Coagulation competence and fluid recruitment after moderate blood loss in young men

Zaar, Morten; Mørkeberg, Jakob; Pott, Frank Christian; Johansson, Pär I.; Secher, Niels H.

doi:10.1097/mbc.0000000000000114

Cited by 9 publications

(17 citation statements)

References 33 publications

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“…However, BL has the opposite effect. The reduction in circulating blood volume causes fluid to shift from the extravascular space to the intravascular space, resulting in haemodilution (Riddez et al 1998;Drobin & Hahn, 1999;Zaar et al 2014). This divergent effect on plasma volume is likely to have contributed to the greater increase in white blood cells during LBNP.…”

Section: Discussionmentioning

confidence: 99%

White blood cell concentrations during lower body negative pressure and blood loss in humans

Helmond

Johnson

Curry

et al. 2016

Experimental Physiology

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What is the central question of this study? Is lower body negative pressure a useful surrogate to study white blood cell responses to haemorrhage in humans? What is the main finding and its importance? We found that lower body negative pressure appears to be a useful surrogate to study the early white blood cell mobilization response during blood loss. Hypovolaemia has been associated with an immune response that might be secondary to sympathoexcitation. We tested the hypothesis that simulated hypovolaemia using lower body negative pressure (LBNP) and real hypovolaemia induced via experimental blood loss (BL) cause similar increases in the white blood cell concentration ([WBC]). We measured [WBC] and catecholamine concentrations in 12 men who underwent an LBNP and a BL protocol in a randomized order. We compared 45 mmHg of LBNP with 1000 ml of BL; therefore, [WBC] and catecholamine concentrations were plotted against central venous pressure to obtain stimulus-response relationships using the linear regression line slopes for both protocols. Mean regression line slopes were similar for total [WBC] (LBNP 183 ± 4 μl mmHg versus BL 155 ± 109 μl mmHg , P = 0.15), neutrophils (LBNP 110 ± 2 μl mmHg versus BL 96 ± 72 μl mmHg , P = 0.15) and lymphocytes (LBNP 65 ± 21 μl mmHg versus BL 59 ± 38 μl mmHg , P = 0.90). Mean regression line slopes for adrenaline were similar (LBNP 15 ± 5 pg ml mmHg versus BL 16 ± 4 pg ml mmHg , P = 0.84) and were steeper during LBNP for noradrenaline (LBNP 28 ± 6 pg ml mmHg versus BL 9 ± 6 pg ml mmHg , P = 0.01). These data indicate that central hypovolaemia elicits a relative leucocytosis with a predominantly neutrophil-based response. Additionally, our results indicate that LBNP models the stimulus-response relationship between central venous pressure and [WBC] observed during BL.

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Section: Discussionmentioning

confidence: 99%

White blood cell concentrations during lower body negative pressure and blood loss in humans

Helmond

Johnson

Curry

et al. 2016

Experimental Physiology

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“…This discrepancy might have occurred due to differences in the rate of blood removal (ϳ43 ml/min in our study vs. ϳ30 ml/min). Additionally, we removed blood into three separate 333-ml aliquots, whereas Zaar et al (39) used two 450 ml aliquots to protocol completion when compared with our protocol. Although ␣ angle was not statistically distinguishable from baseline to protocol termination in both LBNP and BL protocols, the stimulus-response trajectory of CVP-␣ angle was steeper during BL when compared with LBNP.…”

Section: Discussionmentioning

confidence: 99%

“…First, we collected blood only at baseline and at the termination of each protocol. Collecting multiple samples throughout both protocols would have allowed us to identify if a graded hypercoagulable state exists throughout a range of central hypovolemia within each subject (30,39). Second, we did not match CVP between protocols.…”

Section: Methodological Considerationsmentioning

confidence: 99%

“…However, BL has the opposite effect. The reduction in circulating blood volume causes fluid to shift from the extravascular space to the intravascular space, resulting in hemodilution (7,27,39) and a lower blood viscosity (3). The divergent hematocrit and viscosity responses to LBNP and BL may differentially influence coagulation responses during these two protocols, despite similar hemodynamic responses.…”

Section: Our Study Provides Noteworthy Data That Directly Compare Blomentioning

confidence: 99%

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Coagulation changes during lower body negative pressure and blood loss in humans

