The effect of pH on platelet and coagulation factor activities

Chaimoff, C; Creter, D; Djaldetti, M

doi:10.1016/0002-9610(78)90241-6

Cited by 64 publications

(47 citation statements)

References 11 publications

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“…[11][12][13][14] The contributions to thrombin generation from hypothermia and acidosis induced in vivo are revealed recently by Martini et al 15 Using a swine model with four animal groups (control, hypothermia, acidosis, and combined hypothermia and acidosis), Martini et al 15 investigated the independent and combined effects of hypothermia and acidosis on thrombin-generation kinetics. In this study, hypothermia of 32°C was induced using a cold-water blanket with 4°C circulating water and acidosis of pH 7.1 was induced by the infusion of 0.2 mol/L hydrochloric acid.…”

Section: Thrombin Generationmentioning

confidence: 96%

Coagulopathy by Hypothermia and Acidosis: Mechanisms of Thrombin Generation and Fibrinogen Availability

Martini

2009

Journal of Trauma: Injury, Infection &Amp; Critical Care

204

132

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ВведениеОб изменениях кислотно основного состояния (КОС) в условиях церебрального повреждения име ется мало данных. Например, модель двухчасовой ок IntroductionThere are few data on changes of acid base balance (ABB) following a cerebral damage. For example, the model of a two hour occlusion of the middle cerebral Общая терапевтическая гипотермия «заработала» негативную репутацию в лечении мультитравматических паци ентов, и рассматривается как один из факторов в «летальной триаде» шока, ацидоза и гипотермии. Данный факт объясняется отсутствием взаимодействия между ацидозом и гипотермией; эффекты гипотермии на коагуляцию яв ные и сложно обратимые в присутствии ацидоза. Цель работы -определение влияния локального неинвазивного охлаждения головного мозга на метаболические и гемокоагуляционные показатели больных с синдромом острой ишемии мозга. Материал и методы. Материалом исследования явились 113 пациентов с тяжелой черепно мозго вой травмой, в том числе осложненной поражением стволовых структур, которым в различных модификациях про водили охлаждение головного мозга. При этом изучались значения кислотно основного состояния и свертывающей системы артериальной и венозной крови. Результаты. Установлено, что никаких воздействий локальной гипотер мии головного мозга на коагуляцию не происходит, в то время как исходно отрицательные значения избытка бу ферных оснований показывают положительные цифры (сдвиг вправо) к концу охлаждения. Приведены рекомен дации по предупреждению метаболических сдвигов. Заключение: пациентов с очень высоким риском кровотечения можно безопасно охлаждать до температуры головного мозга 32-34°C, даже в присутствии ацидоза от умеренной степени до тяжелой. Это является большим преимуществом локальной гипотермии перед общей. Ключевые слова: кислотно основное состояние, свертывающая система, охлаждение головного мозга, назофарингеальное охлажде ние, общая гипотермия.Systemic therapeutic hypothermia has gained a negative reputation in treating multiple trauma patients and is regarded as one of the factors in the lethal triad of shock, acidosis, and hypothermia. This fact owes to no relationship between acidosis and hypothermia; the effects of the latter on coagulation are evident and complexly reversible in the presence of acidosis. Objective: to determine the impact of noninvasive local brain cooling on the metabolic and blood coagulation indicators of a patient with acute cerebral ischemia. Subjects and methods. The subjects of the study were 113 patients with severe brain injury, including that complicated by the involvement of stem structures, who underwent brain cooling in different modifications. In so doing, the val ues of acid base balance and coagulation system in arterial and venous blood were investigated. Results. Local brain hypother mia was not found to affect coagulation while the baseline negative values of excess buffer bases showed positive values (a right shift) by the end of cooling. Recommendations were given to prevent metabolic shifts. Conclusion. Patients at very high risk for ...

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Section: Thrombin Generationmentioning

confidence: 96%

Coagulopathy by Hypothermia and Acidosis: Mechanisms of Thrombin Generation and Fibrinogen Availability

Martini

2009

Journal of Trauma: Injury, Infection &Amp; Critical Care

204

132

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“…Two studies have shown that raising pH from intragastric levels to pH 7.0 improves the coagulation in patients suffering from gastric hemorrhage and that coagulation is impaired at pH 6.4 and severely impaired at pH 5.4. 26,27 These studies have been the foundation for the treatment of bleeding ulcers with pHraising drugs such as proton pump inhibitors and histamine blockers. However, these pH levels are relevant in the treatment of gastric ulcers but they are not providing us with information regarding effects of pH changes in the blood on the coagulation system as the levels studied are outside what is compatible with survival.…”

Section: Fig 1 a Roteg Registration Of Blood Explaining The Differementioning

confidence: 99%

Acidosis Impairs the Coagulation: A Thromboelastographic Study

Engström

Schött

Romner

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

156

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“…18 Studies have also shown that low pH impairs plasma coagulation and inhibits platelet function. 19,20 The importance of these factors was shown by a large retrospective study demonstrating that an elevated prothrombin time (PT) or partial thromboplastin time (PTT) in the earliest phases of the resuscitative effort (on arrival in the trauma center) was both common and independently associated with increase in all-cause mortality. 21 An elevation in the PTT (> 35 s) was a particularly ominous sign, predicting a 326% increase in mortality compared to patients with a normal PTT when other prognostic indicators were controlled for, with most of the deaths occurring early in the hospital stay.…”

Section: Etiologymentioning

confidence: 99%