Effects of changes in temperature (local and central) on plasma fibrinolytic activity

Dodman, B.; Cunliffe, W.J.; Roberts, Bryan E.; Buchan, C.

doi:10.1136/jcp.26.4.248

Cited by 6 publications

(3 citation statements)

References 7 publications

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“…Investigations of hemostasis during hyperthermia have revealed a similar activation of coagulation [11] and fibrinolysis [23] as in the present experiment but there exists no clear description of the mechanism responsible for these changes on hemostasis. It has, however, been considered that platelet activation in response to increased temperature with a secondary activation of the coagulation factors or changes in endothelial function could be responsible for the alterations in coagulation [11].…”

Section: Discussionsupporting

confidence: 58%

Hypercoagulability in response to elevated body temperature and central hypovolemia

Meyer¹,

Ostrowski²,

Overgaard³

et al. 2013

Journal of Surgical Research

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Background Coagulation abnormalities contribute to poor outcomes in critically ill patients. In trauma patients exposed to a hot environment, a systemic inflammatory response syndrome, elevated body temperature, and reduced central blood volume occur in parallel with changes in hemostasis and endothelial damage. The objective of this study was to evaluate whether experimentally elevated body temperature and reduced central blood volume (CBV) per se affects hemostasis and endothelial activation. Methods Eleven healthy volunteers were subjected to heat stress, sufficient to elevate core temperature, and progressive reductions in CBV by lower body negative pressure (LBNP). Changes in hemostasis were evaluated by whole blood haemostatic assays, standard hematologic tests and by plasma biomarkers of coagulation and endothelial activation/disruption. Results Elevated body temperature and decreased CBV resulted in coagulation activation evidenced by shortened activated partial tromboplastin time (−9% [IQR −7; −4]), thrombelastography: reduced reaction time (−15% [−24; −4]) and increased maximum amplitude (+4% (2; 6)), all P < 0.05. Increased fibrinolysis was documented by elevation of D-dimer (+53% (12; 59), P = 0.016). Plasma adrenaline and noradrenaline increased 198% (83; 346) and 234% (174; 363) respectively (P = 0.006 and P = 0.003). Conclusions This experiment revealed emerging hypercoagulability in response to elevated body temperature and decreased CBV, whereas no effect on the endothelium was observed. We hypothesize that elevated body temperature and reduced CBV contributes to hypercoagulability, possibly due to moderate sympathetic activation, in critically ill patients and speculate that normalization of body temperature and CBV may attenuate this hypercoagulable response.

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Section: Discussionsupporting

confidence: 58%

Hypercoagulability in response to elevated body temperature and central hypovolemia

Meyer¹,

Ostrowski²,

Overgaard³

et al. 2013

Journal of Surgical Research

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“…The patients were kept at rest for 30 minutes before the pre-exercise venepucture. The effect of local heat was studied by placing one arm in a water bath at 45°C for 10 minutes (Dodman, Cunliffe, Roberts, and Buchan, 1973), and blood was sampled from this arm immediately before and after the procedure. P. A. Gordon, G. R. Breeze, J. R. Mann, and J. Stuart…”

Section: Methodsmentioning

confidence: 99%

Coagulation fibrinolysis in sickle-cell disease

et al. 1974

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SYNOPSIS A study of fibrinolytic activity in sickle-cell patients during asymptomatic periods has shown a normal fibrinolytic response to exercise and local heat to the arm. During vasoocclusive crises there was no significant decrease in fibrinolytic activity. These results contrast with earlier reports of decreased fibrinolysis during crisis and a suggestion that fibrinolytic activators might be of value in preventing vasoocclusive episodes.Patients in painful crisis showed a significant rise in fibrinogen concentration and fall in platelet count. The former may contribute to localized vascular sludging by increasing whole-blood viscosity, while the latter probably results from local trapping of platelets in areas of sickling or from subsequent splenic sequestration of damaged platelets. There was no evidence of disseminated, as opposed to localized, intravascular coagulation during crisis.

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“…This allows for better heat dissipation. Some studies have shown that the increase in heat causes a decrease in activated partial thromboplastin time, thromboelastographic reaction time, and platelet count, as well as an increase in fibrinolytic activity [ 42 , 43 ]. There is therefore an early activation of the coagulation system when the body is exposed to heat stress.…”

Section: Blood Volume and Coagulationmentioning

confidence: 99%

Heat-Related Illness in Emergency and Critical Care: Recommendations for Recognition and Management with Medico-Legal Considerations

Savioli

Zanza²,

Longhitano³

et al. 2022

Biomedicines

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Hyperthermia is an internal body temperature increase above 40.5 °C; normally internal body temperature is kept constant through natural homeostatic mechanisms. Heat-related illnesses occur due to exposure to high environmental temperatures in conditions in which an organism is unable to maintain adequate homeostasis. This can happen, for example, when the organism is unable to dissipate heat adequately. Heat dissipation occurs through evaporation, conduction, convection, and radiation. Heat disease exhibits a continuum of signs and symptoms ranging from minor to major clinical pictures. Minor clinical pictures include cramps, syncope, edema, tetany, and exhaustion. Major clinical pictures include heatstroke and life-threatening heat stroke and typically are expressed in the presence of an extremely high body temperature. There are also some categories of people at greater risk of developing these diseases, due to exposure in particular geographic areas (e.g., hot humid environments), to unchangeable predisposing conditions (e.g., advanced age, young age (i.e., children), diabetes, skin disease with reduced sweating), to modifiable risk factors (e.g., alcoholism, excessive exercise, infections), to partially modifiable risk factors (obesity), to certain types of professional activity (e.g., athletes, military personnel, and outdoor laborers) or to the effects of drug treatment (e.g., beta-blockers, anticholinergics, diuretics). Heat-related illness is largely preventable.

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Effects of changes in temperature (local and central) on plasma fibrinolytic activity

Cited by 6 publications

References 7 publications

Hypercoagulability in response to elevated body temperature and central hypovolemia

Hypercoagulability in response to elevated body temperature and central hypovolemia

Coagulation fibrinolysis in sickle-cell disease

Heat-Related Illness in Emergency and Critical Care: Recommendations for Recognition and Management with Medico-Legal Considerations

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