Platelet Sequestration During Hypothermia in Dogs Treated with Sulphinpyrazone and Ticlopidine - Reversibility Accelerated After Intra-Abdominal Rewarming

Pina-Cabral, J M; Ribeiro‐da‐Silva, Alfredo; Dias, Almeida

doi:10.1055/s-0038-1660144

Cited by 22 publications

(14 citation statements)

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“…However, the biological significance of these phenomena and the function of platelets in this specific context remain unclear. Furthermore, these previous studies involved relatively mild hypothermic conditions . In the present study, we exposed the mice to severe hypothermia and discovered new information about platelet activity in hypothermia.…”

Section: Discussionmentioning

confidence: 90%

Hypothermia‐induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model

Horioka

Tanaka

Isozaki

et al. 2019

Journal of Thrombosis and Haemostasis

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BackgroundHypothermia, either therapeutically induced or accidental (ie, an involuntary decrease in core body temperature to <35°C), results in hemostatic disorders. However, it remains unclear whether hypothermia enhances or inhibits coagulation, especially in severe hypothermia. The present study evaluated the thrombocytic and hemostatic changes in hypothermic mice.MethodsC57Bl/6 mice were placed at an ambient temperature of −20°C under general anesthesia. When the rectal temperature decreased to 15°C, 10 mice were immediately euthanized, while another 10 mice were rewarmed, kept in normal conditions for 24 hours, and then euthanized. These treatments were also performed in 20 splenectomized mice.ResultsThe hypothermic mice had adhesion of CD62P‐positive platelets with high expression of von Willebrand factor (vWF) in their spleens, while the status of the peripheral platelets was unchanged. Furthermore, the plasma levels of platelet factor 4 (PF4) and pro‐platelet basic protein (PPBP), which are biomarkers for platelet degranulation, were significantly higher in hypothermic mice than in control mice, indicating that hypothermia activated the platelets in the splenic pool. Thus, we analyzed these biomarkers in asplenic mice. There was no increase in either PF4 or PPBP in splenectomized hypothermic mice. Additionally, the plasma D‐dimer elevation and microthrombosis were caused in rewarmed mice, but not in asplenic rewarmed mice.ConclusionsOur results indicate that hypothermia leads to platelet activation in the spleen via the upregulation of vWF, and this activation causes hypercoagulability after rewarming.

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Section: Discussionmentioning

confidence: 90%

Hypothermia‐induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model

Horioka

Tanaka

Isozaki

et al. 2019

Journal of Thrombosis and Haemostasis

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“…3). In addition to the effects seen on coagulation factors, severe hypothermia results in decreased platelet aggregability and decreased platelet count due to hepatic platelet sequestration [29,30].…”

Section: Mechanisms Of Coagulopathymentioning

confidence: 99%

Coagulopathy in the trauma patient

Schreiber

2005

Current Opinion in Critical Care

117

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Changes in coagulation following trauma are characterized by a complex series of events that may result in either a hypocoagulable or a hypercoagulable state. Routinely analyzed coagulation parameters do not adequately describe this state and they are deficient for guiding its therapy. Several promising new agents are available for treating hemorrhage in coagulopathic trauma patients that should result in improved survival.

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“…These modifications, which could potentially increase bleeding, were not documented in the normothermic control group. Pina-Cabral et al 66 also observed a decrease in platelet count in hypothermic dogs. The presence of platelet clumps was detected inside the hepatic sinusoids.…”

Section: Temperaturementioning

confidence: 85%

Massive Transfusion and Coagulopathy

Hardy

Samama

2003

Transfus Alt Transfus Med

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Massive Transfusion and Coagulopathy ) ( Transfusion Alternatives in Transfusion MedicineMost studies of MT have been conducted in trauma patients and are, for obvious reasons, primarily retrospective or uncontrolled observational studies.9 Given the variable and complex clinical context, the results of these studies have seldom led to definitive conclusions. Furthermore, factors other than the transfusion strategy, related to the trauma itself, may have led to the observed hemostatic abnormalities.10 Unfortunately, conventional teaching has sometimes failed to appreciate the evolution of transfusion practices and the context in which these practices were developed. As a result, anesthesiologists may have been led to inappropriately apply transfusion strategies, e.g., those specifically developed for trauma patients at a time when MWB was available, to a patient receiving red cell concentrates for massive bleeding during elective surgery. The situation can become even more confusing when disseminated intravascular coagulation (DIC) is associated with trauma and/or MT.In this article on MT and coagulopathy, we will attempt to do the following:1. Identify the causes of coagulopathy in massively transfused adult and previously hemostatically competent patients in order to determine the most appropriate transfusion/treatment strategies.2. Differentiate between the elective surgical setting and trauma, hypothesizing that recommendations derived from studies of MT in trauma patients may not apply to elective surgical patients.We searched MEDLINE for published articles on massive transfusion, using the search terms "transfusion," "trauma," "surgery," "coagulopathy," and "hemostatic defects." Articles dealing with obstetrical and pediatric patient populations were not retained, nor were those dealing with specific hemostatic anomalies such as cardiopulmonary bypass (CPB), liver transplantation and pre-existing coagulation disorders. A preliminary version of the text was circulated to experts from the (Perioperative Hemostasis Interest Group) for comments and suggestions. A narrative format was adopted given that the heterogeneity of the published studies was too great and not conducive to a more formal review. Since the nature of blood products available to clinicians has changed over time, the retrieved articles were organized and reviewed by date of publication in order to better understand the evolution of our knowledge of MT and coagulopathy. Variables Responsible for Coagulopathy in Association With Massive Transfusion Platelets HemodilutionSince the publication of Miller' s classic study on coagulation defects associated with massive blood transfusions, thrombocytopenia resulting from hemodilution has been thought to be the most important hemostatic abnormality associated with MT.11 This explanation is intuitively appealing: replacement of lost blood with fluids that do not contain platelets (or coagulation factors) results in a dilutional coagulopathy. However appealing the notion, hemodilution fails to explain s...

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Platelet Sequestration During Hypothermia in Dogs Treated with Sulphinpyrazone and Ticlopidine - Reversibility Accelerated After Intra-Abdominal Rewarming

Cited by 22 publications

References 9 publications

Hypothermia‐induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model

Hypothermia‐induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model

Coagulopathy in the trauma patient

Massive Transfusion and Coagulopathy

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