Biomedical subjects

J Kutti

Publications and source records attributed to J Kutti.

At least 109 records · Page 6Linked to original sources

PubMed1982

Platelet activation in response to phlebotomy. An experimental study of healthy blood donors.

Plasma concentration of beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were measured in three consecutive blood samples from 29 healthy male blood donors. The first sample was collected after 15 min of rest, the second immediately after a phlebotomy of 450 ml blood and the third after a further 15 min of rest. The mean baseline plasma BTG and PF4 values were 68 x 5 and 13.8 +/- 0.7 ng/ml, respectively. The second sample's mean plasma values of these two platelet-specific proteins were significantly higher (88 +/- ( and 24.1 +/- 4.1 ng/ml, respectively). The plasma concentrations of BTG and PF4 in the last sample, however, had returned to baseline levels. It is concluded that significant but short-lasting platelet activation and secretion take place in healthy subjects in response to an acute but comparatively mild blood loss even though the platelets do not participate in the process of hemostasis.

Adolescent↗

PubMed1981

Evidence that circulating immune complexes remove transfused platelets from the circulation.

Fifteen recently diagnosed patients with acute leukemias admitted for induction chemotherapy were selected for study. When thrombocytopenic (venous platelet count less than 20 X 10(9)/l) these patients received prophylactic platelet transfusions. A total of 67 platelet transfusion therapies were administered and evaluated. Using the Raji cell radioimmunoassay, the serum concentrations of circulating immune complexes (CIC) were measured immediately before and 10-12 hr after each platelet transfusion. In 36 instances, elevated values of CIC were present in the recipient's pretransfusion samples. The corresponding posttransfusion values being significantly lower (P less than 0.05). Furthermore, in those 36 instances the mean percentage for the posttransfusion platelet increment was significantly lower (P less than 0.001) than in the remaining 31 instances in which normal pretransfusion values of CIC were measured. We conclude that CIC were an important factor in rapidly removing transfused platelets from the circulation, thereby, adversely affecting the benefit of platelet transfusions.

Acute Disease↗

PubMed1981

Plasma levels of platelet factor 4 in patients admitted to a coronary care unit.

Blood was obtained from 63 consecutive patients within 24 h period after the admission to a coronary care unit for the determination of plasma platelet factor 4 (PF-4) concentration. 28 of the subjects proved to have an acute myocardial infarction (MI), 24 had evidence of ischaemic heart disease (IHD) but no MI, and the remaining 11 patients had no signs of IHD. 40 healthy subjects served as controls. The mean PF-4 value in the MI group was 10.5 +/- 0.8 ng/ml. The corresponding values for patients with and without IHD were 8.7 +/- 0.6 and 8.3 +/- 0.6 ng/ml, respectively. The control mean (5.4 +/- 0.3 ng/ml) was significantly lower (P less than 0.001) than the means for all 3 groups of patients studied. The difference between the group of MI patients and patients with IHD as well as patients without IHD was only of borderline significance (0.10 greater than P greater than 0.05).

Adult↗

PubMed1981

Plasma concentrations of platelet factor 4 in acute myocardial infarction.

The aim was to investigate whether in the acute stage of myocardial infarction (MI) platelet activation, as measured by plasma platelet factor 4 (PF-4), excluding that in ischaemic heart disease (IHD) is taking place. Over a period of 4 d the plasma levels of PF-4 were determined on 44 consecutive patients admitted to a coronary care unit with suspected MI. 21 of them had a definite acute MI (group 1), and 13 had evidence of IHD but no MI (group 2). In the remaining 10 subjects there was no evidence of either MI or IHD. On the first day the mean plasma PF-4 concentrations in group 1 and 2 patients were 11,8 +/- 1.1 and 15.0 +/- 2.3 ng/ml, respectively; the difference between means was not statistically significant. A peak mean PF-4 for group 1 patients (17.5 +/- 4.6 ng/ml) was recorded on the second day of study. The corresponding value for group 2 patients was lower, but not significantly so. In the latter subjects no peak PF-4 was recorded. During the last 2 d of study the plasma PF-4 concentrations tended to decrease, but the means for the 2 groups did not differ statistically. Thus, at no point in time was there a significant difference between the PF-4 values for MI and IHD patients present.

Adult↗

PubMed1981

Platelet kinetics in systemic lupus erythematosus (SLE), with special reference to corticosteroid and azathioprine therapy.

