Operation Everest II: coagulation system during prolonged decompression to 282 Torr

1987 ◽  
Vol 63 (3) ◽  
pp. 1262-1267 ◽  
Author(s):  
M. Andrew ◽  
H. O'Brodovich ◽  
J. Sutton
Keyword(s):  
Factor Viii ◽  
High Altitude ◽  
Sea Level ◽  
Prolonged Exposure ◽  
Venous Blood ◽  
Work Load ◽  
Coagulation Factors ◽  
Coagulation Cascade ◽  
Coagulation System ◽  
Arterial O2 Saturation

Thromboembolic phenomena may occur as humans ascend to high altitude. To investigate the role of the coagulation cascade and its inhibitors in these disorders, venous blood was obtained from eight subjects who participated in the Operation Everest II project. Samples were obtained before and 5 min after completion of a progressive incremental exercise test to exhaustion at sea level and atmospheric pressures of 380 (18,000 ft) and 282 Torr (25,000 ft). Plasma was analyzed for the activity or concentration of factors II, V, VII, VIII complex, IX-XIII, prekallikrein, high-molecular-weight kininogen, fibrinogen, antithrombin III, alpha 2-macroglobulin, alpha 2-antiplasmin, C1-esterase inhibitor, alpha 1-antitrypsin, and protein C. Prolonged exposure to simulated high altitude did not alter the concentration of any of the coagulation factors or inhibitors. Exercise increased the circulating concentrations of the factor VIII complex at sea level, 380, and 282 Torr. However, the increment was less at the simulated high altitudes. The increase in the factor VIII complex was inversely related to arterial O2 saturation and directly related to the work load achieved and blood pH and plasma lactate concentrations. These studies suggest that the gradual development of marked chronic hypoxia does not affect the coagulation cascade.

Home treatment for haemophilia

1978 ◽  
Vol 16 (13) ◽  
pp. 49-50
Keyword(s):  
Factor Viii ◽  
Coagulation Factors ◽  
Home Treatment ◽  
Factor Ix ◽  
Coagulation Cascade ◽  
Haemophilia A ◽  
Haemophilia B ◽  
Prolonged Bleeding ◽  
Factor Deficiency ◽  
Spontaneous Haemorrhage

Haemophilia A is caused by faulty synthesis of Factor VIII of the coagulation cascade. Haemophilia B (Christmas disease) is caused by a deficiency of Factor IX. The two conditions are clinically similar; all patients suffer from prolonged bleeding after trauma and in the more severely affected there is also spontaneous haemorrhage, particularly into joints and muscles. Correction of factor deficiency by plasma concentrates restores haemostasis but the intermittent nature of the haemorrhage, the scarcity of the transfused coagulation factors and their short plasma half-lives in most cases limit treatment to episodes of bleeding.

Role of vitamin K-dependent proteins in the arterial vessel wall

2011 ◽  
Vol 31 (04) ◽  
pp. 251-257 ◽  
Author(s):  
M. L. L. Chatrou ◽  
C. P. Reutelingsperger ◽  
L. J. Schurgers
Keyword(s):  
Vascular Calcification ◽  
Vitamin K ◽  
Independent Predictor ◽  
Vitamin K Antagonists ◽  
Venous Blood ◽  
Coagulation Factors ◽  
Coagulation Cascade ◽  
High Intake ◽  
Smooth Muscle Cell Migration

SummaryVitamin K was discovered early last century at the same time as the vitamin K-antagonists. For many years the role of vitamin K was solely ascribed to coagulation and coagulation was thought to be involved only at the venous blood side. This view has dramatically changed with the discovery of vitamin K-dependent proteins outside the coagulation cascade and the role of coagulation factors at the arterial side. Vitamin K-dependent proteins are involved in the regulation of vascular smooth muscle cell migration, apoptosis, and calcification. Vascular calcification has become an important independent predictor of cardiovascular disease. Vitamin K-antagonists induce inactivity of inhibitors of vascular calcification, leading to accelerated calcification. The involvement of vitamin K-dependent proteins such as MGP in vascular calcification make that calcification is amendable for intervention with high intake of vitamin K. This review focuses on the effect of vitamin K-dependent proteins in vascular disease.

