The Plasminogen-Plasmin System of Newborn Infants

Quie, Paul G.; Wannamaker, Lewis W.

doi:10.1001/archpedi.1960.04020040838005

Cited by 38 publications

(11 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This, together with the observation that low levels of plasminogen persist until the age of 6 months [17], suggests that decreased plasminogen synthesis is the primary mechanism responsible for the significantly lower levels of plasminogen observed in the newborns. Since our methods of collection included the addition of trasylol as an antifibrinolytic agent and immediate processing of the samples, the effect, if any, of in vitro fibrinolysis was minimized.…”

Section: Discussionmentioning

confidence: 91%

“…The inhibitors' levels have been reported to roughly parallel the plasminogen levels in newborns and adults [17], and it also appears that inhibitor levels are lower in the newborn group compared to normal adults. In our study utilizing synthetic substrate-based methods, we demonstrate a slight, but not significant, reduction in a2-AP for the newborn group compared to normal adults in the maternal group.…”

Section: Discussionmentioning

confidence: 92%

See 1 more Smart Citation

Neonatal and maternal fibrinolysis: Activation at time of birth

Suárez¹,

Walenga²,

Mangogna³

et al. 1985

American J Hematol

View full text Add to dashboard Cite

Utilizing chromogenic synthetic substrate-based methods, determination of the plasma concentration of plasminogen, alpha 2-antiplasmin, alpha 2-macroglobulin, and B beta 15-42-related peptides were made at the time of birth in both newborns and mothers. Plasminogen levels were increased in the maternal group (150 +/- 26%), and markedly decreased in the newborn group (67 +/- 14%). The major inhibitors of fibrinolysis, alpha 2-antiplasmin and alpha 2-macroglobulin, were within normal range in both groups. Determination of B beta 15-42-related peptide showed markedly increased levels in the maternal group above control values (115 +/- 102, normal 29 +/- 12); the newborn group showed values only mildly elevated above control values (39 +/- 21). The results demonstrate increased fibrinolytic activity in both groups, though the degree of activation is significantly higher in the maternal group, as reflected by the higher levels of B beta 15-42-related peptides. Fibrinopeptide A levels confirm an activation of coagulation in both maternal and newborn groups (22 +/- 4 ng/ml and 138 +/- 22 ng/ml, respectively) with a significantly increased level in newborns (2-5 ng/ml normal).

show abstract

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 92%

Neonatal and maternal fibrinolysis: Activation at time of birth

Suárez¹,

Walenga²,

Mangogna³

et al. 1985

American J Hematol

View full text Add to dashboard Cite

show abstract

“…Plasminogen was shown to be present in 10.5 week embryo (6), and blood level in creased gradually, reaching the level about 50 % less than adult level soon after the birth (7,8), and reached the adult level in 13 weeks (9). As shown later, plasma plasminogen level does not change much with age (10)(11)(12), although the fibrinolytic activity was shown to decrease in the aged.…”

Section: Variations Due To Age Sex and Racementioning

confidence: 82%

Physiology of Plasminogen: With Special Reference to Activation and Degradation

Takada

Takada²

1988

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

Plasminogen is said to be synthesized in many organs, but the major source of its production is considered to be the liver. The production of plasminogen is observed in fetal life, but its plasma level is low in new born infants, rising rapidly to attain adult levels in about 13 weeks. The plasma levels do not change much with age. Although the fibrinolytic enzyme system is influenced by many factors such as hormones, exercise, emotion, age, sex, nutritional states etc., the plasma levels of plasminogen are relatively stable. In this presentation we would like to discuss three important subjects related to the physiology of plasminogen. The first subject is the activation pathway of the native form of plasminogen (Glu-plg) by various activators in the plasma or clotted plasma. Glu-plg was not easily activated by activators such as urokinase (UK) or tissue plasminogen activator (t-PA), but activated very easily in the presence of fibrin clot. In the presence of purified clot, Glu-plg was partly activated by activators to Glu-plasmin, but also converted to Lys-plg by preformed plasmin, subsequently being activated to plasmin. Glu-plg I (containing two carbohydrate chains) changed conformation more easily upon interaction with fibrin than Glu-plg II (containing one carbohydrate chain) and Glu-plg I was also more easily activated by activators than Glu-plg II. Although Glu-plg was hardly activated by activators in the plasma, Glu-plg was activated easily in the presence of plasma clot. Results of immunoblotting experiments indicated that Glu-plg was mainly activated by activators directly to plasmin, not via Lys-plg in contrast to purified systems. The second subject is the degradation of plasminogen by elastase. Plasminogen may be degraded by proteolytic enzymes such as cathepsin or elastase. The degradation of plasminogen by elastase is shown to give rise to K1 to K3, K4, and mini-pig (containing K5). We have shown that the degradation rate to Glu-plg by elastase increased in the presence of tranexamic acid, indicating that the conformational change of Glu-plg in the presence of tranexamic acid resulted in the exposure of the hydrophobic regions connecting K3, K4 and K5, thus making them accessible to elastase. Consequently, Lys-plg or conformationally altered Glu-plg (possibly bound to fibrin or FDP) is more easily degraded in vivo. The last subject is relationship between plasma plasminogen levels and fibrinolytic activity in various ages. Although plasma plasminogen levels do not change with age, the fibrinolytic activity lowers. We found that t-PA antigen levels increased, PA inhibitor levels decreased, and PA activity decreased with age. These results suggest that the major factor influencing the activity of fibrinolytic system is not plasminogen but other components such as PA, PA inhibitors or inhibitors of plasmin.

