On the inhibitory effect of albumin on platelet aggregation

Jørgensen, Kaj Anker; Stoffersen, Erik

doi:10.1016/0049-3848(80)90289-3

Cited by 127 publications

(52 citation statements)

References 9 publications

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“…Albumin binds to endothelial glycocalyx and maintains the normal permeability of microvessel walls, serving as a carrier for various molecules through its capability of transcytosis across endothelium [59,61,62]. Tang et al [63] demonstrated significantly reduced blood brain barrier permeability in a transient focal ischemia rat model when treated with rt-PA along with albumin, and hence significantly attenuating deleterious effects of rt-PA. Albumin is also an important inhibitor of platelet aggregation [64][65][66]. Albumin also increases the production of the anti-aggregatory prostaglandin (PGD2) from cyclic endoperoxides [65].…”

Section: Albuminmentioning

confidence: 99%

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Investigational Therapies for Ischemic Stroke: Neuroprotection and Neurorecovery

2011

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Stroke is one of the leading causes of death and disability worldwide. Current treatment strategies for ischemic stroke primarily focus on reducing the size of ischemic damage and rescuing dying cells early after occurrence. To date, intravenous recombinant tissue plasminogen activator is the only United States Food and Drug Administration approved therapy for acute ischemic stroke, but its use is limited by a narrow therapeutic window. The pathophysiology of stroke is complex and it involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis, neuroprotection, and neurorestoration. Regeneration of the brain after damage is still active days and even weeks after a stroke occurs, which might provide a second window for treatment. A huge number of neuroprotective agents have been designed to interrupt the ischemic cascade, but therapeutic trials of these agents have yet to show consistent benefit, despite successful preceding animal studies. Several agents of great promise are currently in the middle to late stages of the clinical trial setting and may emerge in routine practice in the near future. In this review, we highlight select pharmacologic and cell-based therapies that are currently in the clinical trial stage for stroke.

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Section: Albuminmentioning

confidence: 99%

“…Albumin also increases the production of the anti-aggregatory prostaglandin (PGD2) from cyclic endoperoxides [65]. The use of albumin also binds plateletactivating factor with high affinity [66,67], and decreases platelet-activating factor induced responses in platelets [68].…”

Section: Albuminmentioning

confidence: 99%

Investigational Therapies for Ischemic Stroke: Neuroprotection and Neurorecovery

2011

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“…34,35 It decreases platelet aggregation 34 and possesses heparin-like activity able to potentialize antithrombin III. 35 Such effects might be useful in view of the current interest in anticoagulation in septic patients.…”

Section: Anticoagulant Effectsmentioning

confidence: 99%

Use of Albumin in the Intensive Care Unit

Dubois

Vincent

2002

Transfus Alt Transfus Med

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( Pa ge 80 )The use of albumin in the critical care setting is a very controversial issue.Although not a new situation, we have seen a renewed interest in this question, especially after the publication of one particular meta-analysis. Much has been said about its publication, but it merits a brief review. Hypoalbuminemia, no longer considered to be "acceptable" or even inevitable in critically ill patients, has also been revisited. We will examine the issue by reviewing studies that have tried to correct the condition, the mechanisms by which it appears and its prognostic value. Finally, a great deal of work has been done to gain a better understanding of albumin and its properties beyond the most commonly accepted, namely maintenance of plasma oncotic pressure. A review of the research will help us to recognize that more randomized controlled trials are warranted. S U M M A R Y DEPARTMENT OF INTENSIVE CARE ERASME HOSPITAL FREE UNIVERSITY OF BRUSSELS BRUSSELS, BELGIUM• Albumin, • Hypoalbuminemia• Meta-analysis• Critical care• Intensive care unit ublication of the Cochrane meta-analysis on the administration of albumin solutions 1 in 1998 generated much debate. The authors concluded that overall relative risk of death in patients receiving albumin solutions was 1.67 compared with non-albumin recipients (Table 1). The study was criticized for many reasons. Not insignificant was the inclusion of studies that did not have mortality as an endpoint, not to mention the heterogeneity of the studies included (different patient populations, different goals in administering albumin, etc). Some studies had 0% mortality in the control group (despite it being highly improbable that a study in an intensive care unit [ICU] setting would result in no mortality) whereas others failed to consider important factors (age, hemodynamic data, etc.).Recently, another meta-analysis on the same issue was published by Wilkes and Navickis 2 in which the authors found no increased risk in mortality when albumin was administered (Table 1). Methodological considerations and inclusion of a larger number of studies could account for this discrepancy. However, the clinician

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“…The abnormal platelet activation caused by hypoalbuminemia can be prevented or corrected by the normalization of the plasma albumin level, or by simply adding albumin to plasma either in vitro or in vivo. 6,41,49 The mechanism, or mechanisms, leading to such an enhanced platelet aggregation as a result of hypoalbuminemia still remain unexplained. There is, however, some evidence to indicate that the abnormal platelet behavior might be caused by an increased rate of endoperoxide and thromboxane A 2 production by the platelets.…”

Section: Platelet Functionmentioning

confidence: 99%