The effects of antenatal drug administration on aggregation of platelets of newborn infants

Corby, Donald G.; Schulman, Irving

doi:10.1016/s0022-3476(71)80122-1

Cited by 92 publications

(17 citation statements)

References 8 publications

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“…%led at day 15. her infant's platelet function and increase susceptibility to bleeding (7,14), cases 1 and 4 were included in the thriving EPT infants lower, the VIII antigen/activity ratio higher and platelets, factors because platelet function was not Part of this study and neither I1 and VII were no different than in group I infants. infant had clinical signs of bleeding.…”

Section: Resultsmentioning

confidence: 99%

Coagulation Studies in Extremely Premature Infants

Barnard¹,

Simmons²,

Hathaway³

1979

Pediatr Res

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SummaryEvidence of developmental evolution of coagulation can be seen when the studies of 10 thriving extremely premature (EPT) infants are compared to normal full-term (FT) infants. The prothrombin time, partial thromboplastin time, and thrombin time all became shorter with increasing gestational age. Fibrinogen levels and platelet counts appear to be comparable to term infant and adult levels. Fibrin degradation products (FDP) of 10 pg/ml or less were found in the thriving EPT infants. When compared to healthy fullterm infants, there is a definite gestational dependency of antithrombin 111 levels. Factors 11 and VII appear to be related to intrauterine maturation after the age of viability (24 wk), but factor VII-X complex does not. The contact factors XI, XII, high molecular weight kininogen (Fitzgerald factor), and prekallikrein (Fletcher factor) are all markedly decreased in thriving EPT infants. The mean factor V level is lower than that found in FT infants. This study confirms a gestational age dependency of factor VIlI activity. The ratio of factor VIlI antigen to factor VIlI clotting activity is increased (2.8 vs 1.01 in FT and adults). Thriving small for gestational age (SGA) infants had coagulation studies which were not statistically different from those of thriving EPT infants. The coagulation changes which occurred in severely ill EPT were mainly in the factors which decrease during intravascular coagulation (factors I, V, and VIII). The present study suggests that because of the high antigen to activity ratio seen in thriving EPT infants, a dysfunctional or fetal factor VlIl may have been produced. However, the further elevation of this ratio in the severely ill EPT infants is in keeping with a pathologic proteolysis or increased endothelial release of factor VIII antigen. SpeculationPrevention of and prompt therapeutic intervention for asphyxia, sepsis, hypovolemia, hypotension, hypothennia, hypoxia, and acidosis may prevent the occurrence of the coagulation changes seen in the severely ill EPT infants. A distinction between abnormal proteolysis versus production of dysfunctional proteins is essential before specific therapies can be designed.

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Section: Resultsmentioning

confidence: 99%

Coagulation Studies in Extremely Premature Infants

Barnard¹,

Simmons²,

Hathaway³

1979

Pediatr Res

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“…6 ADP : Adenosine diphosphate. 6 ATP: Adenosine triphosphate. ported here is contingent on the long term effect of unbound unconjugated bilirubin on platelets.…”

Section: Discussionmentioning

confidence: 99%

“…However, Rozdilsky's observation [32,33] that bilirubin infusion in animals causes a hemorrhagic diathesis suggests that these platelet changes may be of clinical importance. Since a variety of clinical factors {e.g., drugs [6,23] and liver disease [19]) may influence platelet functions in jaundiced patients, any conclusions drawn from clinical studies regarding the action of bilirubin on platelets must be made cautiously. Further clarification of its in vitro action is required.…”

Section: Introductionmentioning

confidence: 99%

Influence of Bilirubin on Human Platelets

Maurer

Caul

1972

Pediatr Res

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“…The abnormalities of neonatal platelet function are less completely understood. In the mid-1970s, differences in the in vitro responses of cord and newborn platelets compared to those from older subjects were identified (3)(4)(5)(6). These abnormalities include a decreased aggregation response to certain agonists including ADP, epinephrine and collagen (3, 4), and decreased secretion of dense granule contents (5,6).…”

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confidence: 99%

Deficient Collagen-Induced Activation in the Newborn Platelet

1990

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ABSTRACT. We have investigated the impaired secretion response of neonatal platelets. We compared the response of washed neonatal and adult platelets to thrombin and collagen, and to specific activators of calcium flux (inositol trisphosphate) and protein kinase C activation (oleoylacetyl glycerol). Neonatal platelets show no impairment ofaggregation, secretion of ['4C]serotonin or phosphorylation of saecific intracellular rotei ins in resDonse to thrombin. inositol trisphosphate, o; oleoyl-acetyl glycerol. ow ever; neonatal platelets have a markedly decreased response to collagen. To further evaluate this deficient response, we examined specific aspects of the collagen activation pathway. Collagen-platelet interaction as measured by adhesion of platelets to collagen-coated dishes showed no difference in adhesion of neonatal platelets compared to adult controls (20.1 f 11.6 versus 18.6 2 9.3%). The presence of GPIa/ Ila, a Mgz+-dependent collagen receptor, was evaluated by flow cytometric analysis of binding of fluorescein-tagged monoclonal antibody, 6F1 (directed against GPIaJIIa). There was no difference either in the percent of platelets that bound antibody (80 versus 81%) or in the mean fluorescence intensity of the adult and neonatal samples. Phosphoinositide hydrolysis was decreased in neonatal platelets in response to collagen but normal in response to thrombin. Neonatal platelets released more arachidonic acid than adult platelets in response to thrombin (29.5 f 3.2 versus 19.6 + 1.8%) but less than adult platelets in response to 10 pg/mL collagen (3.2 2 1.1 versus 9.3 + 3.0%). Thromboxane B2 production was also decreased in response to collagen (52.7 f 12.6 versus 101.4 + 18.7 ng/mL). These results suggest that the deficient collagen response in neonatal platelets may lie in transduction of the collagen signal to phospholipases Az and C . (Pediatr Res 27: 337-343,1990) Abbreviations AA, arachidonic acid IP3, inositol-1,4,5-trisphosphate OAG, oleoyl-acetyl glycerol PIPZ, phosphatidylinositol-4,5-bisphosphate MLC, myosin light chain 47 K, 47000 dalton protein TxAZ, thromboxane A2 TxBz, thromboxane Bz HBSS, Hanks' balanced salt solution clinical importance to those caring for sick and premature infants. The differences in clotting factor activity and fibrinolytic enzymes between cord blood and that of adult controls are well established (1,2). The abnormalities of neonatal platelet function are less completely understood. In the mid-1970s, differences in the in vitro responses of cord and newborn platelets compared to those from older subjects were identified (3-6). These abnormalities include a decreased aggregation response to certain agonists including ADP, epinephrine and collagen (3, 4), and decreased secretion of dense granule contents (5, 6). Neonatal platelets were shown to have decreased endogenous stores of dense granule contents, ADP, and serotonin, although Whaun demonstrated that their uptake and storage of radiolabeled serotonin was as effective as that of adult platelets (6). In addition,...

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The effects of antenatal drug administration on aggregation of platelets of newborn infants

Cited by 92 publications

References 8 publications

Coagulation Studies in Extremely Premature Infants

Coagulation Studies in Extremely Premature Infants

Influence of Bilirubin on Human Platelets

Deficient Collagen-Induced Activation in the Newborn Platelet

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