Duplicate platelet survival studies were carried out on 10 patients with SLE. At the time of the first study 5 of them (group I) were untreated and the remaining 5 (group II) were receiving corticosteroid (CS) therapy. The second study was performed while group I patients received CS and group II patients CS + azathioprine (AT) treatment. Untreated SLE patients were shown to have normal values for platelet mean life-span (MLS) and platelet production rate. CS and AT treatment did not affect either platelet MLS or platelet production rate. The present study also provides further evidence that a state of compensated thrombocytolysis is not present in SLE.

Adult↗

PubMed1980

Plasma beta-thromboglobulin values in thrombocytopenic patients with acute leukemia.

Plasma beta-thromboglobulin (beta-TG) levels were measured in 14 healthy subjects and in 20 acute leukemia (AL) patients, newly diagnosed, with highly variable values for venous platelet counts. For healthy subjects the plasma beta-TG levels ranged 12-38 (mean 17) ng/ml. In this group of patients with AL, a highly significant positive correlation (P < 0.001) between the values for plasma beta-TG and venous platelet count was present. During a thrombocytopenic period, the plasma beta-TG concentraton was measured in nine of the AL patients immediately before and 10 to 12 hours after platelet transfusion therapy. Fourteen platelet transfusions were administered when the patient's highest temperature of the day was < 38.5 degrees C, and 18 when the highest temperature of the day was greater than or equal to 38.5 degrees C. The mean pre-transfusion and post-transfusion beta-TG values for the 14 platelet transfusions were 7 +/- 2 and 20 +/- 5 ng/ml, respectively. The corresponding means for the 18 transfusions given to febrile patients were 5 +/- 2 ng/ml and 11 +/- 2 ng/ml, respectively. Of the pretransfusion values, 11/14 and 14/18 were below the control range. We conclude that the plasma beta-TG values are considerably lower in thrombocytopenic patients than in subjects with normal platelet counts. Further work should provide reference values for plasma beta-TG over a wide range of venous platelet counts.

Adolescent↗

PubMed1980

Platelet transfusion therapy and circulating immune complexes.

30 platelet transfusions were administered to 9 thrombocytopenic patients with acute leukemias. Using the Raji cell radioimmunoassay, the serum concentration for circulating immune complexes (CIC) were determined immediately before and 10--12 h after each transfusion therapy. Elevated serum concentrations for CIC were present in 14 of the pretransfusion samples. After platelet transfusion therapy, a significant (p < 0.02) decrease in the values of CIC occurred. In these 14 transfusion studies the mean percent platelet increment was considerably lower (0.10 > p > 0.05) than the mean for the 16 transfusion studies in which the pretransfusion values for CIC were normal. These results show that CIC probably play an important role in removing transfused platelets from the circulation. Conversely, platelets are able to remove CIC from the circulation.

Acute Disease↗

PubMed1980

Presence of a non-splenic platelet pool in man.

3 asplenic but otherwise healthy men, in whom autologous platelets had been labelled with radioactive sodium chromate, received i.v. infusions of epinephrine in a dose of 0.35 micrograms per kg per min over a period of 20 min. In response to these infusions an increase in the concentration of labelled platelets (average 8% over the basal value) was seen in all 3 subjects. In no case was the maximal increase in the venous haematocrit higher than 1%. Identical experiments were also carried out on 3 intact male volunteers. As compared to the asplenics, the mean maximal increase in platelet-bound radioactivity was considerably higher (41%). It is concluded that a small but significant epinephrine sensitive non-splenic platelet pool is present in humans.

Adolescent↗

PubMed1980

Plasma levels of beta-thromboglobulin and platelet factor 4 in relation to the venous platelet concentration.

The plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) were determined in patients with various hematologic malignancies, and the results were related to simultaneously determined venous platelet counts. All studied patients were in a steady state. The plasma beta-TG concentrations were determined on 69 occasions and the values ranged from 0 to 82 ng/ml. In 33 instances, the venous platelet count was <25 x 10 (9/1) and in two thirds of these samples beta-TG was undedectable. The highest values for plasma beta-TG were found in patients with the highest venous platelet counts. A highly significant correlation (r=0.77, p <0.001) between the values for plasma beta-TG and venous platelet count was present. The plasma concentrations for PF-4 ranged from 0 to 50 ng/ml. Similarly, there was a highly significant relationship (r=0.78, p<0.001) between the values for PF-4 and venous platelet concentration. We conclude, if the plasma levels of beta-TG and PF-4 are used as markers of platelet activation in vivo, it is necessary to simultaneously consider the platelet concentration in the collected blood.

