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Biomedical subjects

T H Thomas

Publications and source records attributed to T H Thomas.

At least 91 records · Page 5Linked to original sources
PubMed1988

Sodium-lithium countertransport activity and its sensitivity to inhibitors with erythrocyte ageing in man.

Sodium-lithium countertransport is believed to depend on a specific protein and since such proteins usually decline with erythrocyte age it would be expected to be reduced in older cells. In fact, sodium-lithium countertransport increased with ageing, whereas the rate constant of the sodium pump decreased. The increase in sodium-lithium countertransport with erythrocyte ageing was due to a phloretin insensitive component that was not present in young erythrocytes. Raised sodium-lithium countertransport in patients with essential hypertension was due mainly to an increased phloretin sensitive component but the phloretin insensitive component was also higher in middle aged erythrocytes. Amiloride had no effect upon sodium-lithium countertransport or unidirectional sodium influx in cells of any age. This suggests that sodium-lithium countertransport is not a mode of action of the sodium-proton exchanger in the erythrocyte.

Aging↗
PubMed1988

High erythrocyte water content causes discrepancy between values of automated and micro-centrifuged haematocrit.

Erythrocyte water content, micro-haematocrit (micro-Hct) and haematocrit (Hct) as derived by Coulter Counter were determined on 41 subjects. Significant discrepancies were observed between manual and automated Hct which could not be explained by abnormal red cell morphology and abnormal plasma osmolality, but appeared to be related to high erythrocyte water content (r = 0.54, p less than 0.001). As human ageing is associated with increased erythrocyte water content, these results question the reliability of Hct readings in the elderly. Further studies need to be performed to evaluate which estimation of Hct should be applied for subjects with high erythrocyte cell water.

Adult↗
PubMed1988

Hypertension and diabetes mellitus: erythrocyte electrolytes and the effect of captopril treatment.

Erythrocyte sodium, potassium and water contents and sodium fluxes were measured in both normotensive and hypertensive patients with either insulin dependent or non-insulin dependent diabetes mellitus. Hypertensive patients were studied again after two months' treatment with captopril. There were no differences in erythrocyte ion contents or concentrations but sodium fluxes may have been lower in insulin dependent patients and in hypertensive patients. The most marked erythrocyte defects associated with hypertension were low erythrocyte water content and increased potassium concentration in non-insulin dependent diabetic patients. Treatment with captopril caused an increase in erythrocyte water and a decrease in ion content and concentration. In non-insulin dependent diabetic patients, who had the greatest increases in erythrocyte water and falls in potassium concentration, frusemide-sensitive sodium-potassium co-transport activity was reduced. The reduction in blood pressure with captopril treatment was related to the initial erythrocyte sodium content.

Biological Transport↗
PubMed1986

Use and misuse of a digoxin assay service.

In a study of the use of a digoxin assay service and its influence on clinical management 285 assay requests were audited over 12 weeks. For 67 (24%) there was no clear clinical indication for the request and for 140 the period between the last dose of digoxin being given and the blood sample being taken was either unknown or inappropriate. Treatment in 64 patients (22%) was changed after the assay result was received [corrected]. 24 of these changes bore no relation to the original clinical indication for requesting the assay, suggesting that such changes were based on the assay result alone. Of samples collected within six hours after the last dose, 15 of 69 (22%) led to a reduction in treatment compared with 10 of 116 (9%) taken after six hours (p less than 0.025), thereby highlighting the danger that incorrectly timed samples may lead to inappropriate clinical decisions.

Clinical Laboratory Techniques↗
PubMed1986

Changing effects on erythrocyte sodium and potassium during the development of chronic renal failure with anaemia in rats.

