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Biomedical subjects

H Wadenvik

Publications and source records attributed to H Wadenvik.

84 records · Page 5Linked to original sources
PubMed1986

The relation between platelet reactivity and coronary angiographic findings in young female survivors of acute myocardial infarction.

In 31 women who had survived their first acute myocardial infarction (MI) studies of platelet reactivity were related to coronary angiographic findings. The results were compared to those obtained from 38 age-matched control women. According to the cardioangiographic findings the group of MI was subdivided into: 9 patients with 1-vessel disease (VD), 10 patients with 2-VD, and 5 patients with 3-VD; 7 subjects did not reveal significant coronary stenosis. When each of these 4 subgroups of MI-patients were compared with the control material significant difference with respect to PF4 was found only for subjects with 1-VD (20.0 +/- 4.8 vs. 10.3 +/- 0.6 ng/ml). As regards BTG the difference was significant for 1-VD and 2-VD patients (69 +/- 12 and 59 +/- 3, respectively vs. 40 +/- 2 ng/ml). The cumulative frequency for secondary aggregation differed only as regards 1-VD patients (78 vs 40%).

Adenosine Diphosphate↗
PubMed1986

Evaluation of platelet reactivity in diabetes mellitus.

Seventeen patients with insulin-dependent diabetes mellitus, all below the age of 45 years, were studied. Five of them had retinopathy but no other micro- or macrovascular diabetic complications. None of them had any other concurrent disorder or were on any medication but insulin. The results were compared to those of 17 healthy volunteers of comparable age. There was no difference between the two groups in venous platelet counts, serum production of thromboxane B2 (TXB2), ADP-induced platelet aggregation or bleeding times. As compared to the controls, the diabetics had significantly elevated blood glucose and glycosylated hemoglobin values. The mean plasma values of beta-thromboglobulin, platelet factor 4 and TXB2 were significantly lower in the patients than in the controls. Thus, our results do not lend support to the current concept that platelet reactivity is enhanced in diabetes mellitus.

Adenosine Diphosphate↗
PubMed1985

Effect of Iloprost (ZK 36 374), a novel prostacyclin analogue, on ADP-induced platelet aggregation.

The effect of Iloprost (ZK 36 374), a chemically stable carboprostacyclin derivative, on ADP-induced platelet aggregation was investigated using platelet-rich plasma obtained from healthy male volunteers. It was shown that Iloprost in a dose-dependent fashion powerfully inhibits both the primary and secondary wave of ADP-induced platelet aggregation. Similarly, Iloprost immediately and most effectively disaggregates preformed platelet aggregates.

Adenosine Diphosphate↗
PubMed1984

Successful treatment of refractory autoimmune haemolytic anaemia by plasmapheresis.

A 16-year-old female was admitted because of rapidly progressive fatigue, severe anaemia and icterus. The S-bilirubin was 190 mumol/l, COHb 7.3% and high amounts of free Hb in plasma were present. The Coombs' direct test was strongly positive with anti-IgG but negative with anti-IgM and anti-C3. Conventional therapy with very high doses of hydrocortisone i.v., cyclophosphamide, azathioprine, and transfusions of washed packed red cells proved ineffective. During 5 consecutive days she also received i.v. infusions of gamma-globulin (25 g each day). Nevertheless, her condition deteriorated and 3 plasma exchanges were carried out with impressive clinical and laboratory effects. After the 3rd plasma exchange, the patient did not require further transfusions of packed red cells. Therapy with corticosteroids could be rapidly reduced and she was discharged after 5 weeks with a normal blood picture. Since then she has remained in excellent health.

Adolescent↗
PubMed1983

Plasma concentrations of platelet-specific proteins in young female acute myocardial infarction survivors and their age-matched female controls.

