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

Saugstad, Ola Didrik; Buø, Laila; Johansen, Harald Thidemann; Røise, Olav; Aasen, Ansgar O.

doi:10.1203/00006450-199210000-00012

Cited by 22 publications

(10 citation statements)

References 20 publications

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“…PMNs appear to be the only blood cells that can efficiently cleave CTAP-III into NAP-2, thereby generating their own activator [34]. Our investigations, thus, link the haemostatic and the inflammatory process and resemble the situation that may be found during lung failure [35][36][37], and during surfactant therapy associated complications such as pulmonary haemorrhage. A study suggesting an increased incidence of this complication in preterm infants following endotracheal administration of a synthetic preparation (Exosurf®) [38] would support this assumption.…”

Section: Discussionmentioning

confidence: 65%

In vitro modulation of induced neutrophil activation by different surfactant preparations

Tegtmeyer¹,

Gortner²,

Ludwig³

et al. 1996

Eur Respir J

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Section: Discussionmentioning

confidence: 65%

In vitro modulation of induced neutrophil activation by different surfactant preparations

Tegtmeyer¹,

Gortner²,

Ludwig³

et al. 1996

Eur Respir J

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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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“…Thrombus formation may occur at many levels; recently, intracardiac thrombi have been increasingly observed 15–17 . However, data on neonatal intracardiac thrombosis are limited to case reports.…”

Section: Discussionmentioning

confidence: 99%

Association of Prothrombin Gene Mutation with Sepsis in a Preterm with Multiple Intracardiac Thrombi

et al. 2005

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We report for the first time, a premature infant with multiple intracardiac thrombi and sepsis, who was heterozygous for the G20210A prothrombin gene variant. Anticoagulant treatment with low molecular weight heparin resulted in the complete disappearance of the thrombi. It may be suggested that prothrombin gene variant associated with sepsis, respiratory distress syndrome, and perinatal asphyxia, as well as other thrombophilic disorders, could be a risk factor for the development of neonatal thrombus.

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

Cited by 22 publications

References 20 publications

In vitro modulation of induced neutrophil activation by different surfactant preparations

In vitro modulation of induced neutrophil activation by different surfactant preparations

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

Association of Prothrombin Gene Mutation with Sepsis in a Preterm with Multiple Intracardiac Thrombi

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