of (+/-)CP 96,345 (100 nM) 10 times smaller than that of FK 888 and GR 82,334 (1 microM). The cytosolic Ca2+ mobilization in response to the NK1 agonist was monitored both by spectrofluorimetric and single-cell image analysis determinations on adherent cells loaded with the Ca(2+)-sensitive fluorescent indicators Fura-2/AM and Indo-1, respectively. [Sar9]-SP (100 nM) produced a rapid increase in the intracellular Ca2+ level in Fura-2/AM loaded cells. Cytosolic Ca2+ mobilization, measured by single-cell image analysis, indicated a concentration-dependent increase in both the ratio and in the number of cells responding to [Sar9]-SP. Either the non-peptide or the peptide selective NK1 receptor antagonists inhibited the increase in Ca2+ level in both the assays. In the spectrofluorimetric experiments the antagonizing effects of (+/-)CP 96,345 (1-100 nM), FK 888 (10 nM-1 microM) and GR 82,334 (10 nM-1 microM) were concentration-dependent. Moreover, the non-peptide antagonist was more potent than the two peptide antagonists, producing an 82.5% inhibition of Ca2+ mobilization at a concentration (10 nM) at which FK 888 and GR 82,334 decreased the response by only 62.3 and 60%, respectively. Stimulation of phosphatidylinositol turnover and calcium mobilization were also induced by 10 nM bradykinin; these effects were influenced neither by the previous administration of the NK1 receptor agonist nor by the three antagonists tested. These results demonstrate that the cellular transduction mechanisms induced in human skin fibroblasts by NK1 receptor stimulation are specifically and effectively antagonized by (+/-)CP 96,345, and that this non-peptide antagonist is more potent than the two peptide antagonists tested.
Biphenyl Compounds↗
Thapsigargin inhibits the response to acetylcholine and substance P but does not interfere with the responses to endothelium-independent agents.
We investigated the influence of the Ca(2+)-ATPase inhibitor thapsigargin (TG) on the vasorelaxant response to different endothelium-dependent and endothelium-independent relaxing agents in an isolated thoracic aorta preparation of the rabbit, precontracted by norepinephrine (NE). Pretreatment with 100 microM L-arginine methyl ester (L-NAME) an inhibitor of nitric oxide (NO) synthesis, completely prevented acetylcholine (ACh)-induced relaxation; the inactive stereoisomer D-NAME did not modify the effect of ACh. The exposure of the preparations to 1 microM TG induced a slowly developing slight increase in the basal tension during 30-min contact. The same concentration of TG also slightly reduced the response to the subsequent administration of NE. The antagonist effect of TG on the ACh response was concentration dependent in the range between 0.1 and 10 microM. A 30-min pretreatment with 1 microM TG appeared to be sufficient to induce a consistent antagonism of the ACh (0.01-10 microM) concentration-relaxant effect curve, since an increase to 60 min did not produce a further significant increment in the degree of the antagonist effect. The concentration-dependent relaxation induced by substance P (SP 0.1-3 nM) was also significantly antagonized by 1 microM TG. The effect of the calcium ionophore A23187 (0.01-1 microM) was reduced by the Ca(2+)-ATPase inhibitor only at the higher concentrations tested (0.3-1 microM). However, a 30-min contact time with 1 microM TG was completely ineffective in antagonizing the concentration-relaxant response curves to the two nitrovasodilators sodium nitroprusside (SNP 0.1-100 microM) and nitroglycerin (NTG 1-300 nM) and to the cyclic GMP analogue 8-Bromo-cyclic GMP (3-100 microM). The effects of the beta-adrenoceptor agonist isoprenaline (ISO 0.1-10 microM) and of the direct adenylate cyclase activator forskolin (FK 0.01-10 microM) were also completely unaffected by 1 microM TG. These results demonstrate that TG affects the response to agents that induce an endothelium-dependent relaxation through receptor-dependent calcium mobilization. However, they do not support the hypothesis that sarcoplasmic pump activity is essential for the development of a vasorelaxant response to endothelium-independent agents.
Acetylcholine↗
The effect of linomide on the migration and the proliferation of capillary endothelial cells elicited by vascular endothelial growth factor.
In order to assess the mechanism of action of the quinoline-3-carboxyamide linomide as an antiangiogenic drug, the effect of linomide was studied in vitro on postcapillary endothelial cells exposed to vascular endothelial growth factor (VEGF). Linomide did not block the spontaneous replication of endothelial cells, but significantly suppressed endothelial cell growth and migration elicited by VEGF. It is concluded that linomide appears to be an effective tool to inhibit VEGF-dependent angiogenesis.
Capillaries↗
Functional and morphological study of the cricopharyngeal muscle in patients with Zenker's diverticulum.