Adolescent↗

PubMed1980

Platelet survival and platelet production in systemic lupus erythematosus (SLE).

Platelet survival studies were carried out on 36 patients suffering from SLE. Twelve of them received no therapy, 17 were on corticosteroids (CS), and the remaining 7 received CS and azathioprin (AT). Ten healthy hospital employees served as controls. Only 1 of our SLE patients had thrombocytopenia (platelet count 42 x 10(9)/l). All the remaining 35 patients had venous platelet counts greater than or equal to 120 x 10(9)l. In the control group the average platelet mean life-span (MLS) was 5.8 +/- 0.3 (range 4.0-6.8) days. In the group of untreated SLE patients 3 out of 12 subjects (25%) had a platelet MLS below the lower range for the controls. The mean platelet MLS in the control group did not differ statistically from any of the means of the three groups of SLE patients studied. The lowest mean for platelet MLS (5.2 +/- 0.6 days) was encountered in the group of patients who received no therapy. The means for platelet MLS in the two groups of SLE patients who received immunosuppressive therapy were higher (6.5 +/- 0.4 and 6.6 +/- 0.4 days, respectively) but did not differ statistically from the mean of untreated patients (0.10 > p > 0.05). The mean platelet production rate in the control group (23 +/- 10(10) platelets per day) did not differ from any of the three groups of SLE patients investigated. In the literature it has been proposed that a state of compensated thrombocytolysis is present in most cases of SLE. The results of the present study do not support this hypothesis, however.

Adrenal Cortex Hormones↗

PubMed1979

Platelet survival and platelet production in acute myocardial infarction.

Thrombokinetic studies were carried out on 26 consecutive patients with myocardial infarction (MI) admitted to a coronary care unit in the acute stage during a two-month period. The results were compared with those of an age-matched control group. In the MI patients, platelet mean life-span was 5.0 +/- 0.3 days and significantly shorter (p greater than 0.01) than in the controls (6.4 +/- 0.4 days). The mean platelet production rate for the patients with MI was significantly higher (p greater than 0.005) than for the controls. On the basis of results reported by others as well as the present data, it is suggested that during the acute phase of MI there is no additional measurable reduction in platelet survival above that observed in chronic coronary artery disease.

Acute Disease↗

PubMed1979

The peripheral platelet count and the isoprenaline-induced splenic platelet pooling in response to beta-adrenoceptor blockade.

Previous reports have shown that a single, oral dose of 50 mg metoprolol (a selective beta-1-receptor antagonist) causes a significant increase in the peripheral platelet count by releasing platelets from the spleen. In the present study 20 healthy volunteers received 50 mg metoprolol and 40 mg propranolol orally. Both drugs induced a statistically significant increase in the platelet count lasting more than 5 h. In addition, the effect of metoprolol and propranolol on beta-adrenoceptor mediated splenic platelet trapping was studied on 7 healthy subjects who received intravenous infusions of isoprenaline before and after the ingestion of these 2 beta-blocking drugs. It was demonstrated that the isoprenaline mediated decrease in the venous platelet count was diminished by both propranolol and metoprolol but the former compound appeared to be more potent in this respect. We conclude that both selective and non-selective beta-receptor blockade causes an increase in the peripheral platelet concentration during rest as well as during beta-adrenoceptor stimulation.

Adrenergic beta-Antagonists↗

PubMed1979

Thrombokinetics in giant cell arteritis, with special reference to corticosteroid therapy.

Duplicate platelet survival studies were carried out on 8 patients with giant cell arteritis (GCA), once before the institution of any therapy, and the second time when they were in a completely asymptomatic phase after having received corticosteroid treatment. The time interval between the studies ranged between 5 and 14 months. In the first study the mean peripheral platelet count was 486 +/- 25 X 10(9)/l and in the second 326 +/- 25 X 10(9)/l. The difference between the means was highly significant (P less than 0.001). The mean life-span of the platelets was normal in the duplicate experiments (6.7 +/- 0.3 and 7.3 +/- 0.4 days, respectively). Platelet production rate was significantly (P less than 0.001) raised in the first experiment but became normal in response to corticosteroid therapy. It is concluded that the thrombocytosis seen in GCA is reactive to the inflammation present in this disease, and it seems reasonable to assume that the reduction in the peripheral platelet count which occurs in response to corticosteroid therapy accurately reflects the clinical improvement of the patient.

