Search PubMed⌕ Search

Biomedical subjects

L O Simpson

Publications and source records attributed to L O Simpson.

At least 91 records · Page 5Linked to original sources
PubMed1986

Blood rheology and myalgic encephalomyelitis: a pilot study.

The blood rheology of EDTA-anticoagulated blood samples from blood donors and subjects considered to have myalgic encephalomyelitis was assessed by multiple shear rate viscometry and by multiple-pressure filterability. Although average viscosities of the two groups were different, the differences did not reach statistical significance. In contrast, the data from multiple-pressure filtration of whole blood showed significant differences between females at the lowest (2.5 cm of water) filtration pressure. It appears that the acute phase of the disorder is associated with changes in blood rheology which could impair microcirculatory blood flow. In contrast, the chronic state does not appear to be associated with rheological abnormalities.

Blood Viscosity↗
PubMed1985

Intrinsic stiffening of red blood cells as the fundamental cause of diabetic nephropathy and microangiopathy: a new hypothesis.

It is proposed that stiffened red cells can interfere with normal microvascular and glomerular function. In diabetics intrinsic stiffening of red cells is intensified during poor metabolic control when plasma osmolarity is increased. Hypoxia, acidosis, catecholamines and other changes in red cell environment also increase red cell stiffness. Exercise proteinuria may help to identify individuals with the greatest intrinsic stiffening of red cells which appears to be due to the disposition of spectrin molecules rather than to changes in the lipid bilayer. Stiffened red cells may impede blood flow in the microcirculation and stimulate an autoregulated vasodilation which increases perfusion pressure, enhancing transudation. In the absence of vasodilation, stasis will lead to vascular occlusion and localised ischaemic necrosis. If diabetic microangiopathy is caused by abnormal haemorheology then the possibility exists that the complications of diabetes might be alleviated or prevented by agents which enhance red cell flexibility and improve blood rheology.

Blood Viscosity↗
PubMed1984

Smoking, abnormal haemorheology and the pathogenesis of coronary heart disease.

Presently held views on the cause of coronary heart disease (CHD) considers hypertension, hypercholesterolemia and cigarette smoking to be the major risk factors. Large scale intervention trials which sought to evaluate the contribution of the major risk factors have failed to provide clear-cut results. Another significant, but clinically unrecognised factor in CHD is abnormal haemorheology which is exacerbated by smoking, and is associated with decreased RBC filterability. It is proposed that coronary heart disease may result directly from haemorheologic causes but occurs more often when lesions in two or more coronary arteries are associated with increased blood viscosity and poorly deformable RBCs. Treatment should be aimed at reducing blood viscosity and RBC stiffening.

Blood Flow Velocity↗
PubMed1983

Morphological changes in the kidneys of mice with proteinuria induced by albumin-overload.

Female CBA/H-T6T6 mice were given daily i.p. injections of 1 ml of saline containing 250 mg of human serum albumin (HSA) for 7 consecutive days. Control mice received the same volume of saline only. At approximately 24 hourly intervals for the 10 days after the first injection, groups of mice (3 HSA and 1 saline-injected) were killed and kidney tissue was taken for light (LM) scanning (SEM) and transmission (TEM) electron microscopy. Small numbers of glomeruli with Bowman's space filled with protein and fine, radially-disposed casts in collecting tubules were observed by LM. SEM revealed focal changes in both endothelium and epithelium, and in a few cases severely damaged epithelial cells were seen. TEM showed numerous small regions of loss or change in shape of foot processes. Epithelial cell branches became increasingly swollen. By the third day after the last injection glomerular morphology appeared to have returned to normal. Although the cause of the proteinuria was attributed to the effects of HSA-induced increased blood viscosity, the focal distribution of the observed morphological changes remains unexplained.

Animals↗
PubMed1983

Echinocytes in the blood of hyperproteinaemic mice with proteinuria. Is the effect of such cells on blood viscosity the cause of the proteinuria?

Early studies in this series failed to obtain evidence for the cause of hyperproteinaemic proteinuria although it was speculated that blood viscosity, increased because of high plasma protein levels, might play a significant role. As we had no means of measuring blood viscosity it was decided to investigate the effects of reducing blood viscosity in a small number of mice made anaemic before subjecting them to albumin overload. All but one of the mice given injections i.p. of 250 mg HSA on 2 successive days developed proteinuria within 24 h of the first injection. This result seemed to show that altered blood viscosity was not a factor in the mechanism of the hyperproteinaemic proteinuria. However, it has been shown that changes in the red cell environment can lead to red cell deformation resulting in an increase in blood viscosity. To check on this possibility another small group of mice were injected with HSA as previously. On the morning after their second injection the mice were bled by percutaneous heart puncture and the blood was examined by scanning electron microscopy. This showed that a vast preponderance of red cells, probably more than 95%, were echinocytes. Although no measurements of blood viscosity were made, it can be speculated that hyperproteinaemic proteinuria is caused by the intraglomerular effects of blood with increased viscosity (because of the red cell transformation) being made more viscous by glomerular filtration. Enhanced protein filtration would occur because of the increase in glomerular pressure needed to restore flow of viscous blood at the efferent arteriole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

The implications of the changes in the nature of the urinary proteins which occur in albumin overload-induced proteinuria in normal mice.

Mice with normal urine were given daily injections of human serum albumin for 7 days. Blood and urine samples were obtained at regular intervals during the first 24 h and daily throughout the injection period, and for 6 days after the injections had been stopped. Control mice which received saline injections were studied in a similar fashion. Albumin-injected mice developed peak urinary total protein concentrations and peak incidence of high and medium mol. wt proteinuria after the third daily injection. Despite the fact that plasma total protein and plasma albumin concentrations remained elevated, both the total urinary protein and the incidence of large proteins fell after the third day. Saline-injected mice did not show unusual changes in the range of total urinary protein, but over the first 3 days a small percentage developed proteinuria. Explanations for the observed changes were sought on the basis that glomerular basement membranes are thixotropic gels and are therefore pressure-dependent. It was concluded that the changes in urinary proteins could be due to the effects of combinations of the following factors: (a) the existence of an auto-regulatory mechanism which by stimulating afferent arteriolar constriction reduced glomerular pressure; (b) the reduction of the protein content of a proteinaceous filtrate because of protein absorption by glomerular epithelial cells; and (c) as both saline-injected and albumin-injected mice developed proteinuria during the first 3 days, it is speculated that volume expansion also contributed to the proteinuria, through its effects at the level of efferent arterioles.

Animals↗