Biomedical subjects
Publications and source records attributed to P Lacombe.
Arterial manifestations of Behçet's disease carry a particularly poor prognosis, especially pulmonary arterial aneurysms. We report herein the successful embolization of multiple bilateral pulmonary arterial aneurysms in a young Algerian man, whose treatment included corticosteroids and immunosuppressive drugs.
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Bronchial artery embolization (BAE) is well accepted and widely used for management of massive and recurrent hemoptysis. Recurrent hemoptysis occurs in 20% of cases. It may be due to partial embolization, recruitment of other systemic collaterals, recanalization of an embolized artery, or progression of primary disease. Severe complications of BAE are limited to spinal cord injury, oesophageal necrosis, and bronchial ischemia. The proper application of bronchial arteriography and embolization techniques depends on a thorough knowledge of the arterial anatomy, a meticulous catheterization technique, the use of nonionic or lowosmolarity contrast materials, and adequate positioning of the catheter. In these optical conditions of safety, BAE is the treatment of choice for severe and recurrent hemoptysis.
The nucleus basalis magnocellularis (NBM) of the rat, equivalent of Meynert's nucleus in the primate, is the origin of the main cholinergic innervation of the cerebral cortex. Stimulation of this area has been previously shown to induced marked, cholinergically mediated, blood flow increases in the frontal and parietal cortices. However, the complete distribution of the cerebrovascular effects of NBM stimulation within the whole brain has not been determined. In the present study, we used the [14C]iodoantipyrine autoradiographic method to measure local cerebral blood flow (CBF) in the unanesthetized rat, chronically implanted with a stimulation electrode. We performed unilateral electrical stimulation of the NBM in order to compare both the interhemispheric differences in blood flow and the differences with a group of sham-stimulated rats. Considerable blood flow increases were found in most neocortical areas, exceeding 400% in the frontal area, compared to the control group. Marked responses also appeared in discrete subcortical regions such as the zona incerta, some thalamic nuclei and structures of the extrapyramidal system. These responses were mostly ipsilateral to the stimulation. The significance and the distribution of these blood flow increases are related first, to anatomical and functional data on mainly the cholinergic projections from the NBM, but also non-cholinergic pathways connected with the NBM, second, to biochemical data on the basalocortical system, and third, to the limited ultrastructural data on the innervation of microvascular elements. This cerebrovascular study represents a step in the elucidation of the function of the basalocortical system and provides data which may be related to certain deficits of degenerative disorders such as Alzheimer's disease in which this system is consistently affected.
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RATIONALE AND OBJECTIVES: To assess the intraobserver reliability of three methods used frequently to evaluate joint destruction in rheumatoid arthritis: the Sharp method, the Larsen method, and the carpo:metacarpal ratio. METHODS: One observer analyzed twice within a 6-week interval 71 radiographs from patients with rheumatoid arthritis. Reliability was estimated by intraclass correlation coefficient (R) and by Altman-Bland graphical method. Correlations were examined by the Spearman's coefficient (r). RESULTS: The intraobserver reliability of each method appeared satisfactory with a good result for the Sharp method (R = 0.97). The correlation was strong (r > 0.80) between the results obtained by Sharp's and Larsen's methods and weaker between the results of the two former methods and the carpo: metacarpal ratio. CONCLUSIONS: Sharp's method should be used preferentially in studies evaluating the radiologic changes in rheumatoid arthritis over time, especially in clinical trials. The carpo:metacarpal ratio may be considered as a complementary method, when wrist destruction is of conceptual importance.
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The aim of this study was to determine whether alpha-chloralose, when associated with an initial period of halothane, is a suitable anesthetic regimen for cerebrovascular studies. For this purpose, rats anesthetized with alpha-chloralose plus halothane induction were first subjected to noxious stimuli, and the behavior, EEG and systemic variables were recorded. During a second step, cortical blood flow was measured with laser-Doppler flowmetry and the time-course of the cerebrovascular reactivity to hypercapnia were measured in artificially ventilated rats anesthetized with either alpha-chloralose (40 mg.kg-1, s.c.) plus halothane induction (1.5% given during the first 45-60 min) or halothane alone (1.5%). Finally, an experimental paradigm was developed that allowed the comparison of the hypercapnic reactivity, both in awake and anesthetized conditions in the same animal. Our results show that the association of alpha-chloralose with halothane leads to stable cardiovascular parameters and immobility of ventilated rats, placed in ear bars without curare, for 3 h without any sign of discomfort. Based on EEG criteria, we found that halothane induction lengthens the duration of alpha-chloralose anesthesia (253 +/- 19 vs. 200 +/- 15 min, P < 0.01). Under alpha-chloralose alone or in association with halothane induction, the vascular reactivity to hypercapnia was considerably impaired (-85% compared to the awake state, P < 0.01), but this impairment was transient, since a control reactivity was restored 150-190 min after induction of anesthesia. Under halothane alone, the vascular reactivity remained reduced throughout the experiment. These results provide evidence that alpha-chloralose plus halothane induction is a suitable anesthetic regimen which displays a temporal window of normal cerebrovascular reactivity.
