[Ocular hypertonia disclosed by the association of central retinal vein and cilioretinal artery occlusions].
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Biomedical subjects
Publications and source records attributed to C Boudet.
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The time-related changes of dopamine (DA) and norepinephrine (NE) pools were investigated in heart, superior cervical ganglion (SCG) and urine in rats treated chronically with guanethidine (50 mg/kg i.p. five days each week). The efficiency of sympathectomy was assessed by the great loss of NE in heart and superior cervical ganglion (SCG) (-96% and -76% respectively of control values on day 18) together with the ready reduction of NE and 3-methoxy-4-hydroxyphenylglycol (MHPG) in urine. The pattern of changes was quite different for DA, which was less readily affected and at a lesser extent than NE in heart and SCG thus suggesting the presence of norepinephrine-independent DA stores. Similarly the urinary excretion of free DA, free 3,4-dihydroxyphenylacetic acid (DOPAC) and free homovanillic acid (HVA) was slightly decreased only from the 9th day, whereas urinary conjugated DA remained unaltered. These results indicate that the greatest portion of urine free and conjugated DA, free DOPAC and free HVA derives from peripheral pools located outside noradrenergic neurons. Alternatively, the time-course of DA sensitivity to guanethidine suggests that a portion of urine DA may originate from DA stored independently from NE in noradrenergic neurons.
Almitrine increases ventilation by stimulating the peripheral arterial chemoreceptors. This study assessed the effects of acute and chronic almitrine treatments on the dopamine (DA) and norepinephrine (NE) contents and utilization rates in the rat carotid body. Almitrine (5 mg/kg ip) caused a 34% reduction in DA content after 30 min. Extending the almitrine treatment for 15 days (one daily ip injection) produced a further progressive diminution in DA stores (-55%; P less than 0.01). The utilization rate of DA measured after inhibiting catecholamine biosynthesis by alpha-methyl-p-tyrosine was strongly reduced by almitrine (-98% after 15 days; P less than 0.01). The effects of almitrine were dose dependent. The noradrenergic activity was much less altered by the drug. The data showed that almitrine can modify the dynamics of DA in rat carotid body producing a decrease in both content and utilization rate.
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Free and sulfated 3,4-dihydroxyphenylacetic acid (DOPAC) were measured in rat plasma after bilateral 6-hydroxydopamine lesions of striatum or mesolimbic tissue (nucleus accumbens + olfactory tubercle). Both lesions selectively reduced plasma DOPAC sulfate levels without altering free DOPAC or catecholamine levels in plasma, sympathetic ganglia or adrenal medulla. The present work confirms our previous findings and suggests that DOPAC sulfate functional state of striatal and mesolimbic dopaminergic neurons.
Bilateral retinal arteritis with multiple aneurysmal dilatations was described for the first time by Kincaid and Schatz in 1983. We have reported a typical case of this disease which occurred in a 49-year-old woman: retinal abnormalities were followed up during two years by repeated fluorescein angiographies. The etiology of the disease and its connexions with periarteritis nodosa are discussed. While the patient was given steroid therapy per os during 16 months, new segmental inflammation of retinal arteries were observed. Inflammation affecting retinal arteries would result in weakening of the arterial wall and aneurysmal outpouchings.
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In man, the major portion of plasmatic and urinary catecholamines is found in a conjugated/sulfate form. The biological characteristics of the conjugates (formation sites, kinetics of appearance and disappearance from the plasma, genetic regulation, influence of biological factors) are different from those of the free forms. Physiopathological data show that the dosage conjugated catecholamines together with that of free amines, provides interesting informations on the integrative level of sympathetic activity and on the regulation of the catecholamines plasma concentrations by conjugation. In these two objectives, the dosage of DA sulfate proves very important.
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The ability of diosmin to inhibit venous catechol-O-methyltransferase (COMT) activity was studied comparing it with tropolone in rat superior mesenteric vein (MV), inferior vena cava (IVC) and saphenous vein (SV). Diosmin inhibited COMT activity in the mesenteric vein after 200 and 400 mg/kg i.p., but only at 400 mg/kg in IVC. The COMT inhibitory effect of diosmin (400 mg/kg) was smaller than that of tropolone (50 mg/kg). Furthermore, diosmin, but not tropolone, increased urinary normetanephrine (NMN) excretion (+56%) at 400 mg/kg and that of 3-methoxy 4-hydroxyphenylglycol (MHPG) in a dose-dependent way, thus suggesting that diosmin may exert an activating effect on sympathetic activity. Both mechanism--local inhibition of COMT and enhanced sympathetic activity--may contribute to increase NE levels in the synaptic clefts of the vascular wall and explain the venoconstrictor effect of this drug.
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Two cases of acute retinal necrosis are reported, the etiology of this affection being priorly defined. The lesions were bilateral in the first case, and retinal detachment developed: the first eye was inoperable, and surgery was unsuccessful for the second eye in spite of a salvage vitrectomy after a classical operation. We therefore treated the second case with immediate and massive corticotherapy, and, mainly, preventive total vitrectomy as soon as the first signs of vitreous retraction appeared and before the occurrence of retinal detachment. This preventive vitrectomy, not previously described to our knowledge, seems to provide favorable results.
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