Rheological approach to the analysis of blood coagulation in endothelial cell-coated tubes: Activation of the intrinsic reaction on the erythrocyte surface

Kawakami, S.; Kaibara, Makoto; Kawamoto, Yoshitaka; Yamanaka, Ko

doi:10.1016/0006-355x(95)00030-d

Cited by 31 publications

(4 citation statements)

References 37 publications

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“…Dehydration increases the hematocrit and blood viscosity both of which could induce thrombotic tendency [4]. Moreover, elevated hematocrit levels are reported to promote activation of factor IX (an intrinsic factor for coagulation cascade) by erythroelastase IX (factor IX-activating enzyme) in erythrocytes, which could further enhance the coagulation pathway [5,6]. In addition, patients with reduced renal function are more likely to develop pulmonary thromboembolism than those with normal kidney function [7].…”

Section: Discussionmentioning

confidence: 99%

Acute pulmonary thromboembolism occurring during treatment with tolvaptan in a patient with autosomal-dominant polycystic kidney disease

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Acute pulmonary thromboembolism occurring during treatment with tolvaptan in a patient with autosomal-dominant polycystic kidney disease

et al. 2017

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“…6 High procoagulant activity associated with loss of lipid asymmetry has been reported in a number of membrane bilayers, including glucosetreated erythrocytes, 10 sickled cells, 29 apoptotic cells, 30 and shed membrane microparticles as those derived from the atherosclerotic plaque. 4 Interestingly, PS exposure under pathological conditions occurs frequently in erythrocytes, and it has often been referred as an "apoptotic-like" even.…”

Section: Discussionmentioning

confidence: 99%

“…1 Exposure of PS at the surface of cell membranes regulates numerous physiological processes in cellular control and signaling, including apoptosis 2 and coagulation. [3][4][5] PS exposure in circulating cells 3,6 or shed membrane microparticles 4 provides a water/lipid surface for the interaction of coagulation factors, leading to an acceleration of thrombin formation. In sickle cell anemia, diabetes or under abnormal oxidative stress, erythrocytes display both a decrease in vitamin E content and an increase in PS externalization, causing an abnormal hypercoagulable state.…”

mentioning

confidence: 99%

α-Tocopherol Modulates Phosphatidylserine Externalization in Erythrocytes

Klein

Deckert

Schneider

et al. 2006

ATVB

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Objective-The aim of the present study was to assess the effect of ␣-tocopherol, the main vitamin E isomer on phosphatidylserine (PS) exposure at the surface of circulating erythrocytes, and to determine consequences on erythrocyte properties. Methods and Results-In vitro ␣-tocopherol enrichment of isolated erythrocytes significantly decreased PS externalization as assessed by lower Annexin V-fluorescein isothiocyanate labeling. Plasma phospholipid transfer protein (PLTP) transfers vitamin E, and both ␣-and ␥-tocopherol accumulated in circulating erythrocytes from PLTP-deficient homozygous (PLTP Ϫ/Ϫ ) mice as compared with wild-type mice. In agreement with in vitro studies, vitamin E-enriched erythrocytes from PLTP Ϫ/Ϫ mice displayed fewer externalized PS molecules than wild-type controls (Ϫ64%, PϽ0.05). The perturbation of phospholipid membrane asymmetry from PLTP Ϫ/Ϫ erythrocytes was accompanied by impairment of their procoagulant properties, with a 20% increase in clotting time as compared with wild-type controls (PϽ0.05). Less pronounced, however still significant, changes were observed in ␣-tocopherol content, procoagulant properties, and PS externalization in erythrocytes of PLTP-deficient heterozygotes. Finally, whole blood coagulation and circulating level of D-dimer, which reflects increased thrombus formation in vivo, were significantly decreased in PLTP Ϫ/Ϫ mice compared with wild-type mice. Conclusions-Vitamin

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“…Global tests, such as Thromboelastogram ® (TEG) or Sonoclot signature, etc., that measure hemostasis in whole blood or citrated blood, with or without activators, appear to closely resemble the in vivo situation, although they do not reflect the interaction(s) between the blood and endothelium [12]. We measured the initiation time of blood coagulation (Ti) from pregnancy 10M till one month after delivery, focusing particularly on the very early postpartum period, using a damped oscillation rheometer that is approximately 160 times more sensitive than that of TEG, to evaluate the risk of thrombus formation [17].…”

Section: T Sagesaka and H Funabashi / Change Of The Initiation Timementioning

confidence: 99%

Change of the initiation time of blood coagulation in pregnancy from 10-months to postpartum

Sagesaka

Funabashi²

2013

Clinical Hemorheology and Microcirculation

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We measured the time of initiation of blood coagulation (Ti) from pregnancy 10-months (36∼40 weeks) till 1-month after delivery, paying particular attention to the very early postpartum period, using a damped oscillation rheometer that is approximately 160 times more sensitive than the Thromboelastogram ® to evaluate the risk of thrombus formation. Blood samples were obtained from healthy volunteers at pregnancy 10-month, 1-hour, 3-hours, 4-days, 7-days, 3-weeks and 1-month after delivery. Ti values at pregnancy 10-month, 1-hour, 3-hours, 4-days, 7-days, 3-weeks, 1-month after delivery and in non-pregnant females were 20.4 ± 2.2, 11.7 ± 1.6, 13.2 ± 3.1, 17.2 ± 2.0, 20.2 ± 1.6, 21.4 ± 4.0, 24.6 ± 3.6, and (25.0 ± 3.4) minutes, respectively. Ti was significantly shorter at pregnancy 10-month, 1-hour, 3-ours, 4-days, 7-days and 3-weeks after delivery than in non-pregnant females. These data show that the blood of pregnant females is more hypercoagulable than nonpregnant females from pregnancy 10-month until 3-weeks post delivery, suggesting that they are at high risk of VTE after discharge from hospital.

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Rheological approach to the analysis of blood coagulation in endothelial cell-coated tubes: Activation of the intrinsic reaction on the erythrocyte surface

Cited by 31 publications

References 37 publications

Acute pulmonary thromboembolism occurring during treatment with tolvaptan in a patient with autosomal-dominant polycystic kidney disease

Acute pulmonary thromboembolism occurring during treatment with tolvaptan in a patient with autosomal-dominant polycystic kidney disease

α-Tocopherol Modulates Phosphatidylserine Externalization in Erythrocytes

Change of the initiation time of blood coagulation in pregnancy from 10-months to postpartum

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