The steady state plasma concentrations of the two platelet-specific proteins beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were determined in two groups of females: 36 acute myocardial infarction (AMI) survivors, and 38 age-matched control subjects. For the AMI patients the mean BTG and PF4 values were 57 +/- 4 and 14.1 +/- 1.7 ng/ml, respectively. These two means significantly exceeded the corresponding means for the controls, 40 +/- 2 and 10.3 +/- 0.6 ng/ml, respectively. Similar results have recently been reported by other workers who investigated patients with coronary artery disease; however, in no previous study were the values for BTG and PF4 related to those obtained for control subjects matched with respect to sex and age. The present results therefore further support the concept that increased platelet activation and secretion is taking place in steady state patients who previously have sustained an AMI.

Adult↗
PubMed1983

Stress and platelet activation.

Severe stress, with increased secretion of adrenaline, is likely to cause platelet activation. The aim of the present study was to investigate if moderate stress, which usually is not accompanied by adrenaline secretion, could induce activation of platelets, as measured by changes in the plasma concentrations of platelet factor 4 (PF-4). Noise stimulation (100 dBA for 10 min) caused a significant increase in the diastolic (10%, p less than 0.01) and mean arterial pressures (4%, p less than 0.01) of 10 healthy male volunteers. The plasma levels of PF-4 and the venous platelet concentrations were, however, unaffected during noise exposure. The results therefore suggest that stress not accompanied by adrenal medullary activation, does not induce platelet activation.

Adrenal Medulla↗
PubMed1983

Plasma platelet factor 4: a potentially useful predictor of ischaemic heart disease?

The aim was to investigate whether plasma platelet factor 4 (PF-4) in suspected acute myocardial infarction (AMI) patients could serve as a prognostic tool and identify patients at risk for future death from AMI or ischaemic heart disease (IHD). Therefore, upon admission to our coronary care unit plasma PF-4 was measured on 109 consecutive patients. 53 of them proved to have AMI, and 50 IHD but no AMI; the remaining 6 had no evidence of IHD. 24 patients died in hospital or during the follow-up period which was an average of 16.7 +/- 2.4 months. The decreased were subgrouped into those dying of AMI (n = 16), and those dying of IHD but with no AMI (n = 8). No deaths from other causes were recorded. As compared with survivors there was a tendency towards higher PF-4 values among those who died of AMI. However, patients who during follow-up suffered death from IHD proved to have significantly (p less than 0.05) higher PF-4 levels than survivors.

Adult↗
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↗
PubMed1977

Apnoea and bradycardia from submersion in "chronically" decerebrated cats.

In "chronically" but not in acutely decerebrated cats, submersion of the head caused apnoea and marked bradycardia, associated with a maintained or slightly raised arterial pressure. Since these reflex adjustments, though very reproducible, occurred with a varying latency and could be induced also by nasal injection of water, they appeared to be, at lest in part, elicited from the upper respiratory passages. Thus, a terrestrial mammal, reputed to shun any form of immersion, can exhibit adjustments during head submersion, similar to those in habitually diving species. This response pattern is basically organized at the lower brainstem level.

Animals↗
PubMedDate not supplied

Detection of platelet antibodies in chronic idiopathic thrombocytopenic purpura (ITP). A comparative study using flow cytometry, a whole platelet ELISA, and an antigen capture ELISA.

Chronic idiopathic thrombocytopenic purpura (ITP) is a consequence of rapid platelet destruction caused by circulating platelet antibodies. In this study we compared three methods for detecting serum platelet antibodies in a population of 65 patients with chronic ITP. In two of the techniques intact platelets were used as the antibody target, i.e. the whole platelet ELISA and the flow cytometric assay; in the third an antigen-specific modified antigen capture ELISA (MACE) was employed. By using the whole platelet ELISA and the flow cytometric assay 35% and 45% of the patients, respectively, displayed an antiplatelet antibody. In most cases (26 or 29 patients) IgG was the predominant antiplatelet immunoglobulin. As analysed using the MACE-technique glycoprotein (GP) Ib/IX-specific antibodies occurred with the same frequency as antibodies specific for GPIIb/IIIa. Moreover, there was a poor correlation between the MACE results on the one hand and results from the intact platelet-based techniques on the other, i.e. several patients were positive in one assay whereas they were negative in the other. We conclude that all three techniques have their merits and demerits; it appears reasonable that they should be used together in the evaluation of the autoimmune process of chronic ITP.

Adult↗