Pharyngo-oesophageal function was investigated in 12 patients with Zenker's diverticulum before and after cricopharyngeal myotomy with or without diverticulectomy using low-compliance, high-frequency oesophageal manometry. Nine healthy volunteers served as controls. The amount of muscle and connective tissue in the cricopharyngeal muscle was also measured by computerized morphometry and compared with findings in cadavers with no history of dysphagia. Preoperative manometry in patients with Zenker's diverticulum showed an incomplete relaxation of the upper oesophageal sphincter (UOS) (the residual UOS pressure at swallowing was 7.9 (range 1-20)mmHg in patients versus 0.2 (-12.5-14) mmHg in controls; P < 0.001) and increased pharyngeal intrabolus pressure (21 (range 0-52) versus 9 (range 0-16) mmHg; P < 0.01), with no pharyngo-oesophageal coordination abnormalities. Both parameters significantly decreased after myotomy. Patients with Zenker's diverticulum had significantly fewer muscle fibres in the cricopharyngeus and the muscle:connective tissue ratio was significantly lower (0.94 (range 0.8-1.4) in patients versus 1.5 (1.4-3.6) in controls; P < 0.05). This study supports the theory that Zenker's diverticulum is caused by an increased intrapharyngeal pressure at swallowing due to incomplete cricopharyngeal muscle relaxation resulting from localized sclerosis.
Adult↗
Calcitonin gene-related peptide selectively increases cAMP levels in the guinea-pig ureter.
Calcitonin gene-related peptide (CGRP, 0.1 microM) and forskolin (10 microM) both produced a time-dependent accumulation of cAMP in homogenates of the guinea-pig ureter, while cromakalim (3 microM) was ineffective. Neither agent did increase the cGMP levels. cAMP accumulation induced by CGRP or forskolin was unchanged by glibenclamide (1 microM). In sucrose gap, the application of forskolin (1-10 microM for 15 s) hyperpolarized the smooth muscle membrane and its effect was greatly enhanced when tested in a low-K+ medium (extracellular K+ reduced from 5.9 to 1.2 mM). The hyperpolarization produced by 10 microM forskolin was reduced and abolished by 1 and 10 microM glibenclamide, respectively, in both normal and low-K+ medium. The present findings demonstrate that CGRP determines a selective cAMP accumulation in the guinea-pig ureter and suggest that elevation of cAMP may be involved in the opening of glibenclamide-sensitive K+ channels in the ureter smooth muscle.
Animals↗
The persistent primitive hypoglossal artery: a rare anatomic variation with frequent clinical implications.
The case of a persistent primitive hypoglossal artery (PHA) in a 72-year-old man dead from myocardial infarction is presented. The autopsy showed the presence of a semicircular marginal infarct on the surface of the left cerebral hemisphere. The PHA anastomized the basilar artery origin with the left internal carotid artery, running through the left hypoglossal canal together with the hypoglossal nerve. The vertebral and posterior communicating arteries were hypoplastic. The PHA represented the morphological base on which the cerebral vascular insufficiency acted, following the generalized circulatory insufficiency due to the myocardial infarct, causing the cerebral infarct. Based on the embryology of the cranial arteries and on the morphological findings we suggest that the persistence of the hypoglossal artery: 1) precedes the vertebral and posterior communicating arteries hypoplasia causing it by competition for the territory of distribution; 2) gives rise to an almost complete dependence of the cerebral circulation from the carotid system with predictable ischemic consequences in the case of a critical reduction of the carotid blood flow; 3) may be associated with an anomalous structure of the vessel wall and exposes the basilar trunk to an unusual haemodynamic stress, predisposing to the onset of aneurysms.
Aged↗
Nitric oxide modulates angiogenesis elicited by prostaglandin E1 in rabbit cornea.
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Alprostadil↗
Course of the caudal hypoglossal rootlet through the vertebral artery.
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Aged↗
Substance P increases cyclic GMP levels on coronary postcapillary venular endothelial cells.
The vasodilating effect of substance P (SP) at the microvascular level is endothelium-dependent. In the present study we evaluated whether SP activates nitric oxide (NO) production by venular endothelial cell. We evaluated NO activation by measuring cyclic GMP levels in cultured endothelial cells isolated from coronary postcapillary venules of bovine origin (CVEC). Our results indicate that 5 min exposure of CVEC to 10 nM SP doubled basal cyclic GMP levels. Cell treatment with the NO synthase inhibitor L-NMMA reduced the basal levels of cyclic GMP and abolished the effect of SP but did not modify the increase in cyclic GMP in response to exogenous NO. These data indicate that a) microvascular endothelium responds in an autocrine fashion to NO with increased cyclic GMP levels, b) SP activates cyclic GMP pathway through NO production.
Animals↗
Enhanced responsiveness of ovalbumin-sensitized guinea-pig alveolar macrophages to tachykinins.