show abstract

“…Since that time the reports on the lytic system of the newborn have been conflicting. Some [11,27,30,32,43] reported increased fibrinolytic activity of cord blood; others [66,80] reported decreased fibrinolytic activity. Boyd [19] also suggested decreased lytic activity of the fetus, and Zilliacus [117] stated that the lytic activity decreases with aging of the fetus.…”

Section: Discussionmentioning

confidence: 99%

Placental Transfer of Intravascular Coagulation between Mother and Fetus

et al. 1971

View full text Add to dashboard Cite

ExtractPregnant sheep of 110-140 days' gestation were used to determine the effect of intravascular coagulation in the mother upon her fetus and the effect of intravascular coagulation in the fetus upon its mother. Because fetal lambs can be delivered and left attached to the mothers via the umbilical cord without placental separation, coagulation studies on a mother and her corresponding fetus could be done simultaneously. When intravascular coagulation was induced in the mothers by administering thromboplastin infusions intravenously, the attached fetal lambs also developed intravascular coagulation with decreased levels in platelets, fibrinogen, and factor V, and prolongation of prothrombin, thrombin, and partial thromboplastin times. When intravascular coagulation was induced in fetal lambs, the dam had a drop in platelet count, a minimal drop in fibrinogen levels, and the appearance of fibrin breakdown products in serum and urine.The factor or factors that crossed the placenta initiating this transfer of coagulation abnormalities are not known. It has been demonstrated that the transfer was not due to fibrin or fibrinogen breakdown products, nor to the infused thromboplastin, and that the trauma of surgery or hypoxia did not contribute to the coagulation abnormalities. The mothers consistently developed fibrin breakdown products in the serum and urine when intravascular coagulation was induced. This was in contrast to the results observed in fetal lambs, which, with one exception, did not show evidence of fibrin breakdown products in serum or urine under identical experimental conditions. These observations suggest the fibrinolytic system of the fetus is inefficient compared with that of the adult; this could be a considerable disadvantage in the presence of intravascular coagulation. SpeculationAs a result of intravascular coagulation in the mother or the fetus a stimulus is produced on the opposite side of the placental barrier resulting in similar changes in the placental partner. This mechanism may be of significance in the etiology of fetal death in eclampsia. Introductionplacentae [4,7,29,33,39,53,69,72,76,82,87,98,111], amniotic fluid embolism [53,68,83,86,88,99, Defects in hemostasis have been described in women 102], retention of a dead fetus [36, 53, 67, 68, 70, 71, with toxemia of pregnancy with preeclampsia or 73, 89, 99, 109, 113], and sepsis [53,68,99]. The eclampsia [28,45,54,68,74,75,94,99], abruptio pathogenesis of coagulation abnormalities has been

show abstract

The Plasminogen-Plasmin System of Newborn Infants

Cited by 38 publications

References 19 publications

Neonatal and maternal fibrinolysis: Activation at time of birth

Neonatal and maternal fibrinolysis: Activation at time of birth

Physiology of Plasminogen: With Special Reference to Activation and Degradation

Placental Transfer of Intravascular Coagulation between Mother and Fetus

Contact Info

Product

Resources

About