FACTOR VIII AND FACTOR XII LEVELS IN BORDERLINE HYPERTENSION

1987 ◽  
Author(s):  
G M Patrassi ◽  
A Santarossa ◽  
F Fallo ◽  
M T Sartori ◽  
M Viero ◽  
...  
Keyword(s):  
Factor Viii ◽  
Coagulation Factors ◽  
Vascular Wall ◽  
Coagulation System ◽  
Factor Xii ◽  
Mortality And Morbidity ◽  
Borderline Hypertension ◽  
Normal Limits ◽  
Coagulant Activity ◽  
Ristocetin Cofactor

Borderline hypertension causes mortality and morbidity rates similar to those associated with estabilished hypertension. However, there is no univocal guideline for its therapeutic management. Hypercoagulability in hypertension has been demonstrated. The aim of our study was to evaluate some coagulation factors in agroup of patients affected by borderlinehypertension. The following tests were carried out: PT and PTT, Factor VIII coagulant activity, FVIII antigen and FVIII ristocetin cofactor, Factor XII and Factor XI activities. These tests were selected for their relationship to the contact coagulative activation near the vascular wall. In our patients statistically significant higher FVIII and FXII coagulant activities than normal control subjects were found. Moreover, an evident even though not statistically significant PTT shortening was seen. Other tests taken into consideration were all within normal limits. Our results suggest that an increased FVIII and FXII synthesis and/or release is present, and an activated coagulation system exists in borderline hypertension. Furthermore, it is not clear why an excess of FVIII:C over FVIIIR:Ag and FVIIIR:RCof was found in our patients. In conclusion, an activation of haemostatic mechanism was found in borderline hypertension. The young age of patients and the absence of evident hypertensive angiopathy are in agreement with an overactivity of blood vessel tone. Haemostatic activation could be an useful marker in favour of the precious management of patients with borderline hypertension.

Recruitments of Sherpa highlanders and non-Sherpa lowlanders v1

2021 ◽  
Author(s):  
Yunden Droma ◽  
not provided Masayuki Hanaoka ◽  
not provided Masao Ota
Keyword(s):  
Single Nucleotide Polymorphisms ◽  
High Altitude ◽  
Sea Level ◽  
Venous Blood ◽  
Genetic Adaptation ◽  
Nucleotide Polymorphisms ◽  
Research Project ◽  
Single Nucleotide ◽  
Altitude Hypoxia ◽  
High Altitude Hypoxia

In order to carry out the research project of genetic adaptation to high-altitude hypoxia in Sherpa highlanders, we recruited Sherpa highlanders in Namche Bazaar village at a high altitude of 3,440 meters (m) above sea level and non-Sherpa lowlanders in Kathmandu city at 1,300 m in Nepal. Venous blood was sampled to obtain plasma and extract DNA in each subject. The concentrations of factors in plasma were measured. The single-nucleotide polymorphisms (SNPs) in the hypoxia-associated genes were genotyped.

Coronary lipid deposition during chronic anemia or high altitude exposure

1961 ◽  
Vol 16 (1) ◽  
pp. 103-106 ◽  
Author(s):  
Louis C. Fillios ◽  
Stephen B. Andrus ◽  
Chikayuki Naito
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Prolonged Exposure ◽  
Tissue Hypoxia ◽  
Lipid Deposition ◽  
High Altitudes ◽  
Chronic Anemia ◽  
Apparent Increase ◽  
Altitude Exposure ◽  
Per Se

Experimental anemia and polycythemia were studied in hypercholesteremic rats. The following results were noted: a) chronic anemia favors a significant increase in endocardial and coronary lipid deposition; b) rats made polycythemic by prolonged exposure to simulated high altitudes also had a marked degree of coronary involvement but no apparent increase in endocardial sudanophilia; whereas c) sea-level cobalt polycythemia does not appear to favor an increase in coronary or endocardial sudanophilia, suggesting that d) polycythemia, per se, does not favor an increase in lipid deposition at these sites. These findings suggest that tissue hypoxia may account for the above increases in coronary sudanophilia, while changes in endocardial sudanophilia appear to be related more closely to the circulating cholesterol for all the groups. Submitted on May 16, 1960

scholarly journals Blood Coagulation in High Altitude Pulmonary Hypertension

1977 ◽  
Author(s):  
I. Singh ◽  
I.S. Chohan
Keyword(s):  
Pulmonary Hypertension ◽  
Factor Viii ◽  
High Altitude ◽  
Blood Coagulation ◽  
Sea Level ◽  
Fibrinolytic Activity ◽  
Plasma Fibrinogen ◽  
Factor V ◽  
Platelet Adhesiveness ◽  
Platelet Factor

Blood coagulation studies were carried out in 38 Indian soldiers who were resident at altitudes between 3690 and 5540 m for 2 years. Compared with 16 sea-level controls, 6 of these 38 subjects who had developed pulmonary hypertension during their stay at high altitude showed a significant increase of plasma fibrinogen, fibrinolytic activity, platelet adhesiveness, platelet factor 3, factor V, and factor VIII. In the remaining 32 subjects who did not develop pulmonary hypertension there was a significant increase of plasma fibrinogen and fibrinolytic activity only.The above differences between subjects who develop pulmonary hypertension at high altitude and those who do not develop pulmonary hypertension suggest that high altitude pulmonary hypertension is of occlusive origin and is dependent on changes in blood coagulation at high altitude.

Beta-adrenergic blockade does not prevent the lactate response to exercise after acclimatization to high altitude

1994 ◽  
Vol 76 (2) ◽  
pp. 610-615 ◽  
Author(s):  
R. S. Mazzeo ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
A. Cymerman ◽  
A. C. Roberts ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Arterial O2 Saturation ◽  
Response To Exercise ◽  
Peak Blood

We examined the extent to which epinephrine influences blood lactate adjustments to exercise during both acute (AC) and chronic (CH) high-altitude exposure. Eleven male sea level residents were divided into a control group (n = 5) receiving a placebo or a drug group (n = 6) receiving 240 mg/day of propranolol. All subjects were studied at rest and during 45 min of submaximal exercise (approximately 50% of sea level maximal O2 uptake) at sea level (SL) and within 4 h of exposure to and after 3 wk residence at 4,300 m (summit of Pikes Peak). Blood samples were collected from the femoral artery for epinephrine and lactate concentration. Exercising blood lactate concentration was significantly different across all altitude conditions such that AC > CH > SL (P < 0.05). For a given arterial O2 saturation, mean exercising blood lactates were lower for the beta-blocked group compared with controls; however, both groups demonstrated similar patterns across all conditions. Epinephrine levels during exercise followed a similar pattern to that of lactate, averaging 0.67, 0.43, and 0.29 ng/ml for AC, CH, and SL, respectively. The correlation between lactate and epinephrine was 0.93 and 0.84 for control and beta-blocked subjects, respectively. Whereas during exercise epinephrine was consistently higher for the beta-blocked group than controls, this difference was only significant during CH exposure. The epinephrine response was related to the extent of hypoxia in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Changes in Coagulation Parameters After Permanent Pacemaker Implantation

2020 ◽  
Vol 3 (2) ◽  
pp. 86-90
Author(s):  
I.D. Yoncheva ◽  
D.E. Biserov ◽  
M.N. Negreva
Keyword(s):  
Pacemaker Implantation ◽  
Coagulation Factors ◽  
Endothelial Damage ◽  
The Body ◽  
Coagulation Cascade ◽  
Coagulation System ◽  
Body Type ◽  
Cardiac Devices ◽  
The One