Aged↗

PubMed1978

The peripheral platelet count in response to adrenergic alpha-and beta-1-receptor stimulation.

The aim of the present work was to investigate the effect of adrenergic alpha- and beta-1-receptor stimulation on the peripheral platelet count. The experiments were carried out on 8 healthy male volunteers using radioisotopically labelled platelets. 3 subjects received i.v. infusions of adrenaline (0.09 microgram X kg-1 X min-1) before and after the ingestion of 40 mg propranolol. In response to the first infusion there was an instant increase in the venous platelet-bound radioactivity (PBR) which amounted to 12% over basal value. This effect of adrenaline seemed to be potentiated by propranolol pretreatment. 5 subjects received i.v. infusions of the highly selective beta-1-receptor agonist H 133/22 (prenalterol, Hässle, Sweden). In response to a cumulative dose of 4.75 mg prenalterol a slight but significant (P less than 0.05) decrease in PBR occurred. It is concluded that alpha-receptor stimulation causes a depletion of platelets from the exchangeable splenic platelet pool resulting in a concomitant increase in the peripheral platelet count. Beta-receptor stimulation has an opposite effect on the spleen. The trapping of platelets by the spleen is mediated both via beta-1- and beta-2-receptors, but the effect of beta-2-receptor stimulation seems to predominate.

Adrenergic beta-Agonists↗

PubMed1978

The exchangeable splenic platelet pool in response to intravenous infusion of isoprenaline.

8 healthy volunteers and 4 asplenic subjects, in whom autologous platelets had been labelled with radioactive sodium chromate, received i.v. infusions of isoprenaline in a dose of 0.03 microgram x kg-1 x min-1 over a period of 6 min. In the former group these infusions caused a significant decrease in the concentration of labelled as well as unlabelled platelets in the peripheral blood. Body surface countings showed that a significant increase in the count rate over the spleen occurred concomitantly with the decrease in the circulating platelet-bound radioactivity (PBR). In the group of asplenic subjects no change in PBR occurred. It is concluded that adrenergic beta-receptor stimulation causes a transitory trapping of platelets in the exchangeable splenic platelet pool.

Adult↗

PubMed1978

Rapid platelet consumption in a case of metastatic osteogenic sarcoma of the breast.

An operation was carried out on an elderly female because of an osteogenic sarcoma of the breast. One year later she developed a state of rapid thrombocytolysis resistant to high dose prednisolone therapy and spleenectomy. At autopsy a large single metastasis was found in the right atrium and tumour emboli in the pulmonary artery. It is suggested that the shortening in platelet survival might have had an immunological background. Trapping of fibrinous material within tumour emboli and mechanical platelet destruction caused by the tumour appear to have been contributing factors.

Aged↗

PubMed1978

Assessment of a tissue transport-medium in preservation of tissue-fixed immunoglobulins and complement demonstrated by direct immunofluorescence. A pilot study with skin from SLE patients.

The present work was undertaken in order to test the value of a tissue transport-medium (Histocon) for direct immunofluorescence studies. For this purpose one skin biopsy was performed on each forearm of 26 patients with systemic lupus erythematosus. One of the specimens was left in ice-cold Histocon solution for 4, 8, or 20 hours, and the other was immediately quick-frozen. The results of the immunofluorescence tests with the two methods yielded similar results. It is concluded that the solution allows the preservation of tissue-fixed immunoglobulins and complement during short periods of transport.

Adult↗

PubMed1978

Peripheral platelet count in response to salbutamol before and after adrenergic beta-receptor blockade.

The effect of salbutamol (a comparatively selective adrenergic beta2-receptor agonist) on the peripheral platelet concentration was studied before and after the ingestion of either 50 mg metoprolol or 40 mg propranolol. The study was carried out on healthy males volunteers and autologous 51Cr-labelled platelets were employed at the experiments. Salbutamol was infused intravenously over a period of 6 min in a dose of 0.27 microgram.kg(-1). min(-1). Prior to metoprolol and propranolol administration a statistically significant lowering in platelet-bound radioactivity (PBR) was obtained in response to the salbutamol infusions. This salbutamol-induced fall in PBR was completely blocked by propranolol but was left unaffected by metoprolol. It is concluded that adrenergic beta2-receptor stimulation induces a transient lowering of the peripheral platelet count.

Adrenergic beta-Antagonists↗