Platelet and Fibrinogen Kinetics in Patients with Aorto-Femoral Dacron Grafts: Evaluation of Period of Maximum Risk from Thrombosis

1979 ◽  
Author(s):  
R.C. Kester ◽  
S.M. Rajah ◽  
C.N. McCollum ◽  
P. Learoyd ◽  
M. Pepper
Keyword(s):  
Blood Flow ◽  
Survival Time ◽  
Antithrombotic Therapy ◽  
Favourable Outcome ◽  
Fractional Catabolic Rate ◽  
Flow Conditions ◽  
Arterial Grafts ◽  
Catabolic Rate ◽  
Post Operation ◽  
Iodine 125

The thrombogenicity of Dacron arterial grafts may lead to eventual closure, although Dacron aorto-femoral grafts rarely thrombose because of wide calibre and rapid blood flow. The less favourable outcome of Dacron grafts with narrow diameter or suboptimal flow may be improved by antithrombotic therapy during the “thrombogenic period” of graft maturation. To evaluate this period, platelet and fibrinogen kinetics using, Chromium 51 and Iodine 125 respectively, were measured pre-operation and at 3, 6 and 9 months, in 10 patients after aorto-femoral Dacron bypass. Six age-matched volunteers were simultaneously studied. Platelet survival time was reduced 8.8 to 7.4 days (p<0.01) and platelet turnover increased at 3 months post-operation compared with pre-operative levels 39 to <47/103/days. Similarly, fibrinogen T½ life was decreased 3.7 to 3.4 days and fractional catabolic rate increased at 3 months 0.27 to 0.34 (p< 0.01). These indices of thrombogenic activity returned to pre-operative levels by 9 months. We suggest that Dacron aorto-femoral grafts remain thrombogenically active for about 9 months. Where blood flow conditions are suboptimal or graft diameters are small, it may be prudent to use antithrombotic therpy to protect patency.

Some Factors Influencing Metabolism and Distribution of Fibrinogen in Man and Rabbits

1977 ◽  
Vol 37 (02) ◽  
pp. 243-252
Author(s):  
Yi-Hsiang Chen ◽  
E. B Reeve
Keyword(s):  
Plasma Fibrinogen ◽  
Synthesis Rate ◽  
Fibrinogen Concentration ◽  
Fractional Catabolic Rate ◽  
System Parameters ◽  
Catabolic Rate ◽  
Simultaneous Decrease ◽  
Normal Males ◽  
Healthy Females ◽  
Made In

SummaryTo shed some light on the homeostatic regulation of plasma fibrinogen, metabolic studies were made in healthy females, and in normal, thyroidectomized, and thyroxine-treated rabbits. In females, compared with normal males, plasma fibrinogen concentration, plasma and interstitial fibrinogen decreased consequent to an increased fractional catabolic rate and a normal fibrinogen synthesis rate. The interstitial/plasma fibrinogen ratio remained unchanged. In normal rabbits, with increasing body weight fractional catabolic rate and catabolic rate decreased, while fibrinogen concentration and plasma fibrinogen remained constant owing to a simultaneous decrease in fibrinogen synthesis. In addition, fractional transcapillary transfer rate and transcapillary flux also decreased resulting in a shrinkage of interstitial fibrinogen. Thyroidectomy and thyroxine-injection markedly altered fibrinogen metabolism: thyroid hormone accelerated fibrinogen catabolism but also stimulated synthesis. The net result was an increase in plasma fibrinogen and fibrinogen concentration. The interstitial/plasma fibrinogen ratio decreased in thyroxine-treated, and increased in thyroidectomized animals. This study defines the variations of the fibrinogen system parameters in these physiologic and pathologic conditions, and illustrates some patterns of alterations in fibrinogen metabolism.

Catabolism of Human Fibrinogen Fragment D in Normal Subjects and Patients with Liver Cirrhosis

1980 ◽  
Vol 44 (03) ◽  
pp. 146-149 ◽  
Author(s):  
Nicole Ardaillou ◽  
Jeannine Yvart ◽  
Philippe Le Bras ◽  
Marie-José Larrieu
Keyword(s):  
Liver Cirrhosis ◽  
Clearance Rate ◽  
Plasma Clearance ◽  
Normal Subjects ◽  
Fractional Catabolic Rate ◽  
Human Fibrinogen ◽  
Plasma Pool ◽  
Catabolic Rate ◽  
Chloramine T

