ISSN:0953-7104    

DOI:10.3109/09537109109006033

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Haemostasis is abnormal in uraemic patients with end-stage chronic renal failure. There is a risk of bleeding due to a failure of primary haemostasis,1yet at the same time arteriovenous shunt thrombosis is common2and the incidence of occlusive arterial disease is increased.3Both bleeding and thrombotic tendencies thus co-exist. There is a great deal of information about the former, less about the latter.

ISSN:0953-7104    

DOI:10.3109/09537109109006021

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Thrombolytic therapy has galned increasing acceptance in the clinical arena in recent years, but is fraught with three primary problems: delays in time to lysis, reocclusion, and haemorrhage. Inasmuch as the platelet is a critical determinant of thrombosis and, at the same time, interacts with molecular elements important in fibrinolysis, this anuclear cell plays a central role in the outcome of thrombolytic therapy. Platelet-rich thrombi are less sensitive to thrombolysis than platelet-poor thrombi, and reocclusive thrombi are richer in platelets than are thrombi that form de novo. Moreover, upon exposure to the fibrinolytic milieu, the platelet becomes transiently activated and, consequently, retards the progress of the lytic process; with continued exposure, however, the platelet becomes progressively inhibited and, as a result, bleeding times prolong and haemorrhagic risk increases. The molecular events that lead to these changes in platelet function during thrombolysis are, indeed, complex, and serve as the primary focus of this review.

ISSN:0953-7104    

DOI:10.3109/09537109109006022

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

We describe a platelet defect characterised by absence of aggregation to adrenaline and lack of secondary aggregation to ADP and platelet-activating factor (PAF) in a male subject without a significant bleeding tendency. The platelets also exhibited a decreased response to the phorbol ester PMA and to vasopressin polypeptides.We obtained evidence that the defect did not involve the cyclooxygenase pathway and that it was not dependent on altered intraplatelet levels of cyclic AMP (cAMP). Furthermore, adrenaline-stimulated cAMP production was normal.Irreversible aggregation was obtained in response to a combination of two stimuli at subaggregating concentrations. This observation indicates that the lack of a bleeding tendency in this subject may be ascribed to subthreshold concentrations of agonists in vivo overcoming the defect to a single agonist.

ISSN:0953-7104    

DOI:10.3109/09537109109006023

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

The effects of nifedipine and propranolol, alone and in combination, on collagen-induced platelet aggregation were studied in healthy volunteers using whole blood impedance aggregometry.No significant inhibition of platelet aggregation was found after the in vitro addition of propranolol, nifedipine or nifedipine vehicle or after nifedipine ex vivo. No interaction was found between in vitro propranolol and nifedipine, either in vitro or ex vivo.

ISSN:0953-7104    

DOI:10.3109/09537109109006024

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Previous evidence has suggested that plasmin, in addition to its proteolytic action on fibrin, may affect platelet function. To test the effects of plasmin generated in vivo by the thrombolytic agent streptokinase (SK) on platelet-dependent vascular occlusion, we have used a well-established canine model of experimental coronary artery stenosis which produces platelet aggregate-dependent cyclical variations in coronary blood flow. Infusion of SK into 22 dogs at doses sufficient to cause a systemic lytic state led to complete abolition of cyclical blood flow reductions (CFR's) at sites of coronary artery injury. Inhibition of coronary platelet occlusion was associated with marked prolongations of the bleeding time (from 3.2±0.6 min before to 14±5 min after SK infusion, mean±SD, n = 22). Despite the striking effects of SK on in vivo platelet-vessel wall interactions, only platelet aggregation in response to collagen was diminished among the ex vivo parameters of platelet function that were studied simultaneously. Platelet aggregation in response to other agonists, thromboxane A2 production, monoclonal antibody binding to platelet membrane glycoprotein (Gp) IIb-IIIa, Gp Ib-dependent botrocetin-induced platelet aggregation and platelet levels of cyclic AMP were not significantly altered. Therefore the thrombolytic agent streptokinase appears to cause important inhibitory effects on in vivo platelet reactivity with injured vascular intimal surfaces, possibly due to localised changes in platelet aggregate formation in the microenvironment of exposed collagen. These findings suggest that plasmin generated by thrombolytic agents may exhibit platelet inhibitory activity, and that this effect may be important in reestablishing blood flow in certain forms of platelet-mediated arterial thromboses.

ISSN:0953-7104    

DOI:10.3109/09537109109006025

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Platelet aggregation to four different agonists was measured in platelet-rich plasma from 17 patients with nutritional vitamin B12deficiency; 10 of these patients were also iron deficient. Impaired aggregation to ADP, collagen, epinephrine and ristocetin was found for 4, 8, 10 and 6 patients, respectively. Bleeding manifestations were seen in 5 patients, one belonging to the vitamin B12deficiency group and 4 to the combined deficiency group. Three of these 5 patients had normal platelet aggregation. These results show that impaired platelet aggregation is common in nutritional vitamin B12deficiency but that this impairment does not reliably correlate with a clinical bleeding tendency.

ISSN:0953-7104    

DOI:10.3109/09537109109006026

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

The uraemic state is commonly complicated by a haemorrhagic tendency due to an abnormality of the primary haemostatic response. Whilst renal anaemia contributes to the defect, platelet dysfunction has also been implicated. Tests of coagulation and platelet reactivity performed ex vivo on anticoagulated blood samples have not provided an adequate explanation for the haemostatic defect. We have therefore studied events at the site of tissue injury by serial assays of beta-thromboglobulin (BTG), thromboxane B2(TxB2) and fibrinopeptide A (FPA) in blood samples issuing from a standardised skin bleeding time incision in 7 uraemic subjects and matched healthy controls. Generation of TxB2and FPA were normal, but the concentration of BTG in bleeding time blood was markedly reduced throughout the first 5 min in the uraemic subjects. We conclude that a defect of platelet release occurring at the site of tissue injury may contribute to the haemostatic abnormality in uraemia and this finding could be relevant to the therapeutic strategy adopted in the management of bleeding episodes.

ISSN:0953-7104    

DOI:10.3109/09537109109006027

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

ISSN:0953-7104    

DOI:10.3109/09537109109006028

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

Based upon experimental data, we advance the hypothesis that ketanserin, a 5-HT2serotonergic receptor antagonist, may provide protection against pathologies resulting from platelet-vessel wall interactions such as myointimal proliferation, vasospasms and thrombus formation. Clinical data support the possibility that such a vascular protection is operational also in man.

ISSN:0953-7104    

DOI:10.3109/09537109109006029

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor