Simulated Hypergravity Activates Hemostasis in Healthy Volunteers

Abstract

Background Hypergravity may promote human hemostasis thereby increasing thrombotic risk. Future touristic suborbital spaceflight will expose older individuals with chronic medical conditions, who are at much higher thromboembolic risk compared with professional astronauts, to hypergravity. Therefore, we tested the impact of hypergravity on hemostasis in healthy volunteers undergoing centrifugation. Methods and Results We studied 20 healthy seated men before and after 15 minutes under 3 Gz hypergravity on a long‐arm centrifuge. We obtained blood samples for hemostasis testing before, immediately after, and 30 minutes after centrifugation. Tests included viscoelastic thromboelastometry, platelet impedance aggregometry, endothelial activation markers, blood rheology testing, microparticle analyses, and clotting factor analysis. Exposure to hypergravity reduced plasma volume by 12.5% ( P =0.002) and increased the red blood cell aggregation index ( P <0.05). With hypergravity, thrombelastographic clotting time of native blood shortened from 719±117 seconds to 628±89 seconds ( P =0.038) and platetet reactivity increased ( P =0.045). Hypergravity shortened partial thromboplastin time from 28 (26–29) seconds to 25 (24–28) seconds ( P <0.001) and increased the activity of coagulation factors (eg, factor VIII 117 [93–134] versus 151 [133–175] %, P <0.001). Tissue factor concentration was 188±95 pg/mL before and 298±136 pg/mL after hypergravity exposure ( P =0.023). Antithrombin ( P =0.005), thrombin‐antithrombin complex ( P <0.001), plasmin‐alpha2‐antiplasmin complex (0.002), tissue‐plasminogen activatior ( P <0.001), and plasminogen activator inhibitor‐1 ( P =0.002) increased with centrifugation. Statistical adjustment for plasma volume attenuated changes in coagulation. Conclusions Hypergravity triggers low‐level hemostasis activation through endothelial cell activation, increased viscoelasticity, and augmented platelet reactivity, albeit partly counteracted through endogenous coagulation inhibitors release. Hemoconcentration may contribute to the response.