Symptomatic splenic infarction complicating adult Kawasaki disease.
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Biomedical subjects
Publications and source records attributed to P Lacombe.
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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.
In the present study, we have investigated the effects of an activation of the ascending serotonergic pathway on the cerebral blood supply to a number (63) of well-defined neuroanatomical structures. To this end, we have measured the local cerebral blood flow during electrical stimulation of the dorsal raphe nucleus. Measurement of regional blood flow was performed in the conscious rat through the use of the [14C]iodoantipyrine autoradiographic technique. Stimulation of the dorsal raphe nucleus induced increases (> 15% compared to control) in cerebral blood flow in 17 structures of which statistical significance (P < 0.05) was achieved in nine; raphe stimulation significantly decreased flow in three regions. The greatest increases (+71 and +46%) were found in the frontal sensorimotor and posterior parietal cortices. Other increases were noted in relay stations of the extrapyramidal and limbic systems. Stimulation induced a decrease in two regions of the primary auditory system and in the lateral habenular nucleus. These results show that activation of the serotonergic pathway in the conscious rat effects regional cerebral blood flow heterogeneously, differing from the widespread increase in glucose utilization that we previously observed using the same experimental paradigm. Statistical analyses indicated that activation of the dorsal raphe nucleus resulted in a global modification of the flow-metabolism ratio. Moreover, in 19 out of 31 regions analysed, this ratio is significantly altered as compared to control. The dichotomy between raphe-induced changes in flow and glucose-metabolism could be explained by one or both of two hypotheses; firstly there could be a direct serotonergic innervation of cerebral resistance vessels; secondly, during raphe stimulation it could be that glucose use is not the primary determinant of tissue perfusion.
BACKGROUND: Aneurysms of the subclavian artery are rare in childhood and may be due to traumatic, infectious or congenital causes. CASE REPORT: A 15 year-old boy presented with a sudden left visual disturbance plus decreased muscle strength and paresthesias of the left arm; these manifestations disappeared within 15 minutes. His neurological examination on admission was normal. The right arm radial pulse was weak and the blood pressures of the right and left arms were significantly different. Doppler showed a right subclavian artery aneurysm containing several clots, that was confirmed by angiography. There were no signs of inflammation or indication of autoimmune disease. This aneurysm might have been caused by trauma as the patient had had a violent cervical traumatism after a diving accident 2 years earlier. The aneurysm was surgically removed and the right vertebral artery arising from it was reimplanted. Histological examination of the aneurysm gave no evidence of etiology. The post-surgical MRI showed no brain abnormaly. CONCLUSIONS: This aneurysm is probably of post-traumatic origin. The cerebral disturbance could be due to embolism or transient ischemia; the latter is more compatible with the normal NMR.
The distribution of serotonergic nerves in major basal and isolated small pial arteries (diameter > or = 50 microns) was investigated immunohistochemically using an antibody directed against tryptophan-5-hydroxylase (TPOH), the rate-limiting enzyme in the synthesis of 5-hydroxytryptamine (5-HT or serotonin), and compared to that of the noradrenergic system labeled for the selective noradrenaline (NA) synthesizing enzyme, dopamine-beta-hydroxylase (DBH). In addition, the possible peripheral and/or central origins of the cerebrovascular serotonergic (TPOH-positive) nerve fibers were examined. Strongly labeled TPOH-immunoreactive (TPOH-I) fiber bundles were observed in major basal arteries and gave rise to small varicose fibers organized in a meshwork pattern. The highest density of TPOH-I fibers was found in the middle cerebral artery followed by the anterior cerebral and the anterior communicating arteries, with a moderate to low density in the internal carotid and the vertebro-basilar trunk. Of the isolated pial arteries, only the larger ones (diameter > 75 microns) were significantly endowed with TPOH-I varicose fibers. However, free floating TPOH-I nerves were observed coursing through the pia-arachnoid membranes and reaching small pial vessels. In contrast, DBH-I nerve fibers were fine and were visualized primarily as numerous varicosities distributed in a circumferential manner around the vessel wall. A very high density of DBH-I varicosities was seen in the rostral part of the circle of Willis, with the internal carotid being the most richly supplied followed by the anterior cerebral and the anterior communicating arteries; comparatively, the middle cerebral artery was moderately innervated. The differences in distribution pattern and density between TPOH-I and DBH-I cerebrovascular fibers clearly suggest that these two innervation systems are not exactly superimposable. Superior cervical ganglionectomy caused an almost complete disappearance of TPOH-I nerves in all vascular segments, with some residual fibers in selected vessels. Lesion of the central serotonergic component with the neurotoxin 5,7-dihydroxytryptamine had virtually no effect on the TPOH-I fibers in the major basal and isolated pial arteries. These results strongly suggest that the serotonergic innervation of major cerebral as well as pial arteries has a prominent peripheral origin closely related to the sympathetic system. Processing of superior cervical ganglion slices for TPOH immunocytochemistry, however, failed to unequivocally detect TPOH-I neurons.
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