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Cholinergic projections from the basal forebrain are capable of influencing local cortical blood flow (CoBF). The effect of age on this influence was investigated by measuring CoBF and tissue gas partial pressures (PtO2, PtCO2) by mass spectrometry in conscious young adult (2-4 months) and aged (22-28 months) Fischer 344 rats. Electrical stimulation (50 microA) of the substantia innominata (SI) increased frontal (+100.9%) and parietal (+28.4%) CoBF in young rats, but the effects were less in aged rats (frontal, +48.6%, P < 0.05; parietal, +18.9%, difference N.S.). Frontal PtO2 was increased in young but not aged rats (P < 0.01.). During standard hypercapnia, changes in CoBF, PtO2 and PtCO2 did not differ between young and aged rats. Under physostigmine infusion (0.15 mg/kg/h, i.v.), the CoBF increases to SI stimulation were approximately doubled in both cortices, in young and aged rats, and PtO2 increases were also significantly greater. However, frontal PtO2 increases were significantly smaller in aged (+7.6%) than in young (32.7%) rats, as were frontal PtCO2 reductions. We conclude: (i) the influence of the SI on frontal CoBF and PtO2 is substantially reduced with age; (ii) although physostigmine treatment potentiates this influence in both groups, the beneficial effects are relatively limited for aged rats.
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The aim of this study was to determine the distribution within the whole brain of the vascular effects of stimulation of the substantia innominata. This basal forebrain nucleus is the major cholinergic input in the neocortex in the rodent. The local cerebral blood flow was measured by the autoradiographic [14C]iodoantipyrine technique in a group of control and a group of stimulated unanesthetized rats. The substantia innominata was electrically stimulated through a chronically implanted electrode. The stimulation induced blood flow increases exceeding 200% in the hemisphere ipsilateral to the stimulation and 100% in the contralateral hemisphere compared to the control group. The ipsilateral vasodilations were observed not only in the cortical areas but also in some subcortical structures. Comparison with previous data suggests that part of the effects is due to cholinergic neurons of the substantia innominata and part to non-cholinergic neurons and indirect effects. However, only two out of eight stimulated rats displayed this response. The low reproducibility of the results is discussed, considering the stimulation paradigm which has been developed for future measurements of the cerebral glucose utilization which requires a long duration stimulation period.
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Despite the increasing number of publications devoted to the cerebrovascular role of NO, its precise influence in awake animals is still poorly characterized. The effect of nitric oxide synthase (NOS) inhibition on the cerebrovascular CO2 reactivity was therefore studied in conscious rats. Regional CBF was measured using the [14C]iodoantipyrine technique and brain tissue sampling. The CO2 reactivity was determined 60 min after administration of 30 mg kg-1 N omega-nitro-L-arginine methyl ester (L-NAME). Blockade of NOS by L-NAME significantly decreased CBF in all 11 brain regions studied (-17 to -49%) and increased arterial pressure from 117 +/- 12 to 147 +/- 11 mn Hg. In control conditions, CO2 responsiveness ranged from 1.3 +/- 0.4 in the hypophysis to 6.4 +/- 0.6 ml 100 g-1 min-1 mm Hg-1 in the parietal cortex. Following L-NAME injection, the reactivity to hypercapnia was significantly attenuated in all structures, the magnitude of the reduction ranging from 57% in the medulla to 74% in the cerebellum. This result shows that NO is an important mediator of the hypercapnic vasodilation in the conscious rat.
We report a case of acute myocardial infarction occurring in a patient with severe aortic stenosis and left ventricular hypertrophy. A coronary angiogram performed during the acute phase of evolving myocardial infarction excluded coronary obstruction as the cause of acute myocardial infarction in this patient.
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Few cases of transcatheter coronary fistula closure have been reported. High flow coronary fistulae are usually treated by surgery. This case report presents a 5.4 liters/min flow coronary fistula percutaneously closed by steel coils. This large flow needed the packing of 25 coils, 10-15 cm long, for its total occlusion.
This study sought to determine whether the cortical cholinergic projections from Meynert's nucleus are actually the target of the cholinesterase inhibitor physostigmine, which presents the ability to increase cortical blood flow. To this aim, the multiregional cerebrovascular effects of physostigmine in rats with and without lesion of the substantia innominata (SI), the equivalent of Meynert's nucleus of primates, were investigated. Unilateral SI lesions were made using ibotenic acid in three groups of rats. Four to 11 days later, the cortical choline acetyltransferase (ChAT) activity was measured in one group to assess the efficacy of the lesion. In the two other groups, the regional cerebral blood flow was measured using the [14C]iodoantipyrine technique, under physostigmine (0.2 mg/kg/h iv) or control conditions. SI lesion induced 27-59% fall in cortical ChAT activity in the ipsilateral hemisphere with the frontal area most affected. Despite these large biochemical differences, the lesion had little cerebrovascular effects. Side-to-side blood flow differences did not exceed 11% and did not strictly overlap the ChAT depletion. Physostigmine increased flow (38-66%) in all cortical areas, with no frontal predominance. Despite these considerable vasodilations, there were no significant differences between the lesioned and the intact hemisphere, nor any significant interaction between physostigmine and SI lesion. Thus, physostigmine does not actually activate the SI neuron terminals. This result suggests that cholinesterase inhibitors cannot be used as presynaptic markers of the cholinergic activity of this nucleus and casts doubts on their specificity as enhancement therapeutic agents in Alzheimer's disease.