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Biomedical subjects

A M Peters

Publications and source records attributed to A M Peters.

At least 271 records · Page 15Linked to original sources
PubMed1982

Indium-111 autologous leucocyte scanning: comparison with radiology for imaging the colon in inflammatory bowel disease.

Indium-111 autologous leucocyte scanning was compared with barium enema for assessing the extent of colonic disease in Crohn's colitis and ulcerative colitis. Scanning was shown to be as accurate as conventional radiology in colitis, reliably distinguishing active from inactive disease. The results suggest that 111In-leucocyte scanning is an accurate, non-invasive, alternative technique for imaging the extent of disease in colitis.

Colitis, Ulcerative↗
PubMed1982

Platelet kinetics in congenital heart disease.

The survival of 111indium labelled platelets has been determined in a series of 47 subjects comprising nine with cyanotic congenital disease (Eisenmenger's syndrome), seven with congenital heart disease associated with left to right shunts, six with primary pulmonary hypertension, six with peripheral vascular disease, 11 with cardiac disorder associated with low cardiac output and eight normal volunteers. Compared with the value in the normals of 9.5 days, mean survival was significantly shortened in those with Eisenmenger's syndrome (8.4 days) and with peripheral vascular disease (8.5 days). It was normal in patients with left to right shunts (9.5 days). Gamma camera imaging in selected patients failed to reveal any abnormal sites of deposition of labelled platelets except in one patient with peripheral vascular disease who had bilateral abnormal activity in his lower limbs and a shortened platelet survival (8.0 days). From theoretical considerations, it was concluded that the reduction in platelet survival in Eisenmenger's syndrome was such that, had it been the result of pulmonary intravascular platelet deposition, abnormal activity should have been visible on chest scanning with the gamma camera. The absence of scintigraphic evidence of abnormal platelet deposition in the lungs of these patients, combined with the linear configuration of their platelet survival curves, suggests that the accelerated platelet destruction is in the reticuloendothelial (RE) system rather than intravascular. Indirect evidence in favour of increased RE destruction of platelets in Eisenmenger's syndrome was the finding of an approximate doubling of intrasplenic platelet transit time, indicating abnormal platelet pooling within the spleen.

Blood Platelets↗
PubMed1982

Factors controlling the intrasplenic transit of platelets.

The kinetics of 111In platelets have been investigated in human subjects using a gamma camera and computer system. Time activity curves were recorded over the spleen, chest and liver, following intravenous bolus injection of autologous radio-labelled platelets. Splenic blood flow expressed as the percentage of total blood volume entering the spleen in unit time, and intrasplenic platelet transit time were calculated from the time activity curves. Spleen size was recorded from the camera images. Splenic blood flow increased with increasing spleen size (r = 0.56, P less than 0.001). Platelet transit time showed an inverse relationship with a semi-quantitative estimate of splenic perfusion (i.e. splenic blood flow per unit volume spleen; r = 0.64, P less than 0.001) but was not related to spleen size. At high rates of estimated splenic perfusion transit time appeared to reach a minimum value of about 7 min, whereas at low rates of estimated perfusion, transit time rose sharply to reach levels greater than 20 min. The effect of polycythaemia, taken to indicate high intrasplenic haematocrit on platelet transit time, was also investigated. Patients with secondary polycythaemia had elevated transit times (19 min SEM 1.6, n = 10) compared with primary polycythaemia (9.7 min SEM 0.8, n = 5) and normals (9.6 min SEM 0.5, n = 5). It was concluded that splenic perfusion was important in determining the duration of platelet transit.

Blood Platelets↗
PubMed1982

Kinetics of heat damaged autologous red blood cells. Mechanism of clearance from blood.

The kinetics of radiolabelled heat damaged red cell (HDRBC) distribution have been studied in humans using a gamma camera, and compared with the kinetics of other blood cells. Liver uptake of 111In labelled HDRBC was completed within about 10 min of injection; splenic uptake was biphasic with a half time of about 5 min over the first 20 min following injection, and a later half time much longer than this. Activity initially present in the lung fields cleared within 24 h. The rate constants of liver uptake of 99mTc labelled HDRBC and of 111In labelled platelets were very similar; the rate constants of splenic uptake of these 2 particles were also very similar up to about 20 min following injection when the splenic platelet levels became constant and the HDRBC level continued to slowly rise. Splenic uptake and blood clearance of red cells coated with IgG (IgG-RBC), in contrast to HDRBC, were monoexponential. It was concluded that: (1) the blood clearance of HDRBC was due to pooling within, and to irreversible extraction by, the spleen; (2) liver uptake of HDRBC, which was irreversible, was completed within 10 min of injection; (3) IgG-RBC clearance was due to irreversible extraction by the spleen; (4) HDRBC uptake in the lung was unrelated to reticuloendothelial function, and represented prolonged transit through the lung microvasculature.

Blood Platelets↗
PubMed1982

Elution of 111Indium from reticuloendothelial cells.

Measurement of isotope accumulation in an organ is often used to assess that organ's removal of blood cells labelled with the isotope. This technique is only valid if the isotope does not elute from the organ. Elution of 111In from the liver and spleen has been investigated in 14 subjects following intravenous injection of heat-damaged erythrocytes labelled with 111In. The elution rate from the spleen was found to be low, about 2% of the initial activity per day. The liver accumulated activity with respect to its initial uptake at a rate of about 5% per day. Bone marrow was not visualised except in two patients in whom it was identifiable in the initial scan.