SummaryThe catabolism of human fragment D, (FgD), obtained by plasmin digestion of fibrinogen has been investigated in normal subjects and patients with liver cirrhosis and the results compared with those obtained for fibrinogen (Fg). Fg was labelled with I-125 and Fg D with I-131 using the chloramine T method. The plasma disappearance curves of both labelled proteins fitted a two exponential curve. In controls the plasma clearance rate of Fg D was greater than that of Fg as shown by the marked difference between the half-lives of these two tracers: 8,9 and 83,5 hours for Fg D and Fg respectively. The fractional catabolic rate of Fg D was 3.38 times the plasma pool per day. In nine patients with liver cirrhosis, catabolism of Fg was not modified. In contrast, catabolism of Fg D was significantly reduced with a half life of 13.0 hours and a low fractional catabolic rate. These results suggest the role of the liver in the catabolism of Fg D in man.

scholarly journals Increased Apolipoprotein AI Production Rate and Redistribution of High-Density Lipoprotein Size Induced by Estrogen plus Progestin as Oral Contraceptive

2009 ◽  
Vol 94 (12) ◽  
pp. 4891-4897 ◽  
Author(s):  
Laurence Duvillard ◽  
Guillaume Dautin ◽  
Emmanuel Florentin ◽  
Aline Jeannin ◽  
Jean-Paul Pais de Barros ◽  
...  
Keyword(s):  
Oral Contraceptive ◽  
High Density Lipoprotein ◽  
Production Rate ◽  
Density Lipoprotein ◽  
High Density ◽  
Pool Size ◽  
Fractional Catabolic Rate ◽  
Fed State ◽  
Catabolic Rate ◽  
Estrogen Plus Progestin

Context: The impact of estrogen plus progestin as an oral contraceptive on high density lipoprotein (HDL) apolipoprotein (apo) AI metabolism in humans is poorly understood. Objectives: This study was designed to measure the in vivo effect of Moneva (30 μg ethinylestradiol, 75 μg gestodene) on HDL apoAI production rate and fractional catabolic rate. Design: Using 13C-leucine, we performed two kinetic studies in the fed state in 10 normolipidemic young women, before and 3 months after beginning Moneva. Results: On Moneva, serum triglycerides increased by 12% (P = 0.03) in the fed state, whereas low-density lipoprotein and HDL cholesterol remained unchanged. HDL apoAI pool size and production rate were increased by 9.2% (67.3 ± 7.1 vs. 61.6 ± 6.7 mg · kg−1; P = 0.05) and 26.5% (14.3 ± 2.7 vs. 11.3 ± 2.2 mg · kg−1 · d−1; P = 0.02), respectively. HDL apoAI fractional catabolic rate was not significantly modified. Three-month treatment by Moneva induced a shift of HDL size distribution from HDL2 toward HDL3 (HDL3 = 51.5 ± 8.1 vs. 46.5 ± 9.2% of total HDL; P = 0.02) and an increase in the proportion of apoAI among HDL components (38.8 ± 4.3 vs. 34.4 ± 2.8%; P = 0.01). Conclusion: Oral contraception by estrogen plus progestin induces changes in HDL apoAI metabolism characterized by an increase in production rate and pool size, with a higher proportion of HDL3 particles. Whether or not these changes are beneficial to prevent atherosclerosis has to be explored further.

Pulse oximeter signal at various blood flow conditions in anin vitro model

1995 ◽  
Vol 33 (1) ◽  
pp. 87-91 ◽  
Author(s):  
L. -G. Lindberg ◽  
M. Vegfors ◽  
C. Lennmarken ◽  
P. Å. Öberg
Keyword(s):  
Blood Flow ◽  
Pulse Oximeter ◽  
Flow Conditions ◽  
Vitro Model

Interactions of increased pO2 and pCO2 effects in producing convulsions and death in mice

1961 ◽  
Vol 16 (1) ◽  
pp. 1-7 ◽  
Author(s):  
John R. Marshall ◽  
Christian J. Lambertsen
Keyword(s):  
Carbon Dioxide ◽  
High Pressure ◽  
Blood Flow ◽  
Latent Period ◽  
Survival Time ◽  
Brain Blood Flow ◽  
Time Data ◽  
Cortical Depression ◽  
Survival Time Data ◽  
Very High

In 379 mice subjected to from 1 to 11 atm. of pO2 and 0 to 304 mm Hg of pCO2 for 90 minutes, oxygen was convulsigenic at pressures greater than 3 atm. and lethal at greater than 4 atm. Carbon dioxide in 1 atm. of O2 was not convulsigenic but was lethal at very high tensions. In the presence of O2 at high pressure (OHP) small elevations of CO2 tension shortened the preconvulsive latent period, whereas CO2 tensions greater than 120 mm Hg inhibited convulsions. Survival time in OHP was shortened by the addition of CO2. An interaction between OHP and CO2 effects is suggested by both the preconvulsive latent period and survival time data. The effects of CO2 on OHP and electroshock convulsions are compared and possible reasons for differences are discussed in light of the previously demonstrated general cortical depression and inhibition of convulsions by CO2. The potentiation of OHP convulsions by low CO2 tensions is probably due to effects on brain blood flow. Although death can occur without convulsions there is a tendency for animals susceptible to convulsions to be also susceptible to the lethal properties of OHP with CO2. Submitted on July 28, 1960

scholarly journals Overestimation of the lipoprotein fractional catabolic rate(FCR) measured in short duration experiments.