Rats were studied 7 days and 17 days after the onset of renal failure which was induced by a surgical technique. Plasma urea, creatinine (PCr) and potassium had increased after 7 days; plasma potassium increased much more after 17 days but PCr was slightly lower. Renal failure caused resetting of erythropoietic control to a lower level of packed cell volume (PCV). After 7 days renal failure some rats had a low PCV, whereas others still had a normal PCV apparently due to slower erythrocyte destruction of pre-renal failure cells. After 7 days renal failure, rats with a normal PCV had an increased erythrocyte membrane leak to potassium that resulted in a low erythrocyte potassium [K+]RBC. This was accompanied by an increase in active sodium pump units [increased ouabain sensitive sodium flux (Fo) and its rate constant (ko)] that caused erythrocyte sodium ([Na+]RBC) to fall. The increased active pump units retarded the fall in [K+]RBC and may have extended the life of the normal erythrocytes in the renal failure environment. The PCV was below normal in all rats after 17 days renal failure. [K+]RBC was increased and since ko was normal there appeared to be compensation to produce erythrocytes with reduced membrane leak to potassium with longer standing renal failure. PCr was only related to PCV after 17 days renal failure and not in the earlier phase of erythrocyte destruction. The changes in erythrocyte membrane permeability were very significantly related to PCV after 17 days.

Anemia↗
PubMed1984

A model for erythropoiesis in experimental chronic renal failure.

Chronic renal failure (CRF) in rats was induced by various subtotal nephrectomy procedures. Plasma creatinine concentrations ([Creat]p) were consistently elevated in partially nephrectomized (PNX) rats (P less than 0.001) and renal function ([Creat]p-1) was correlated with the amount of intact renal tissue (r = 0.624, P less than 0.001). Red blood cell (RBC) production in uraemic and non-uraemic rats was assessed using the recovery of packed cell volume (PCV) and the production of reticulocytes in response to acute blood loss (5, 10, 15 and 20 ml kg-1 body wt). PCV recovery was significantly delayed and failed to reach pre-bleed values for up to 28 d in PNX rats compared with full recovery within 8 d in controls. Linear relationships between the index of reticulocyte production (RP1) and blood loss induced falls in PCV were found in PNX (r = -0.679, P less than 0.001) and control rats (r = -0.696, P less than 0.001). The index of RBC production was lower in PNX rats compared with controls. This was attributed to a reduced erythropoietin (Ep) mediated reticulocyte response to acute blood loss in PNX rats. PNX rats developed a normocytic, normochromic form of anaemia in which the red blood cell volume (RBCV) and plasma volume (PV) were both appropriate for measured PCVs. The reduced RBC production response in experimental CRF may explain the development of anaemia in PNX rats, even though steady state erythropoiesis may eventually be established at a reduced level of PCV. Furthermore, the quantitative evaluation of RBC production in response to acute blood loss provides a further model for the assessment of agents which may stimulate erythropoiesis in CRF.

Anemia↗
PubMed1983

Kinetics of adherence of Actinomyces viscosus to saliva-coated silica and hydroxyapatite beads.

Adherence of 14C-labelled strains of Actinomyces viscosus to uncoated and saliva-coated silica and hydroxyapatite beads had both loose and firm components, probably reflecting different subpopulations of bacteria within a single culture. Adherence was characterized by the proportion of bacteria available for each type of adherence and a constant (Kb) for each combination of bacterial strain and bead surface. Loose adherence, which was greater with silica than with hydroxyapatite beads, always involved many more bacteria than firm adherence. Firm adherence was greater with A. viscosus WVU627 than A. viscosus TF11. The association rate constants (Ka) for loose and firm adherence were similar, indicating simultaneous processes, but the dissociation rate constant (Kd) was lower for loose adherence than for firm adherence. Removal of loosely adhering bacteria by washing may only reflect their distance from the bead surface. Silica beads were convenient for studying bacterial adherence and formed an acceptable coating of salivary glycoprotein.

Actinomyces↗
PubMed1979

Renal function after long-term treatment with lithium.

