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Biomedical subjects

F C Rose

Publications and source records attributed to F C Rose.

177 records · Page 10Linked to original sources

Cholesterol crystal embolization in rat brain: a model for atheroembolic cerebral infarction.

Acute and delayed effects of embolizing cerebral surface vessels with cholesterol crystals were studied by direct observation in anesthetized rats and rabbits, using an open-skull technique, and by histological examination of brains at intervals of one day and one week following embolization. The number and size spectrum of crystals, which were infused into the ipsilateral internal carotid artery, were believed to approximate those released by a rupturing large atheromatous plaque in man, but the other lipid materials contained in such plaques were intentionally excluded. It was found that cholesterol crystals had only limited ability to impede blood flow in the 20--80 mu diameter arteries in view. They were also inert within the lumen, causing no vessel wall reaction even after a week; nor was any evidence seen of a thrombogenic effect. Local caliber changes in the containing artery were reproducibly seen, with dilatation of the arterial segment proximal to the embolus and narrowing of the segment in front. These changes appeared to represent an active response of the vessel wall, rather than a passive response to alterations in intraluminal pressure. The difficulty in subsequently locating cholesterol emboli histologically was confirmed. Possible therapeutic implications for atheroembolic cerebral infarction in man were discussed.

Animals↗

Differential contributions of major lipid components of atheroma to outcome of cerebral atheroembolism. A study in an animal model.

Cerebral atheroembolism, in which mainly lipid emboli are released from rupturing atheromatous plaques, may occur without apparent effect, or result in cerebral ischemia and infarction. The reasons behind these unpredictable consequences were sought in the interaction, in vitro and in an animal model, between the main lipid components of advanced plaques. Pure preparations of representative lipids were each harmless when embolized into the cerebral circulation. In contrast, combinations in proportions similar to those in advanced human plaques caused infarction, whether these were synthetic mixtures or extracts from plaques of the entire lipid fraction. The most important physical interaction between the lipids was aggregation of crystals by oils. Between cholesterol and the mainly liquid esters, this created in vitro a range of glutinous aggregates. Triglyceride lowered the melting point of esters, increasing their oiliness, and reduced the cohesiveness of aggregates in the face of operative mechanical forces through a fall in viscosity. Phospholipid, acting principally as an emulsifying agent, promoted dispersion of the oil, secondarily freeing the crystals from its aggregating effect. In the plaque, the balance of these factors will determine the size and number of particles likely to embolize, and, therefore, the clinical outcome should the plaque rupture.

Animals↗

Diverging trends in cerebrovascular disease and ischaemic heart disease mortality.

The trends in age adjusted and age and sex specific mortality rates for the period 1968-1980 are compared for ischaemic heart disease and cerebrovascular disease. For both sexes and at all ages over 45 the mortality rates for cerebrovascular disease have fallen significantly. However, the mortality rates for ischaemic heart disease are rising significantly for males aged 55-64 and females aged 45-64. The divergence in trend is particularly noticeable for females aged 45-64. Possible hypotheses are discussed explaining this divergence in trend between two cardiovascular diseases of assumed similar aetiology.

Actuarial Analysis↗

Motor neurone disease.

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Bulbar Palsy, Progressive↗

Trigger factors and natural history of migraine.

Trigger factors are important for two main reasons. Firstly, they may provide some clues as to the pathogenesis of migraine. Secondly, by avoidance of them, drug therapy may be obviated. There are at least sixty trigger factors in migraine but the mechanism by which they produce migraine attacks varies.

Arylsulfotransferase↗

Failing memory.

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Acetylcholine↗

CT changes associated with migraine.

In order to determine further the correlation between severe migraine and cerebral atrophy, a group of patients attending either the Charing Cross Hospital migraine clinic or outpatient clinics at the National Hospital, Queen Square, was investigated by computed tomography. The results confirm an association between atrophy and migraine of more than 5 years duration, probably more severe in men than women. The most striking changes were seen in those men who suffered from attacks lasting less than 6 hr.

Adolescent↗