A Clinical Study of Blood Fibrin

Foster, D. P.

doi:10.1001/archinte.1924.00120030036005

Cited by 16 publications

(2 citation statements)

References 5 publications

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“…Pregnant women are widely regarded as predisposed to coagulation disorders for a variety of reasons (Kennan 1955, Mammen 1964, Scott 1968, and not least because of profound alterations occurring in the clotting system during normal pregnancy (Todd et al 1965). Of the factors affected, mention should be made here only of the progressive increase in plasma fibrinogen concentration (Gram 1921, 1922, Foster 1924, Ratnoff et al 1954, Gillman et al 1959) demonstrable from the early month of gestation well into the postnatal period, since hyperfibrinogenaemia has been considered as contributing importantly to the prevailing hypercoagulable state (Hardaway 1966).…”

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confidence: 99%

Fibrinogen Turnover in Pregnancy

Regoeczi

Hobbs

1969

Scandinavian Journal of Haematology

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15 turnover studies in 8 pregnant rhesus monkeys using iodine‐labelled fibrinogen showed that fractional catabolic rates of this protein were similar to those in control females, whereas the absolute catabolic rates were significantly elevated. Intermediate, non‐clottable labelled breakdown products of fibrinogen were present in the circulation of these monkeys. The implication of these findings are briefly discussed.

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confidence: 99%

Fibrinogen Turnover in Pregnancy

Regoeczi

Hobbs

1969

Scandinavian Journal of Haematology

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“…McLester (5) has attempted to utilize blood fibrin determinations as an index of liver function. Foster (6) made fibrin determinations in numerous clinical conditions. He found a marked elevation with the toxemia of pregnancy, the fibrin level running parallel with the severity of the symptoms.…”

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Blood Fibrin in Upper Gastrointestinal Tract Obstruction

Haden

Orr

1927

Journal of Experimental Medicine

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Foster and Whipple (1-4) have studied the blood fibrin in a number of experimental conditions. They have shown that fibrin is a very labile protein with wide fluctuations due to a variety of stimuli. The site of production is mainly the liver where there is a constant manufacture to supply the continuous utilization in the animal body. Injury to any tissue except the liver causes some increase in the fibrin content of the blood. If the liver is seriously injured a decrease is observed. With mild liver injury there is a rise instead of a fall.Dead or injured tissue and non-specific inflammation seem the only factors needed to excite an increased production, It seems quite probable also that any cell injury even without inflammatory reaction will cause this characteristic rise. McLester (5) has attempted to utilize blood fibrin determinations as an index of liver function. Foster (6) made fibrin determinations in numerous clinical conditions. He found a marked elevation with the toxemia of pregnancy, the fibrin level running parallel with the severity of the symptoms. With nephritis no increase was observed. Liver atrophy showed a very low value and lobar pneumonia a very high value.We have made a series of plasma fibrin determinations for comparison with data previously observed in the toxemia incident to upper gastrointestinal tract obstruction. Methods.All experiments were done on dogs. All operations were done under anesthesia with aseptic technique. The cardiac end of the stomach and pylorus were obstructed by ligation with tape. The jejunum was obstructed by severing the intestine and turning in the cut ends. The hematocrit reading was obtained by centrifuging 10 cc. of blood mixed with 2 cc. of 1.6 per cent sodium oxalate. The

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Studies in Epilepsy

Lennox¹,

Allen²

1928

Arch NeurPsych

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A Clinical Study of Blood Fibrin

Cited by 16 publications

References 5 publications

Fibrinogen Turnover in Pregnancy

Fibrinogen Turnover in Pregnancy

Blood Fibrin in Upper Gastrointestinal Tract Obstruction

Studies in Epilepsy

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