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Biomedical subjects

K G Schmidt

Publications and source records attributed to K G Schmidt.

At least 109 records · Page 6Linked to original sources
PubMed1986

A simple method of granulocyte enrichment of crude white cell suspensions labelled with 111In.

A simple method of granulocyte enrichment of a 111In-labelled mixed white cell suspension is described. The method rests on preferential sedimentation by gravity of the granulocytes during labelling. In the 50 studies performed, the granulocytes constituted on average 90% of the 111In-labelled white cells injected for abscess detection. The modest degree of artefactual granulocyte pooling in the lungs and the results of the scintigraphic studies suggest that the method described is well-suited for scintigraphic localization of infectious and inflammatory processes.

Abscess↗
PubMed1986

The use of indium-111-labelled platelets for scintigraphic localization of gastrointestinal bleeding, with special reference to occult bleeding.

Gamma-camera imaging of the abdomen after injection of autologous 111In-labelled platelets was applied for localization of gastrointestinal bleeding in a study of 22 patients. In 15 studies showing scintigraphic signs of bleeding, the clinical presentation included occult bleeding in 6, melaena in 4, and bloody stools in 5. Scintigraphy could be done repeatedly for up to 1 week after a single tracer injection. The time interval between the injection and scintigraphic visualization of bleeding ranged from 10 min to 68 h, being longest in cases of occult bleeding. In most cases the scintigraphic findings were supported by other diagnostic modalities, including surgical removal of presumed sources of bleeding. In seven studies without scintigraphic signs of bleeding a probable source of bleeding was identified by other means in one patient. The 111In-platelet method seems to be a promising method for localization of gastrointestinal bleeding which may prove particularly useful in cases of occult or recurrent bleeding.

Adolescent↗
PubMed1985

Scintigraphic localization of occult gastrointestinal bleeding using a combination of 111In-labelled platelets and 99mTc sulphur colloid.

Repeated scintigraphy was performed for 6 days after the injection of autologous 111In-labeled platelets in a patient showing signs of recurrent occult gastrointestinal bleeding. Colonic activity was observed 142 h post injection, at which time a superimposed study using 99mTc sulphur colloid pinpointed the source of bleeding in the transverse colon.

Aged↗
PubMed1985

Kinetics and in vivo distribution of 111-In-labelled autologous platelets in chronic hepatic disease: mechanisms of thrombocytopenia.

The kinetics and distribution in vivo of autologous 111-In-labelled platelets were studied in 20 patients with chronic hepatic disease. The patients, 16 of whom were thrombocytopenic, exhibited a shortened platelet mean life time, a reduced platelet recovery and a normal platelet turnover, the latter 2 of which were positively correlated to the platelet count. Platelet in vivo recovery was negatively correlated to the spleen volume. In accordance with this, scintigraphic studies revealed that the spleen was the major organ of platelet sequestration and destruction, the role of the liver being almost negligible. Signs of platelet destruction in the bone marrow were also found. Our results indicate that splenic platelet pooling and accelerated platelet destruction, accompanied by inability of the bone marrow to compensate for the thrombocytopenia are the main causes of the thrombocytopenia accompanying chronic hepatic disease.

Adult↗
PubMed1985

Kinetics and distribution in vivo of 111In-labelled autologous platelets in idiopathic thrombocytopenic purpura.

The kinetics of autologous 111In-labelled platelets were studied in 26 patients with ITP. The platelet mean life time (MLT) was considerably shortened, the platelet in vivo recovery slightly lowered and the platelet turnover normal. Comparative studies of the kinetics of simultaneously injected 111In- and 51Cr-labelled platelets in 10 patients showed the MLT and turnover of 51Cr-platelets to be shorter and higher, respectively, than those of 111In-platelets, suggesting that 51Cr-labelling in ITP may underestimate platelet MLT and overestimate platelet turnover. Our results confirm that accelerated platelet destruction is an important pathogenetic factor in ITP, and that the platelet concentration may be influenced by increased splenic platelet pooling and by inability of the bone marrow to respond adequately to the low platelet count. Our scintigraphic studies showed that the spleen played an important role for platelet destruction in most patients, with the liver contributing in some patients.

Adolescent↗
PubMed1985

Kinetics of 111In-labelled platelets in healthy subjects.

25 healthy subjects underwent platelet kinetic and scintigraphic studies following injection of 111In-labelled platelets. Using the multiple hit model, platelet mean lifetime averaged 185.3 hours (range 141.2-225.6), and platelet in vivo recovery averaged 56% (range 42-89). The platelet disappearance pattern was almost linear. However, in comparison with simultaneously injected 51Cr-labelled platelets (7 subjects studied), the 111In-platelet survival curves were slightly more curved. Our results indicate that this may be ascribed to a slight degree of elution of 111In from the circulating platelets. The plateau or even slight increase in circulating activity following the initial steep decline in activity appears mainly to reflect reversible sequestration of platelets in the spleen and maybe in the liver. Using a semiquantitative scintigraphic approach, we estimated 45%, 25% and 30% platelet destruction to occur in the spleen, liver and bone marrow, respectively. Our results indicate that the discrepancy between the course of circulating platelet-bound activity and of chest wall activity reflects platelet destruction in the bone marrow.