Helmond

Johnson

Curry

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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van Helmond N, Johnson BD, Curry TB, Cap AP, Convertino VA, Joyner MJ. Coagulation changes during lower body negative pressure and blood loss in humans. Am J Physiol Heart Circ Physiol 309: H1591-H1597, 2015. First published September 9, 2015; doi:10.1152/ajpheart.00435.2015.-We tested the hypothesis that markers of coagulation activation are greater during lower body negative pressure (LBNP) than those obtained during blood loss (BL). We assessed coagulation using both standard clinical tests and thrombelastography (TEG) in 12 men who performed a LBNP and BL protocol in a randomized order. LBNP consisted of 5-min stages at 0, Ϫ15, Ϫ30, and Ϫ45 mmHg of suction. BL included 5 min at baseline and following three stages of 333 ml of blood removal (up to 1,000 ml total). Arterial blood draws were performed at baseline and after the last stage of each protocol. We found that LBNP to Ϫ45 mmHg is a greater central hypovolemic stimulus versus BL; therefore, the coagulation markers were plotted against central venous pressure (CVP) to obtain stimulus-response relationships using the linear regression line slopes for both protocols. Paired t-tests were used to determine whether the slopes of these regression lines fell on similar trajectories for each protocol. Mean regression line slopes for coagulation markers versus CVP fell on similar trajectories during both protocols, except for TEG ␣°angle (Ϫ0.42 Ϯ 0.96 during LBNP vs. Ϫ2.41 Ϯ 1.13°/mmHg during BL; P Ͻ 0.05). During both LBNP and BL, coagulation was accelerated as evidenced by shortened R-times (LBNP, 9.9 Ϯ 2.4 to 6.2 Ϯ 1.1; BL, 8.7 Ϯ 1.3 to 6.4 Ϯ 0.4 min; both P Ͻ 0.05). Our results indicate that LBNP models the general changes in coagulation markers observed during BL. blood coagulation; hemorrhage; lower body negative pressure; blood coagulation tests; humans; central hypovolemia NEW & NOTEWORTHYOur study provides noteworthy data that directly compare blood coagulation activation induced by lower body negative pressure to those observed during blood loss in conscious humans.HEMORRHAGE IS ONE OF THE LEADING causes of accidental death (1) and is the leading cause of death on the battlefield (8, 9). Activation of the coagulation system is vital following a hemorrhagic injury to reduce the risk of exsanguination. Consequently, studying the activation of the coagulation system during blood loss (BL) is of upmost importance so new therapies and treatment algorithms, such as fluid resuscitation, can be developed. However, using invasive methods to experimentally induce BL is challenging to perform in humans.Lower body negative pressure (LBNP) is a technique that is used as a noninvasive surrogate to study many of the physiological responses to BL (4, 15, 18). LBNP sequesters circulating blood in the lower body, thereby reducing central blood volume and mimicking hemodynamic responses generated during BL (4,15,18). However, it is unclear if markers of coagulation system activation respond similarly during these protocols. Reductions in central blood volume by LBNP (38) ...

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“…Central hypovolemia elevates hemostatic activity whether it is provoked by controlled bleeding [1] , [2] , simulated bleeding by lower body negative pressure (LBNP) [3] , [4] , or orthostatic stress [5] . The hemostatic system is composed of several components that create a dynamic balance between coagulation and fibrinolysis, to reduce bleeding after injury while maintaining or restoring vascular patency.…”

Section: Introductionmentioning

confidence: 99%

Platelet Activation after Presyncope by Lower Body Negative Pressure in Humans

et al. 2014

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Central hypovolemia elevates hemostatic activity which is essential for preventing exsanguination after trauma, but platelet activation to central hypovolemia has not been described. We hypothesized that central hypovolemia induced by lower body negative pressure (LBNP) activates platelets. Eight healthy subjects were exposed to progressive central hypovolemia by LBNP until presyncope. At baseline and 5 min after presyncope, hemostatic activity of venous blood was evaluated by flow cytometry, thrombelastography, and plasma markers of coagulation and fibrinolysis. Cell counts were also determined. Flow cytometry revealed that LBNP increased mean fluorescence intensity of PAC-1 by 1959±455 units (P<0.001) and percent of fluorescence-positive platelets by 27±18%-points (P = 0.013). Thrombelastography demonstrated that coagulation was accelerated (R-time decreased by 0.8±0.4 min (P = 0.001)) and that clot lysis increased (LY60 by 6.0±5.8%-points (P = 0.034)). Plasma coagulation factor VIII and von Willebrand factor ristocetin cofactor activity increased (P = 0.011 and P = 0.024, respectively), demonstrating increased coagulation activity, while von Willebrand factor antigen was unchanged. Plasma protein C activity and tissue-type plasminogen activator increased (P = 0.007 and P = 0.017, respectively), and D-dimer increased by 0.03±0.02 mg l−1 (P = 0.031), demonstrating increased fibrinolytic activity. Plasma prothrombin time and activated partial thromboplastin time were unchanged. Platelet count increased by 15±13% (P = 0.014) and red blood cells by 9±4% (P = 0.002). In humans, LBNP-induced presyncope activates platelets, as evidenced by increased exposure of active glycoprotein IIb/IIIa, accelerates coagulation. LBNP activates fibrinolysis, similar to hemorrhage, but does not alter coagulation screening tests, such as prothrombin time and activated partial thromboplastin time. LBNP results in increased platelet counts, but also in hemoconcentration.

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Coagulation competence and fluid recruitment after moderate blood loss in young men

Cited by 9 publications

References 33 publications

White blood cell concentrations during lower body negative pressure and blood loss in humans

White blood cell concentrations during lower body negative pressure and blood loss in humans

Coagulation changes during lower body negative pressure and blood loss in humans

Platelet Activation after Presyncope by Lower Body Negative Pressure in Humans

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