Daily urine volumes, plasma creatinine concentrations, and creatinine clearance were measured in 106 patients with unipolar and bipolar affective disorders attending a "lithium" clinic. Urine volumes exceeded 3.51 in only six patients, plasma creatinine concentrations exceeded 150 mumol/1 (1.7 mg/100 ml) in only five, and creatinine clearance was below 50 ml/min in 16. Renal function was assessed by measuring creatinine clearance and renal tubular function, including response to 20 hours of water deprivation, in a representative sample of 30 patients from the lithium clinic and 30 psychiatric patients matched for age and sex who were taking other psychotropic drugs. Creatinine clearance and tubular function, including urine osmolality after water deprivation, were not significantly different between the two groups. Urinary excretion of arginine vasopressin (AVP), however, was much greater in the lithium-treated patients, who therefore had a diminished tubular responsiveness to AVP. The findings do not support suggestions that long-term lithium treatment results in seriously impaired renal function, renal damage, and polyuria. Compared with other series, however, the patients were being maintained with low serum lithium concentrations, which apparently area as effective prophylactically as higher concentrations.

Adult↗
PubMed1979

Hypertension and hyperkalaemia responding to bendrofluazide.

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.

Adult↗
PubMed1978

Severe hyponatraemia. A study of 17 patients.

17 patients with severe hyponatraemia (none had cardiac failure or had lately had an operation) all had excessively high plasma-antidiuretic hormone (A.D.H.). Only 13 had features typical of the syndrome of inappropriate secretion of A.D.H. (S.I.A.D.H.). Plasma-A.D.H. was not related to either plasma-sodium or diagnosis. There were as many patients with chest infection as with carcinoma of the lung. Plasma-sodium and plasma-A.D.H. returned rapidly towards normal in the patients with chest infection or volume depletion but these concentrations corrected much more slowly in patients with carcinoma of the lung. The increase in plasma-sodium in patients with chest infection was too rapid to be produced by water-deprivation treatment and was due to return of plasma-A.D.H. to normal. The term S.I.A.D.H. implies an understanding of pathophysiology that does not exist. As a diagnosis it does not help in management or prognosis. A simpler, more descriptive terminology such as "hyponatraemia with carcinoma of the lung" would be more useful and less confusing in the clinical situation.

Aged↗
PubMed1978

Effect of carbamazepine on plasma and urine arginine-vasopressin.

1. Five normal subjects were studied before and during treatment with carbamazepine. 2. Plasma sodium, plasma and urine arginine-vasopressin and urine osmolality were measured during a day of water deprivation, before and during drug treatment. 3. During treatment with carbamazepine plasma sodium increased wheras plasma and urine arginine-vasopressin and urine osmolality decreased. Plasma and urine arginine-vasopressin were signifi"antly correlated with urine osmolality. However, carbamazepine did not affect the osmolality of urine produced by the kidney, in response to endogenous arginine-vasopressin. 4. Plasma and urine arginine-vasopressin were significantly correlated with plasma sodium on both control and drug-treatment days, but the relationships of plasma and urine arginine-vasopressin to plasma sodium were different during carbamazepine treatment, as compared with the control period. 5. It is suggested that the threshold of the hypothalamic osmoreceptors for release of arginine-vasopressin is modified by carbamazepine, and that this may be either a direct action or secondary to another action of the drug.

Adult↗
PubMed1978

Sodium losing renal disease: Two cases and a review of the literature.

Two patients with sodium-losing renal disease were studied in detail. Both presented with shock and hypotension which was attributed at first to other causes, as was the recurrent hyponatraemia in one of them. In both patients the cause of the sodium loss was probably unrelieved urinary obstruction which has been reported previously to cause water loss but not sodium loss. Both patients had severe hyponatraemia when they were sodium depleted, which has previously been attributed to water retention from excessive secretion of antidiuretic hormone. Plasma arginine vasopressin concentrations were raised in one patient but not in the other. The cause of the water retention in the other patient is not known. One of the patients, like others described in the literature, was only able to vary his sodium excretion within narrow limits. He became sodium depleted on a normal intake and oedematous when he was given saline intravenously. We suggest that the term sodium-losing renal disease should be replaced by the term 'fixed sodium' excretion renal disease.

Adult↗