Adolescent↗
PubMed1984

Acute platelet activation induced by smoking. In vivo and ex vivo studies in humans.

Indices of acute in vivo platelet activation in response to cigarette smoking were sought in 10 healthy subjects. Judging by platelet aggregate ratio, platelet factor 4 and beta-thromboglobulin measurements, platelet activation took place from 10 to 30 min after smoking in most subjects. These signs correlated well with the results of scintigraphic studies showing signs of accumulation of 111-In-labelled platelets in the spleen in response to smoking.

Adult↗
PubMed1984

Release of platelets into the circulation induced by gamma globulin treatment in a case of idiopathic thrombocytopenic purpura.

The kinetics and distribution in vivo of 111In-labelled platelets prior to and during intravenous high-dose gamma globulin therapy in a 3-months-old child with idiopathic thrombocytopenic purpura were evaluated. Concomitantly with a prompt increase in platelet concentration we found evidence for release of platelets into the circulation, presumably to a large extent originating from the spleen and liver. Our results support the concept that, in response to high-dose gamma globulin therapy, platelets are not only forced to remain in but are also released into the circulation, presumably as a result of mobilization of platelets adhering to cells of the monocyte-macrophage system.

Blood Platelets↗
PubMed1984

Scintigraphic visualization of haemostatic and thromboembolic processes using 111Indium-labelled platelets.

Five cases of scintigraphic imaging of haemostatic and thromboembolic processes after injection of autologous 111In-labelled platelets are presented. The site of a liver puncture, atherosclerotic plaques in the abdominal aorta, deep vein thrombi, pulmonary embolism and the tip of an indwelling venous catheter could be visualized. Activity measurements corresponding to atherosclerotic plaques suggest that an increased sensitivity of this method may be achieved by extending the investigation period to 4-5 days after injection of 111In platelets.

Aged↗
PubMed1984

Malaria-induced immune thrombocytopenia.

On return from Liberia, a previously healthy 36-year-old man showed signs of malaria accompanied by severe haemolysis and slight thrombocytopenia. We found evidence of a platelet-associated IgG being responsible for the thrombocytopenia, inasmuch as the direct platelet suspension immunofluorescence test was strongly positive, the indirect immunofluorescence test and tests for drug-dependent antibodies at the same time being negative. We suggest that autoimmunity may be a contributing mechanism for platelet destruction in acute malaria.

Adult↗
PubMed1984

Exercise-induced changes in the in vivo distribution of 111In-labelled platelets.

In order to throw some light on the mechanisms underlying exercise-induced thrombocytosis, we investigated 15 healthy persons subjected to short-term vigorous pedalling on a bicycle ergometer 1 d after injection of autologous 111In-labelled platelets. Scintigraphic studies during the post-exercise period showed the spleen to be the major platelet-releasing organ. There was, however, a considerable interindividual variability manifested as signs of a contributing platelet release from the lungs in some cases and of deposition of a surplus of released platelets in the liver of others. Our results also seem to be compatible with the existence of an intravascular marginal platelet pool.

Adolescent↗
PubMed1984

Are young platelets released in excess from the spleen in response to short-term physical exercise?

With a view to throwing some light on the age characteristics of platelets released into the blood in response to short-term physical exercise, we conducted exercise experiments on 23 healthy subjects previously injected with different platelet populations labelled with 111In and 51Cr. Based on comparative platelet kinetic studies of pre- and post-exercise platelets and on exercise experiments carried out while labelled-platelet populations of different age composition were circulating, we cannot support the concept that the platelets released into the blood in response to exercise are enriched with young platelets. In addition, we found that simultaneously-injected large and small platelets were released to the same extent in response to exercise, but that the sequestration patterns of large and small platelets seem to be different.

Adolescent↗
PubMed1983

Comparative studies of the function and morphology of 111In- and 51Cr-labelled human platelets.

Comparative studies of the aggregability in vitro and ex vivo, and of the surface/volume ratio of 111In- and 51Cr-labelled human platelets were carried out. The ADP-induced aggregation in vitro of 111In-platelets was superior to that of 51Cr-platelets, as was that of 51Cr-platelets labelled in plasma as compared to 51Cr-platelets labelled in buffer. These differences seemed to be reversed in vivo, as identical collagen-induced aggregation responses were observed ex vivo when comparisons were made between 111In- and 51Cr-platelets, and between labelled and unmanipulated platelets. Morphometric determination of the surface/volume ratios of the labelled platelets indicated a higher degree of platelet activation of 51Cr-platelets labelled in buffer as compared to those labelled in plasma. In this respect, no difference seemed to be present between 111In- and 51Cr-platelets. The results of the ex vivo aggregation studies were unaffected by the time spent by the platelets in the circulation within 24 h post-injection, by platelet isolation yield, and by the medium used in 51Cr-labelling. Our results indicate that it will be possible to conduct comparative studies of simultaneously induced aggregation ex vivo of different platelet populations labelled with 111In and 51Cr.

Blood Platelets↗