1. We have evaluated the ability of substance P (SP), neurokinin A (NKA) and the selective NK2 receptor agonist [beta-Ala8]-NKA(4-10) to induce superoxide anion (O2-) production and prostanoid (prostaglandin E2, thromboxane B2) release from alveolar macrophages (AMs) isolated from control or actively sensitized guinea-pigs. 2. The dose-response curves for NKA and SP were shifted to the left (three orders and one order of magnitude, respectively) in AMs isolated from sensitized animals, with no variation in maximal effects. 3. By evaluating the effects of [beta-Ala8]-NKA(4-10), we observed that not only was the concentration-response curve shifted to the left in both the functional parameters examined, but also maximal effects were significantly enhanced in AMs isolated from sensitized guinea-pigs. 4. This varied responsiveness seems to be specific for tachykinins, as it was not reproduced by another AM stimulant, the bacterial peptide N-formylmethionyl-leucyl-phenylalanine (fMLP). 5. Only small amounts of beta-glucuronidase were released following tachykinin or ovalbumin stimulation both in control and sensitized AMs. 6. These results indicate that AMs isolated from sensitized guinea-pigs show an increased responsiveness to NK2 receptor stimulation and further stress the role played by AMs in allergic lung diseases.
Animals↗
Primary Kaposi's sarcoma of intraparotid lymph node.
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Aged↗
[The effect of vasoactive factors on the growth of of coronary endothelial cells].
The aim of this study was to evaluate the effect of adenosine and bradykinin on endothelial cell growth at capillary level. DNA synthesis was measured in subconfluent capillary endothelial cells obtained from coronary venules (CVEC) after exposure to adenosine or bradykinin. Our results indicate that adenosine and bradykinin induced a dose-dependent proliferation of CVEC. Maximal effect was observed at the dose 100 microM concentration for adenosine and 0.1 microM concentration for bradykinin.
Adenosine↗
Fenestration of the vertebrobasilar junction.
A fenestration of the vertebrobasilar junction was found in an 80-year-old man during autopsy. It was associated with thrombosis of the vertebral arteries which had caused a left Wallenberg syndrome. The left limb of the fenestration presenting the same transverse diameter as that of the remaining part of the basilar artery appeared to be its direct (true) origin. The right limb had a lesser transverse diameter and appeared to bridge the lateral surface of the rostral end of the right vertebral artery and the basilar trunk. According to the authors, this fenestration could have been caused by the persistence of the cranial part of a primitive lateral vertebrobasilar anastomosis, rather then by the usual incomplete fusion of the primitive paired basilar arteries.
Aged↗
Giant coronary aneurysm associated with aortic mucoid medionecrosis.
A case of sudden death due to rupture of a dissecting aneurysm of the ascending aorta in a 38-year-old man is presented. The patient had a clinical history of severe hypertension. The autopsy also revealed the presence of a voluminous aneurysm of the right coronary artery and a solitary multilocular cyst of the right kidney. It is thought that a prodromal influenza-like syndrome and the renal lesion could have played a role in causing the vascular pathology.
Adult↗
Primary intrasellar coccidioidomycosis simulating a pituitary adenoma.
The case of a 68-year-old woman who had relatively acute, unilateral ophthalmoplegia is reported. Radiological studies indicated a mass lesion involving the pituitary gland and left cavernous sinus. Pathological tissue obtained by the transsphenoidal approach revealed the presence of a Coccidioides granuloma. This pathological entity should be considered when evaluating patients with a pituitary mass and ophthalmoplegia.
Adenoma↗
Ultrastructural findings on the interface between hydroxylapatite and oral tissues.
Two patients were treated with surgical implantation of synthetic, granular, nonporous hydroxylapatite to correct bone defects around dental implants. Ultrastructural examination of biopsy specimens taken several months later showed that the hydroxylapatite material was encapsulated mostly by fibrous connective tissue, without any signs of active inflammation. Osteoid and mature bone were also present in many areas. Under the electron microscope, an electron-dense delimiting band was detected at the interface of the tissue and the material. A polygonal, networklike structure, originating from the electron-dense layer and penetrating into the periphery of the hydroxylapatite granules, was also observed. These findings confirm the results of previous studies, in which it was hypothesized that the electron-dense structures were of a mucopolysaccharide nature and might prove the close bond between the hydroxylapatite and the tissues.
Alveolar Process↗
Basilar arterio-venous pseudoparallelism due to persistence of embryonal venous pattern.
A vascular malformation, consisting of a venous vessel bridgeing the right inferior petrosal sinus and the anterior spinal veins, was found in the posterior fossa. The vessel presented a ring-like course around the right trigeminal root, and it was parallel and dorsal to the basilar artery. The malformation was associated with cutaneous and hepatic angiomas and peri-osteal lipomas. It had been clinically silent for 52 years, when it thrombosed causing death. The authors think that, within a general mesenchymopatic state, this is a result of the persistence of an embryonal cerebral venous pattern.
Autopsy↗