The utilization of glutamine by the retina: an autoradiographic and metabolic study.
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Biomedical subjects
Publications and source records attributed to J Marshall.
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The ultrasonic radiation utilised in phacoemulsification procedures for the removal of cataractous lenses results in the widespread production of discrete lesions in the corneal endothelium. The morphology of this induced damage has been examined in rabbit and man using both scanning and transmission electron microscopy. The illustrated results are related to both the duration of the ultrasonic exposure and to the mechanisms of damage.
The responses of corneal endothelium to a 2-minute exposure of ultrasound from a clinical phacoemulsification device have been studied by specular microscopy and both scanning and transmission electron microscope. Healing of lesions occurred in two ways, and these were related to lesion size. Small lesions healed by a process of rosette formation, and large lesions were repaired by a process of endothelial dedifferentiation and migration. All damaged areas were re-covered with endothelial cells within 24 hours of exposure, and at this time corneal thickness had returned to control levels. The implications are discussed in relation to the phacoemulsification procedure.
A patient with temporal arteritis developed a variety of ischaemic lesions in the eyes. Infarction of the inner retina and optic nerve head was delineated on presentation by white swelling in the retinal nerve fibre layer. The role of interrupted axoplasmic transport in the production of this sign is discussed. Outer retinal infarction was also noted on presentation and subsequently gave rise to striking pigmented scars.
Tinofedrine, a new derivative of l-norephedrine, was examined for cerebral vasodilator activity in man. Ten patients with reduced cerebral blood flow (CBF) and multi-infarct dementia were given the drug intravenously. Cerebral blood flow increased significantly by 28% from a mean of 43.3 to 55.5 ml/100 g/min.
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Cerebral blood-flow (C.B.F.) was measured in 38 patients with haematocrit values (Hct) in the range 0-47--0-53 and was found to be significantly lower than in 43 patients with Hct in a lower range (0-36--0-46). After reduction of Hct in the higher Hct group by venesection, flow increased by a mean of 50%. This improvement in flow was largely due to a reduction in viscosity. Hct around the generally accepted upper limit of normal may be an important factor in the causation of occlusive vascular disease.
Cerebral blood-flow (C.B.F.) has been measured in 16 patients with polycythaemia of differing severity. The mean C.B.F. was 37-9 ml/100 g/min, which is significantly below the normal level of 69-1 (S.D. 9-3) ml/100 g/min (P less than 0-001). C.B.F. measurement was repeated after venesection in 15 of the patients. Lowering the haematocrit from a mean of 0-536 to a mean of 0-455 was associated with a 73% increase in mean C.B.F. (P less than 0-001) and a 30% reduction in whole-blood viscosity. Low C.B.F. was found at haematocrit levels between 0-46 and 0-52. Haematocrit levels that are currently acceptable in the management of polycythaemia may therefore be too high.
Autoradiographs of frog retinas incubated with radioactively labelled taurine show heavy grain density over (i) cells in the position of amacrine interneurones, (ii) the inner plexiform (synaptic) regions, giving a striated appearance, (iii) photoreceptor cells and their synaptic terminals, and (iv) the pigment epithelium. The inner retina, the photoreceptor cell layer and the pigment epithelium all have uptake systems for taurine with apparent Km's in the high affinity range (Km, 20-50 micron; Vmax, 13-33 nmoles/g/min). In vivo subcutaneously injected taurine was taken up by the pigment epithelium and then passed to the photoreceptors and inner retina over about 10 days. The total level of nucleide in the retina remained constant for at least 6 weeks. There was little or no metabolism of the labelled taurine during this time.
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The phenomenon of shunting of blood in association with various intracranial lesions is well known; however, usually clinical symptoms are attributable to the lesion and not to the redistribution of regional cerebral blood flow (rCBF). We report three patients investigated by angiography and rCBF studies in whom symptoms appeared to be due to a hemodynamic steal within one cerebral hemisphere, between hemispheres, and from the brain into a tumor, respectively.
The clinical, angiographical, operative and histological records of 52 patients undergoing carotid endarterectomy for transient cerebral ischaemic attacks were reviewed. Thrombus or other friable material was present in 66 per cent of the 24 patients operated upon within 4 weeks of a clinical attack, but in only 21 per cent of the 28 patients in whom the time interval was longer. The data favour an embolic explanation for the clinical episodes and further suggest that thrombus formation on atheromatous stenosis and ulceration is intermittent.
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