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Biomedical subjects

T Rimmer

Publications and source records attributed to T Rimmer.

7 recordsLinked to original sources
PubMed1994

Clinical relevance of intraoperative embolization detected by transcranial Doppler ultrasonography during carotid endarterectomy: a prospective study of 100 patients.

A study was performed to investigate the clinical significance of microembolization detected by transcranial Doppler ultrasonography (TCD) by determining the quantity and character of emboli and correlating these with neurological and psychometric outcome, fundoscopy, automated visual field testing and computed tomographic brain scans in 100 consecutive patients undergoing carotid endarterectomy. Embolization was detected in 92 per cent of successfully monitored operations. Most emboli were characteristic of air and not associated with adverse clinical outcome. However, more than ten particulate emboli during initial carotid dissection correlated with a significant deterioration in postoperative cognitive function. A relationship between persistent particulate embolization in the immediate postoperative period, and both incipient carotid artery thrombosis and the development of major neurological deficits was observed. Immediate intervention, based on TCD evidence of embolization, has the potential to avert neurological deficits resulting from particulate embolization.

Aged↗
PubMed1994

Impaired contraction and endothelium-dependent relaxation in isolated resistance vessels from patients with insulin-dependent diabetes mellitus.

1. An increase in capillary blood flow and pressure has been implicated in the pathogenesis of diabetic microangiopathy. Abnormal vascular reactivity of the resistance vasculature may play a contributory role by permitting alterations in regional haemodynamics. 2. We have studied the contractile behavior of isolated resistance arteries from normotensive patients with insulin-dependent diabetes mellitus and non-diabetic matched control subjects. Contractile responses to potassium (123 mmol/l), noradrenaline (10(-8) to 3 x 10(-5) mol/l) and angiotensin II (10(-11) to 3 x 10(-8) mol/l) were recorded. Relaxation studies were performed in maximally contracted vessels using acetylcholine (10(-8) to 10(-5) mol/l) and bradykinin (10(-9) to 10(-6) mol/l) (endothelium-dependent) and sodium nitroprusside (10(-9) to 10(-5) mol/l) (endothelium-independent). 3. The maximal contractile responses to potassium (P < 0.05), noradrenaline (P < 0.01) and angiotensin II (P < 0.01) were depressed in diabetic patients. Relaxation to acetylcholine was impaired (P < 0.05), but was normal with bradykinin and sodium nitroprusside. 4. These results suggest that there may be a defect in the endothelial cell acetylcholine receptor excitation-coupling in diabetes mellitus rather than a decreased ability to synthesize and release endothelium-derived relaxing factor. Impaired contraction and endothelium-dependent relaxation of resistance arteries in diabetic patients may contribute to the development of diabetic microangiopathy by causing an increase in tissue blood flow, a rise in capillary pressure and, as a result, an increase in vascular permeability.

Acetylcholine↗
PubMed1993

Resistance of diabetic rat electroretinogram to hypoxemia.

PURPOSE: To investigate the mechanisms of the known electroretinographic abnormalities of diabetic rats and to explore effects of hypoxemia. METHODS: Subretinal and vitreal microelectrodes were used to isolate the retinal and retinal pigment epithelial components of the electroretinogram. Normoxic and hypoxemic recordings were taken from nine normal and six streptozotocin-diabetic, anesthetized, paralyzed, and ventilated pigmented rats. RESULTS: When inspired O2 was reduced the retinal pigment epithelial c-wave component of most of the normal rats diminished, whereas those of the diabetic rats, though initially smaller, were more resistant to the episode of hypoxemia (P = 0.0061). A similar trend was seen in other components. CONCLUSION: It is proposed that the reduced sensitivity of the diabetic electroretinogram to hypoxemia results from a reduced dependency of the diabetic retina on oxygen. This reduced dependence may follow from a shift in adenosine triphosphate production whereby oxidative phosphorylation is reduced by the high level of retinal intracellular glucose (Crabtree effect). A reduced oxygen demand would cause a transient increase in retinal PO2, leading to a reduction in retinal blood flow. The resulting chronic hypoperfusion of the retinal circulation may deprive the retina of vital, non-energy-related substances.

Animals↗
PubMed1990

Hypoxic viscosity and diabetic retinopathy.

Diabetic and sickle retinopathy have features in common--for example, venous dilatation, microaneurysms, and capillary closure preceding neovascularisation. Bearing in mind that haemoglobin in poorly controlled diabetes is abnormal and that extremely low oxygen tensions (known to cause sickling) exist in the healthy cat retina, we wished to explore the possibility that diabetic blood, like that of sickle cell disease, may become more viscous when deoxygenated. To do this we measured whole blood viscosity, under oxygenated and deoxygenated conditions, of 23 normal persons, 23 diabetic patients without retinopathy, and 34 diabetic patients with retinopathy. The shear rate used was 230 s-1, which is similar to that thought to prevail in the major retinal veins. The viscosity of blood from normal persons, corrected for packed cell volume, did not change significantly on deoxygenation: mean 4.54 (SD 0.38) cps, versus, 4.57 (0.39) paired t test, p = 0.66. Similarly the blood from diabetics without retinopathy showed no change: 4.42 (0.45) versus 4.42 (0.30), p = 0.98; whereas the blood from patients with retinopathy changed from 4.82 (0.48) to 4.95 (0.63), p = 0.027. The hypoxic viscosity ratio (deoxygenated divided by oxygenated viscosity) correlated with total serum cholesterol (r = 0.44, p = 0.018) but not with HbA1, serum glucose, triglycerides, or age. A disproportionate increase in venous viscosity relative to arterial viscosity would lead to increased intraluminal and transmural pressure and therefore exacerbate leakage across capillary walls.

Adult↗
PubMed1989

Long-term follow-up of retinal blood flow in diabetes using the blue light entoptic phenomenon.

The blue light entopic phenomenon was used to measure retinal blood flow in 87 diabetics and 10 normal controls in a longitudinal study. The time interval between the initial and final studies was 21-39 months (mean 31.4). The retinal blood flow velocity did not change in the 10 subjects in the control group nor in those nine patients with no retinopathy, all but one of whom remained free of retinal lesions. In the 24 with background retinopathy the flow velocity fell significantly from 0.71 (SD 0.35) mm/s to 0.48 (0.13) mm/s (p less than 0.01). The velocity also decreased in the preproliferative group of 16 patients from 0.62 (0.39) mm/s to 0.41 (0.14) mm/s (p less than 0.05). The retinopathy status changed in 11 of this group. In those with proliferative retinopathy (now treated) and those treated previously there was no change in flow velocity.

Adult↗
PubMed1988

Retinal blood velocity in patients with leukocyte disorders.

The blue light entoptic phenomenon was used to measure retinal blood velocity in eight patients with chronic granulocytic leukemia, six patients with leukopenia, and matched control subjects. The retinal leukocyte velocity of the leukemic patients was 0.53 +/- 0.26 (mean +/- SD) mm/s, whereas that of the matched control subjects was 0.46 +/- 0.14 mm/s. There was no significant difference between these two groups (power: 96% for a difference of 0.2 mm/s and 66% for 0.1 mm/s). There was also no significant difference between the leukocyte velocities of the leukopenic patients and control subjects (0.47 +/- 0.19 mm/s and 0.55 +/- 0.14 mm/s, respectively; 89% power for a difference of 0.2 mm/s, 59% for 0.1). There was a correlation between the leukocyte count and the number of leukocytes seen in the entoptoscope. The results suggest that retinal vascular autoregulation can compensate for changes in leukocyte numbers that might have been expected to alter retinal blood flow.

Adult↗