Activation of the Kallikrein‐kinin System in Premature Infants With Respiratory Distress Syndrome (Rds)

Saugstad, Ola Didrik; Harvie, Ann; Langslet, A

doi:10.1111/j.1651-2227.1982.tb09557.x

Cited by 12 publications

(9 citation statements)

References 9 publications

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“…These data are basically in accordance with our previous findings (6). During the first day of life, mean plasma prekallikrein in both groups of RDS patients was 63% of the values found in premature control patients without RDS.…”

Section: Discussionsupporting

confidence: 82%

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Activation of the Plasma Kallikrein-Kinin System in Respiratory Distress Syndrome

et al. 1992

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Section: Discussionsupporting

confidence: 82%

“…We have previously shown that preterm babies with RDS have low plasma prekallikrein and kallikrein inhibition levels, indicating that the plasma kallikrein-kinin system might be activated in this condition (6).…”

Section: Abbreviationsmentioning

confidence: 99%

Activation of the Plasma Kallikrein-Kinin System in Respiratory Distress Syndrome

et al. 1992

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“…HMD occurs as a consequence of the relative inability of the immature lung to synthesise surfactant in amounts sufficient for neonatal respiratory adaptation [11]. However, this is not the only pathogenic factor, as other mechanisms might also be involved [25,29].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of complement activation in premature newborn infants with hyaline membrane disease

et al. 1993

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Fifteen premature newborns with hyaline membrane disease causing acute respiratory distress were evaluated for complement activation. A high intrapulmonary right-to-left shunt and marked arterial-alveolar oxygen difference indicated the severity of the respiratory failure. Twenty preterm healthy infants served as controls. Total haemolytic activity, plasma concentrations of complement components and regulatory proteins (C3, C4, C1-inhibitor, factors H and I) as well as activation products (C3a, C3dg, C1rsC1-inhibitor, C3b(Bb)P) gave no evidence of significant complement activation. Functional activity of the ubiquitous regulatory protein C1-inhibitor was significantly reduced without impact on classical pathway activation. These data suggest that, in contrast to the adult form of respiratory distress syndrome, the low-pressure pulmonary oedema characterising hyaline membrane disease is not mediated by activation of the complement system.

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“…Timeplasma concentrations of the main kallikrein antiprotease dependent studies in preterm infants with mild, moder-C, esterase (22)-In plasma the IRDS infants, ate, and severe IRDS on the activation of clotting, fibrihowever, we have found higher kallikrein activity and nolysis, and kinin-kallikrein in plasma and its relation to lower PKKI than in plasma the reference the inflammatory process in the lung (38,39) will further indicating activation of the kinin-kallikrein system in the elucidate the role of this activation process in the patho-IRDS group, which is in agreement with findings of genesis of IRDS. Saugstad et al (23,24). Activation of the kinin-kallikrein system results in the formation of bradykinin (25,26).…”

Section: Discussionmentioning

confidence: 99%

Activation of the Plasma Clotting, Fibrinolytic, and Kinin-Kallikrein System in Preterm Infants with Severe Idiopathic Respiratory Distress Syndrome

Brus

Vanoeveren²,

Okken

et al. 1994

Pediatr Res

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We studied the activation pattern of clotting, fibrinolysis, and kinin-kallikrein during the first 5 d of life in 10 preterm infants with signs of severe idiopathic respiratory distress syndrome (IRDS) after birth (IRDS group) and in 12 healthy preterm infants (reference group). We found systemic activation of clotting, fibrinolysis, and kininkallikrein in the IRDS infants within 12 to 24 h of birth, represented by increased median thrombin-antithrombin I11 complex formation (90 ng/mL versus 10 ng/mL in the reference group, p < 0.05), increased mean tissue-type plasminogen activator plasma concentrations (11.8 ng/mL versus 3.5 ng/mL in the reference group, p < 0.05), and increased mean plasma kallikrein activity (182.6% versus 162.0% of maximal activated human plasma in the reference group,p < 0.05), respectively. Clotting activation was accompanied by a significant decrease of the platelet count. Clotting and fibrinolytic activity decreased in the IRDS group during the first 2 to 3 d of life. Kinin-kallikrein activation was accompanied by decreased plasma kallikrein inhibitor activity values and did not change throughout the study period. Plasma factor XI1 activity was not significantly increased in the IRDS infants during the first 2 d of life but did significantly increase thereafter. The cause of simultaneous activation of clotting, fibrinolysis, and kinin-kallikrein in our IRDS infants has not yet been clarified. However, this activation process may contribute to lung injury such as that described in the adult respiratory distress syndrome.(Pediatr Res 36: 647-653, 1994) Abbreviations IRDS, idiopathic respiratory distress syndrome CPP, cryoglobulin poor plasma AT 111, antithrombin 111 T-AT 111, thrombin-antithrombin I11 F XIIa, factor XI1 activity t-PA, tissue-type plasminogen activator PKKI, plasma kallikrein inhibitor activity % AHP, percentage of maximal activated human plasma % NHP, percentage of normal human plasma Intraalveolar and intravascular deposition of fibrin has been found in preterm infants suffering from IRDS (1, 2). These fibrin depositions are likely to contribute to respiratory insufficiency. Intraalveolar fibrin, a major component of hyaline membranes, inactivates considerable amounts of surfactant (1-3). Intravascular fibrin, found at autopsy in the lungs of preterm infants who died of severe IRDS, decreases surfactant synthesis due to impaired lung perfusion (1, 2). These intraalveolar and intravascular fibrin depositions are the result of activation of the clotting system represented

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Activation of the Kallikrein‐kinin System in Premature Infants With Respiratory Distress Syndrome (Rds)

Cited by 12 publications

References 9 publications

Activation of the Plasma Kallikrein-Kinin System in Respiratory Distress Syndrome

Activation of the Plasma Kallikrein-Kinin System in Respiratory Distress Syndrome

Evaluation of complement activation in premature newborn infants with hyaline membrane disease

Activation of the Plasma Clotting, Fibrinolytic, and Kinin-Kallikrein System in Preterm Infants with Severe Idiopathic Respiratory Distress Syndrome

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