Effects of Low Temperature on Shear-Induced Platelet Aggregation and Activation

Zhang, Jianning; Wood, Jennifer R.; Bergeron, Angela L.; Mcbride, Latresha Itreshu; Ball, Chalmette; Yu, Qinghua; Pusiteri, Anthony E.; Holcomb, John B.; Dong, Jing‐fei

doi:10.1097/01.ta.0000093366.98819.fe

Cited by 62 publications

(43 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…10 Small amounts of thrombin generated by contact-activation 11 or cold-activation of plasma activate factor V or factor VIII, accelerating both extrinsic and intrinsic coagulation [12][13][14] and activating platelets. [15][16][17] The phenomenon of cold-activation of plasma has been known for some decades, [18][19][20][21] but the exact thrombin amount generated in cold-activated recalcified plasma was not quantified. The present sensitive INCA technique allows the measurement of lowgrade contact activation of frozen/thawed plasma.…”

mentioning

confidence: 99%

Intrinsic Hemostasis Activation by Freezing and Thawing of Plasma

Stief

Otto

Renz

2007

Clin Appl Thromb Hemost

View full text Add to dashboard Cite

Low-grade contact activation of hemostasis is clinically relevant. Freezing/thawing of plasma was studied in the intrinsic coagulation activity assay. Normal plasmas were frozen at −80°C or −20°C and thawed at 37°C or 23°C. These plasmas and unfrozen samples were activated by SiO2 -CaCl2. Freezing/thawing of normal plasma induced about 100-fold more thrombin activity at 5 minutes coagulation reaction time than the respective unfrozen samples. Freezing at −80°C induces more artificial changes than freezing at −20°C. In 9 of 10 plasmas of patients receiving coumarin, nearly no additional thrombin is generated within a 12-minute coagulation reaction time. Minor procoagulant changes of plasma might be dangerous in patients with insufficient liver function, who might not tolerate a therapy with fresh frozen plasma, which behaves as a procoagulant because of its matrix changes. The intrinsic coagulation activity assay allows the measurement of low-grade contact activation of frozen/thawed plasma.

show abstract

mentioning

confidence: 99%

Intrinsic Hemostasis Activation by Freezing and Thawing of Plasma

Stief

Otto

Renz

2007

Clin Appl Thromb Hemost

View full text Add to dashboard Cite

show abstract

“…However, other investigators have reported the opposite, that refrigeration (< 21 days) retards the release of α-granule contents such as β-thromboglobulin [12,39,40]. Refrigerated platelets spontaneously form aggregates [41,42], respond better to agonists than room temperature platelets [11,[43][44][45][46][47][48][49][50][51], and adhere better to von Willebrand factor (vWf) under shear stress [52,53]. Furthermore, a recent study shows that systemic hypothermia of 31-34 °C in mice accelerates thrombus formation in arterioles and venules [43], indicating that exposure to temperatures below the physiological norm may activate platelets in vivo.…”

Section: Room Temperature Versus Refrigerated Storagementioning

confidence: 99%

Platelet Storage Temperature – How Low Can We Go?

Josefsson

Hartwig

Hoffmeister

2007

Transfus Med Hemother

View full text Add to dashboard Cite

Transfusion of human platelets, stored in blood banks as concentrates, is the treatment of choice for thrombocytopenia and bleeding. To be clinically effective, transfused platelets must circulate and retain sufficient function to recognize and react to vascular damage. Storage at room temperature is limited to 5-7 days because of the risk of bacterial growth and loss of platelet functionality, as platelets do not tolerate refrigeration. Once chilled, platelets are detected and rapidly removed from circulation despite high functionality. We recently defined a clearance mechanism for short-term (2 h) refrigerated platelets: α_Mβ₂ receptors on hepatic macrophages recognize clustered βGlcNAc residues on platelet GPIbα receptors on refrigerated platelets. Here we review current knowledge of the mechanisms of platelet removal, the changes that occur in platelets after short and extended refrigeration, and methods to preserve platelet concentrates long-term for transfusion.

show abstract

“…Shivering also raises intracranial pressure (ICP) and requires the use of several pharmacological agents to inhibit these efects along with skin warming to address physical discomfort [20,21]. Another side efect of wholebody cooling is the risk of shear-induced platelet aggregation, which can develop as blood viscosity increases at low temperatures [22]. Even a minor amount of coagulation can cause a blockage of the microcirculation of the brain and heart, which ironically creates the exact problem that hypothermia atempts to treat [21].…”

Section: Systemic Hypothermiamentioning

confidence: 99%

Hypothermia in Stroke Therapy: Systemic versus Local Application

Huber¹,

Duan²,

Chandra³

et al. 2017

Hypoxia and Human Diseases

View full text Add to dashboard Cite

Presently, there are no efective, widely applicable therapies for ischemic stroke. There is strong clinical evidence for the neuroprotective beneits of hypothermia, and surfacecooling methods have been utilized for decades in the treatment of cerebral ischemia during cardiac arrest, but complications with hypothermia induction have hindered its clinical acceptance in ischemic stroke therapy. Recently, the microcatheter-based local endovascular infusion (LEVI) of cold saline directly to the infarct site has been proposed as a solution to the drawbacks of surface cooling. The safety and eicacy of LEVI in rat models have been established, and implementation in larger animals has been similarly encouraging. A recent pilot study even established the safety of LEVI in humans. This review seeks to outline the major research on LEVI, discusses the mechanisms that mediate its superior neuroprotection over surface and systemic cooling, and identiies areas that warrant further investigation. While LEVI features improvements on surface cooling, its core mechanisms of neuroprotection are still largely shared with therapeutic hypothermia in general. As such, the mechanisms of hypothermia-based neuroprotection are discussed as well.

show abstract

Effects of Low Temperature on Shear-Induced Platelet Aggregation and Activation

Cited by 62 publications

References 33 publications

Intrinsic Hemostasis Activation by Freezing and Thawing of Plasma

Intrinsic Hemostasis Activation by Freezing and Thawing of Plasma

Platelet Storage Temperature – How Low Can We Go?

Hypothermia in Stroke Therapy: Systemic versus Local Application

Contact Info

Product

Resources

About