AbstractThe connection between venous thrombotic events in patients with implanted pacemakers and changes in coagulation factors has been the basis of numerous scientific studies for years. Results show that the effect on the coagulation system is a long-term and dynamic process, as well as presence of a significant dependence with many concomitant cardiovascular diseases.Advances in medicine in recent decades and increase in life expectancy of patients with implanted cardiac devices (ICD) increase the risk of a variety of complications. These adverse events may be associated with development of thrombosis, change in the stimulation threshold, need for ablation due to concomitant rhythm pathology and others. Analysis of data from literature shows unequivocally that placement of endocardial electrodes leads to activation of the coagulation system in the body. On the one hand, this is a result of the direct traumatic moment and endothelial damage in the early post-procedure period, and subsequently, the presence of electrodes of the foreign body type in some individuals can provoke a procoagulation state.More in-depth research is needed in this area to clarify the answers to these questions, namely: in which phase of the coagulation cascade are the changes most significant; is there a way to anticipate these changes and prevent them accordingly; is disturbed homeostasis of coagulation temporary or persistent.These questions will be answered after sufficient data have been accumulated on these changes and how to modulate them.

scholarly journals Activation of factor VIII by factor IXa

Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 744-751 ◽  
Author(s):  
ME Rick
Keyword(s):  
Factor Viii ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Coagulation Factors ◽  
Factor Ix ◽  
Coagulation Cascade ◽  
Related Protein ◽  
Factor Ixa ◽  
Baseline Levels ◽  
High Concentrations

Abstract Thrombin causes an increase in factor VIII coagulant (VIII:C) activity, which is followed by a decay of VIII:C activity to below baseline levels. It has been suggested that a similar interaction of trace amounts of thrombin and factor VIII is a necessary prerequisite before factor VIII can participate in the coagulation cascade. In the current study, factor IXa, a serine protease with structural similarities to thrombin, is shown to cause an increase and subsequent fall in VIII:C in a manner qualitatively similar to the reaction with thrombin. The reaction is inhibited by a human inhibitor to factor IX and the interaction appears to involve only VIII:C, since factor-VIII-related protein (VIII:RP) is not changed on polyacrylamide gel electrophoresis (PAGE) or radioimmunoassay during the reaction. Phospholipid increases the activation of factor VIII by factor IXa, and high concentrations of diisopropylfluorophosphate and hirudin inhibit the reaction. The physiologic significance of the interaction of factor IXa with factor VIII is not entirely clear since the concentration of factor IXa needed for activation is much greater than the concentration of thrombin required for similar activation of factor VIII. Factor IXa is most likely to play a role in the intrinsic cascade acting as an initial activator of factor VIII, since factor IXa precedes thrombin in this clotting sequence. In addition, factor IXa may be important wherever relatively high local concentrations of factor IXa and factor VIII occur, particularly in the presence of phospholipid, which may serve to localize the coagulation factors.

scholarly journals Activation of factor VIII by factor IXa

Blood ◽  
1982 ◽  
Vol 60 (3) ◽  
pp. 744-751
Author(s):  
ME Rick
Keyword(s):  
Factor Viii ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Coagulation Factors ◽  
Factor Ix ◽  
Coagulation Cascade ◽  
Related Protein ◽  
Factor Ixa ◽  
Baseline Levels ◽  
High Concentrations

Thrombin causes an increase in factor VIII coagulant (VIII:C) activity, which is followed by a decay of VIII:C activity to below baseline levels. It has been suggested that a similar interaction of trace amounts of thrombin and factor VIII is a necessary prerequisite before factor VIII can participate in the coagulation cascade. In the current study, factor IXa, a serine protease with structural similarities to thrombin, is shown to cause an increase and subsequent fall in VIII:C in a manner qualitatively similar to the reaction with thrombin. The reaction is inhibited by a human inhibitor to factor IX and the interaction appears to involve only VIII:C, since factor-VIII-related protein (VIII:RP) is not changed on polyacrylamide gel electrophoresis (PAGE) or radioimmunoassay during the reaction. Phospholipid increases the activation of factor VIII by factor IXa, and high concentrations of diisopropylfluorophosphate and hirudin inhibit the reaction. The physiologic significance of the interaction of factor IXa with factor VIII is not entirely clear since the concentration of factor IXa needed for activation is much greater than the concentration of thrombin required for similar activation of factor VIII. Factor IXa is most likely to play a role in the intrinsic cascade acting as an initial activator of factor VIII, since factor IXa precedes thrombin in this clotting sequence. In addition, factor IXa may be important wherever relatively high local concentrations of factor IXa and factor VIII occur, particularly in the presence of phospholipid, which may serve to localize the coagulation factors.

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