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Biomedical subjects

R W Ross Russell

Publications and source records attributed to R W Ross Russell.

8 recordsLinked to original sources
PubMed1988

Cause and treatment of insufficiency in the cerebral circulation.

The term cerebrovascular insufficiency describes reversible attacks of focal cerebral ischaemia affecting patients with extensive extracranial artery disease. The attacks are caused by failure of collateral blood supply and are often related to minor reductions in blood pressure. Characteristic clinical features such as jerking, involuntary movements and loss of vision in response to bright light may allow insufficiency attacks to be distinguished from other varieties of focal cerebral ischaemia. The treatment of patients with cerebral insufficiency aims to increase collateral blood supply by surgical removal of arterial obstruction and by medical therapy to prevent episodes of systemic hypotension.

Cerebrovascular Circulation↗
PubMed1987

Amaurosis fugax under the age of 40 years.

Sixteen patients who presented under the age of 40 years with amaurosis fugax have been studied. Follow up from the time of presentation was one to 13 years with a median of 3 years. One patient whose attacks of uniocular visual loss were associated with headache developed a permanent uniocular field defect. None of the other patients has suffered permanent visual loss, or had symptoms of cerebral or myocardial ischaemia. All angiograms were normal and it is suggested that carotid angiography is unnecessary in this age group. Four out of ten patients studied demonstrated evidence of platelet hyperaggregability to low concentrations of arachidonic acid and adenosine diphosphate with spontaneous aggregation. However, in six patients treated with aspirin, including three with previous platelet hyperaggregability, there was no change in the frequency of their attacks implying that the observed platelet abnormalities were not the cause of the amaurosis fugax.

Adenosine Diphosphate↗
PubMed1986

Recirculation after cerebral ischemia. Simultaneous measurement of cerebral bloodflow, brain edema, cerebrovascular permeability and cortical EEG in the rat.

The 4-vessel occlusion rat model of cerebral ischemia was modified to permit the simultaneous measurement of cerebral blood flow (hydrogen clearance), brain edema (specific gravity), cerebrovascular permeability (14C-AIB) and electrocardiogram. Surgery was performed in one stage in the anesthetised, paralysed and ventilated rat and severe hemispheric ischemia was produced in all animals. Electrode implantation did not alter cortical specific gravity or Ki for 14C-AIB. During 4-vessel occlusion mean cortical CBF was 5.8 +/- 1.4 ml-1 100 g-1 min. and this was associated with an isoelectric ECoG; 15 min of ischemia produced a significant reduction in mean cortical specific gravity (increase in brain edema). Following 15 min ischemia, 180 min of recirculation were permitted. Post-ischemic blood flow showed an immediate hyperemia (CBF = 202 +/- 12 ml-1 100 g-1 min.) followed by hypoperfusion (CBF = 58 +/- 8 ml-1 100 g-1 min). There was an early further decrease in cortical specific gravity. Further recirculation led to a significant increase in cortical specific gravity (resolution of brain edema). The transfer constant (Ki) for 14C-AIB was not altered at any stage in recirculation. This appears to be a model of pure cytotoxic edema until 180 min recirculation after 15 min cerebral ischemia. Recirculation permitted return of cortical electrical activity.

Animals↗
PubMed1985

Mortality and stroke after amaurosis fugax.

One hundred and ten patients who had presented with amaurosis fugax and were treated medically were studied retrospectively. Follow up from the time of presentation was six to nineteen years with a median of eight years. The mortality and frequency of strokes in this group was compared with populations matched for age and sex. Life expectancy in patients with amaurosis fugax was reduced. Ischaemic heart disease was the most frequent cause of death and occurred at a greater rate than in the general population (p less than 0.01). The indicence of stroke was higher than in the Oxfordshire Community Stroke Project 1981-1983 (p less than 0.01). Comparing our results to those published for cerebral transient ischaemic attacks, patients with amaurosis fugax have a similar mortality rate but probably have a lower incidence of stroke. Patients with amaurosis fugax who have an occluded or narrowed proximal internal carotid artery have a greater risk of subsequent stroke than those with a normal carotid artery, or an arteriogram (p less than 0.01).

Adolescent↗
PubMed1979

Retrograde cerebral embolism.

Cerebral embolism may complicate lesions of the subclavian arteries or aortic isthmus distal to the origins of the vertebral or carotid arteries. This may be due to retrograde propagation of occlusive thrombus. In other cases the vessels are patent but there are periods of reverse blood flow, creating a potential for reflux of embolic material to the ostia of the neck vessels.

Adult↗
PubMed1979

[Effects of nicergoline on cerebral blood flow (author's transl)].

Cerebral blood flow (CBF) was measured before and after i.v. injection of the cerebral vasodilator 10-methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) in 13 patients with cerebrovascular disease. CBF increased in seven. The possibility is discussed that the effect of the drug in the other patients may have been masked by a fall of CBF which occurs during sequential measurement of patients at rest. Nicergoline is an alpha-adrenergic receptor blocking agent which affects cerebral blood flow by reducing cerebrovascular resistance. The present study was undertaken to assess the acute effect of the drug on cerebral blood flow and blood pressure in patients with cerebrovascular diseases.

Cerebrovascular Circulation↗
PubMed1977

Cerebral blood-flow in polycythaemia.

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.

Aged↗