Erythrocytes↗
PubMed1981

Analysis of heat-damaged erythrocyte clearance curves.

The rate of clearance from the blood of heat-damaged erythrocytes (HDE) is used routinely as a quantitative assessment of splenic function. The time taken for the value at 3 min to fall by 50% (t0.5)is usually taken as the index of function. The clearance of HDE is dependent on three processes: splenic blood flow, splenic HDE extraction ratio and intrasplenic transit time of "unextracted' HDE, returning to the circulation. Exponential analysis of the clearance curve can resolve these three functions. Simple methods of analysis, however, such as t0.5, which are applied directly to the curve, may be weighted in favour of any one of them. In this paper, a large number of clearance curves have been analysed and the components of splenic function resolved. The t0.5, the percentage fall in HDE between 8 and 28 min (C20), the rate constant at 8 min (K8) and the rate constant of the tail of the curve (alpha 2) have been correlated with these components. K8 showed a close correlation with splenic blood flow, and alpha 2 with the rate of HDE phagocytosis. In general, the correlation between the various components of splenic function was better with C20 than with t0.5. This is explained predominantly by the fact that the t0.5 includes liver clearance. The t0.5 should therefore be used with caution as an estimate of splenic function, which can be usefully assessed by applying alternative simple methods of analysis described.

Erythrocytes↗
PubMed1981

Measurement of red cell volume and splenic red cell pool using 113m indium.

Using the lipophilic chelating agent, acetylacetone, red cells have been radiolabelled with the short-lived, generator-produced isotope, 113mIn. Following re-injection of these labelled cells, red cell volume has been measured and compared with corresponding values using 99mTc labelled red cells in 18 patients, and with 51Cr labelled red cells in five patients. 99mTc slightly overestimated red cell volume in relation to 113mIn, but 51Cr values were identical to 113mIn values. There was a close correlation between splenic red cell pool measured with 99mTc and with 113In. It was concluded that the intracellular stability and gamma emission of 113mIn make this isotope a superior alternative to 99mTc and 51Cr in measurements of red cell volume and splenic red cell pool.

Chromium Radioisotopes↗
PubMed1981

Measurement of splenic function in humans using heat damaged autologous red blood cells.

Functional hyposplenism, a clinical entity which has only recently been recognised, is usually assessed quantitatively by the rate of clearance of radiolabelled heat damaged erythrocytes (HDE) from the circulation. Based on recent observations on the kinetics of HDE, we have developed a 3 compartmental model of HDE distribution between the spleen and blood, and calculated, in a large series of clearance curves, splenic blood flow, HDE intrasplenic transit time and splenic HDE extraction ratio. Transit time (about 15 min) was of the same order as platelet transit time and extraction ratio (about 35%) was similar to that recorded in animals. Thr relationships between blood flow, transit time and extraction ratio provided evidence in support of 2 separate functional compartments, of which only one was engaged in phagocytosis, present within the spleen.

Erythrocytes↗
PubMed1981

Spleen function and platelet kinetics.

In patients suffering from various platelet abnormalities, quantitative scanning after injection of indium-111 (111In) labelled platelets showed three different patterns of platelet destruction and distribution. In patients with a normal platelet life span but with evidence of increased splenic pooling, the spleen tended to be the main site of destruction. In patients with a moderately reduced platelet life span, the distribution of destruction in the system and variable destruction in the marrow. However, because of its rapidity this destruction was difficult to quantify, and it was difficult in these cases to distinguish reliably between spleen pool, sequestration, and destruction. Destruction of platelets on the liver appeared to be unimportant in all three groups. 111In, because of its physical characteristics, is preferable to chromium-51 as a platelet label in the assessment of abnormal platelet kinetics.

Adolescent↗
PubMed1980

The measurement of arterial perfusion of the liver in man using the radioisotope xenon-133.

The washout from the liver of xenon-133 injected into the thoracic aorta of human subjects undergoing cardiac investigation was monitored externally with a sodium iodide scintillation detector. The washout curve displayed an initial peak of activity, followed by a brief decline, and then a second, slower rise. The initial peak was thought to be due to isotope arriving in the liver via the hepatic artery, and the second rise due to isotope arriving via the portal vein. A method of analysis is presented which uses the height of this arterial peak to calculate arterial perfusion of the liver.

Hepatic Artery↗
PubMed1980

Use of 111Indium-labeled platelets to measure spleen function.

The distribution of 111In-labelled platelets following intravenous bolus injection has been studied using a gamma camera and computer system. Liver uptake, which accounted for about 10% of the dose, was completed between 6 and 10 min after injection. Blood pool and splenic 111In, which accounted for the remainder of the dose, reached constant levels simultaneously about 20 min after injection. The kinetics of splenic uptake are consistent with a two compartmental model in which circulating and splenic platelets are in dynamic equilibrium with each other. From analysis of the kinetics, splenic blood flow and the mean transit time of platelets through the spleen have been calculated in normal subjects and in patients with haematological disorders. Blood flow, which was about 200 ml per min in normals, tended to increase with increasing spleen size. Transit time was not dependent on spleen size; it was about 10 min in all but one of the subjects.

Blood Platelets↗