Enhanced platelet aggregation and activation under conditions of hypothermia

Xavier, Ruben G.; White, Ann E.; Fox, Susan C.; Wilcox, Robert G.; Heptinstall, Stan

doi:10.1160/th07-03-0189

Cited by 54 publications

(42 citation statements)

References 24 publications

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“…OHCA patients often develop postresuscitation stress responses after cardiac arrest, presumably due to the low-flow state during cardiac arrest, followed by a reperfusion injury, which causes the procoagulative systemic inflammatory response syndrome (Adrie et al, 2005;Koch et al, 2013). Furthermore, several studies have shown increased platelet activity in conjunction with mild induced hypothermia (Xavier et al, 2007;Högberg et al, 2009;Scharbert et al, 2010;Ortmann et al, 2012). These factors that strengthen hemostasis in OHCA patients during hypothermia are offset by delayed and slower clot formation demonstrated with thromboelastometry in this and previous studies (Heinius et al, 2002;Shimokawa et al, 2003;Martini et al, 2008;Rundgren and Engström, 2008;Spiel et al, 2009;Ivan et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Wide Temperature Range Testing with ROTEM Coagulation Analyses

Kander

Brokopp

Friberg

et al. 2014

Therapeutic Hypothermia and Temperature Management

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Mild induced hypothermia is used for neuroprotection in patients successfully resuscitated after cardiac arrest. Temperature-dependent effects on rotational thromboelastometry (ROTEM(®)) assays with EXTEM(®), FIBTEM(®), or APTEM(®) in cardiac arrest patients have not previously been studied. Ten patients with out-of-hospital cardiac arrest who underwent induced hypothermia were studied during stable hypothermia at 33°C. ROTEM temperature effects on EXTEM, FIBTEM, and APTEM assays were studied at temperatures set between 30°C and 42°C. Citrated whole blood test tubes were incubated in temperature-adjusted heating blocks and then investigated at respective temperature in the temperature-adjusted ROTEM. The following variables were determined: clotting time (CT), clot formation time (CFT), α-angle, and maximum clot firmness (MCF). The results from hypo- and hyperthermia samples were compared with the samples incubated at 37°C using the Wilcoxon matched-pairs signed-rank test. A p-value of <0.05 was considered significant. CT-EXTEM(®) and CT-APTEM(®) were prolonged by hypothermia at 30°C (p<0.01 for both) and 33°C (p<0.05 for both). Hyperthermia at 42°C shortened CT-EXTEM (p<0.05) and CT-APTEM (p<0.01). CFT-EXTEM(®) and CFT-APTEM(®) were markedly prolonged by hypothermia at 30°C, 33°C, and 35°C (p<0.01 for all except CFT-EXTEM, 35°C [p<0.05]). The α-angle-EXTEM was markedly decreased at 30°C, 33°C, and 35°C (p<0.01) but increased at 40°C (p<0.05) and 42°C (p<0.01); α-angle-APTEM showed similar results. MCF was unchanged at different temperatures for all tests. ROTEM (EXTEM, FIBTEM, and APTEM assays) revealed a hypocoagulative response to in vitro-applied hypothermia in the blood of cardiac arrest patients reflected in the prolonged clot initiation and decreased clot propagation. Hyperthermia showed the opposite effects. Clot firmness was not affected by temperature.

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Section: Discussionmentioning

confidence: 99%

Wide Temperature Range Testing with ROTEM Coagulation Analyses

Kander

Brokopp

Friberg

et al. 2014

Therapeutic Hypothermia and Temperature Management

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“…Peroxides and thromboxane A 2 cause new platelets to adhere to the old ones, a positive feedback phenomenon termed platelet aggregation, which rapidly creates a platelet plug inside the vessel [36].…”

Section: Positive Feedback Of Platelet Aggregationmentioning

confidence: 99%

Physiological Positive Feedback Mechanisms

Abdel-Sater¹,

Arabia²,

Ahmed³

et al. 2011

Am. J. Biomed. Sci.

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In positive feedback mechanisms, the response to a stimulus does not stop or reverse it but instead keeps the sequence of events going up. At first glance, this would appear to be a counter to the principle of homeostasis, since a positive feedback loop has no obvious means of stopping. Not surprisingly, therefore, the positive feedback is less common in nature than the negative one. A positive feedback mechanism can be harmful, as in case of fever that causes metabolic changes pushing it to be higher. However, in some instances, the body uses this mechanism for its advantage. A good example of significant positive feedback is the childbirth. Ovulation, coagulation, platelet aggregation, inflammation and shock are other instances in which the positive feedback plays a valuable role.

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“…However, the evidence on how hypothermia per se affects platelet function is contradictory. Whereas some authors proposed an inhibition of platelet function at in vivo and in vitro hypothermia [3,4,[12][13][14][15][16], others suggested platelet activation [17][18][19][20]. Most studies were carried out at temperatures below 28 C and therefore may not reflect platelet function at the clinically relevant degrees of mild and moderate hypothermia.…”

Section: Introductionmentioning

confidence: 99%

Mild and moderate hypothermia increases platelet aggregation induced by various agonists: a whole bloodin vitrostudy

Scharbert¹,

Kalb²,

Essmeister

et al. 2009

Platelets

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The mechanisms causing temperature-dependent bleeding, especially in hypothermic patients, warrant clarification. Therefore the aim of this study was to investigate platelet aggregation at the clinically important temperature range of 30-34 degrees C. After obtaining informed consent citrated whole blood was drawn from 12 healthy adult male volunteers, who had not taken any medication in the previous 14 days. After venipuncture blood samples were incubated at 37 degrees C until platelet testing. Platelet aggregation was performed in whole blood using the impedance aggregometer Multiplate at five different test temperatures between 30 degrees C and 34 degrees C. Aggregation responses at 37 degrees C served as controls. At temperatures of mild and moderate hypothermia (30-34 degrees C), overall platelet aggregation was increased compared to 37 degrees C. Increases were recorded in response to collagen, thrombin receptor activating peptide and ristocetin between 31 degrees C and 34 degrees C and in response to adenosine diphosphate between 30 degrees C and 34 degrees C. Overall platelet aggregation is increased at mild and moderate hypothermia down to 30 degrees C. These results indicate that bleeding complications reported in mildly hypothermic patients are not due to hypothermia-induced platelet inhibition. The pathomechanism of the overall increased platelet aggregation between 30 degrees C and 34 degrees C requires further detailed study.

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Enhanced platelet aggregation and activation under conditions of hypothermia

Cited by 54 publications

References 24 publications

Wide Temperature Range Testing with ROTEM Coagulation Analyses

Wide Temperature Range Testing with ROTEM Coagulation Analyses

Physiological Positive Feedback Mechanisms

Mild and moderate hypothermia increases platelet aggregation induced by various agonists: a whole bloodin vitrostudy

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