1992 ◽  
Vol 15 (9) ◽  
pp. 541-546 ◽  
Author(s):  
Gerard CHAMPARNAUD ◽  
Khadija OUGUERRAM ◽  
Thierry MAGOT ◽  
Claude LUTTON
Keyword(s):  
Short Duration ◽  
Fractional Catabolic Rate ◽  
Catabolic Rate

scholarly journals In vivo behavior of human radioiodinated antithrombin III: distribution among three physiologic pools

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 13-19 ◽  
Author(s):  
TH Carlson ◽  
TL Simon ◽  
AC Atencio
Keyword(s):  
Endothelial Cell ◽  
Antithrombin Iii ◽  
Young Men ◽  
Fractional Catabolic Rate ◽  
Kinetic Behavior ◽  
Exponential Curve ◽  
Catabolic Rate ◽  
Total Body ◽  
Endothelial Receptor

Abstract It has recently been shown that antithrombin III (AT) distributes between plasma, a noncirculating vascular-associated pool and an extravascular pool in rabbit. Study of the in vivo behavior of autologous human 131I-AT demonstrates that in humans AT also distributes among three pools that are analogous to those found in rabbit. From the in vivo kinetic behavior of the 131I-labeled AT, the fractions of total-body AT in the plasma, noncirculating vascular- associated, and extravascular pools were calculated to be 0.393 +/- 0.015, 0.109 +/- 0.016, and 0.496 +/- 0.014, respectively. From three- exponential plasma radioactivity disappearance curves, an average plasma fractional catabolic rate, j3, of 0.576 +/- 0.034 day-1 was obtained for five healthy young men. This is almost identical to the result obtained if plasma 131I-AT disappearance is assumed to fit a two- exponential curve (0.546 +/- 0.038), where the constant C2 from *Ap(t) = C1e-a1t + C2e-a2t is assumed to be equal to 1 - C1. The fraction of the total vascular AT catabolized daily, j3.5, was calculated to be 0.457 +/- 0.034, and the fractional catabolic rate of total-body AT, jT, averaged 0.2271 +/- 0.0176. The results give further support to a model of in vivo behavior in which the vascular AT distributes between plasma and an endothelial receptor. Thus, the latter may serve to mediate activation of AT for its reaction with coagulation proteases and to mediate its entrance into the endothelial cell, where it is either transported to the extravascular fluids or is catabolized.

scholarly journals Interaction of size-fractionated heparins with lipoprotein lipase and hepatic lipase in the rat

1992 ◽  
Vol 285 (3) ◽  
pp. 731-736 ◽  
Author(s):  
G Liu ◽  
M Hultin ◽  
P Østergaard ◽  
T Olivecrona
Keyword(s):  
Body Weight ◽  
Lipoprotein Lipase ◽  
Hepatic Lipase ◽  
High Plasma ◽  
Detectable Effect ◽  
Fractional Catabolic Rate ◽  
Enzymic Digestion ◽  
Catabolic Rate ◽  
Rat Livers ◽  
Plasma Activity

Heparin and heparin partially depolymerized by enzymic digestion were separated into six size fractions. Hep 1 (tetrasaccharides), with a mean M(r) of 1200, did not release significant amounts of either lipoprotein lipase (LPL) or hepatic lipase (HL) on intravenous injection into rats. Hep 2 (mainly octa- and deca-saccharides), with a mean M(r) of 2400-3000, released both lipases. To evoke the same plasma activity of LPL and HL required about 10 times more by weight, or about 40 times more molecules, of this heparin than of hep 5 (mean M(r) 12,000, similar to conventional heparin). Hep 5 impeded binding and degradation of 125I-labelled bovine LPL by perfused rat livers. In contrast, hep 2 had no detectable effect on these processes. This demonstrates a difference between the sites in the liver that mediate binding, uptake and degradation of LPL, and the extrahepatic sites that bind functional LPL, and the hepatic sites that bind functional HL. After injection of 3.25 mg of hep 5/kg body weight, plasma LPL activity rapidly rose and then remained high for at least 1 h. With hep 2, plasma LPL also rose rapidly, but then decreased to almost basal by 1 h. When a labelled triacylglycerol emulsion was injected 1 h after the heparins, the fractional catabolic rate was enhanced in the rats that had received conventional heparin, as expected from the high plasma LPL activity, but decreased compared with controls in rats that had received hep 2, indicating that available LPL had been depleted through enhanced transport to and uptake in the liver.

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