Modulation of tissue fibrinolysis from hypoxia and hyperoxia

Risberg, Bo; Stenberg, Björn

doi:10.1016/0049-3848(85)90055-6

Cited by 18 publications

(5 citation statements)

References 17 publications

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“…The rabbits exposed to hypoxia appear to correspond to this more mildly affected group of thrombocytopenic infants as they did not exhibit evidence of coagulopathy and their platelet count was stable. The exact mechanism(s) responsible for the increased platelet turnover in the hypoxic rabbits remains unclear, however, the possibilities also include elevated platelet associated IgG or activation of the fibrinolytic system (1,(24)(25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Hypoxia on Platelet Survival and Site of Sequestration in the Newborn Rabbit

et al. 1988

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SummaryThrombocytopenia occurs frequently in sick neonates that have experienced perinatal asphyxia. This study investigated the effect of one component of asphyxia, hypoxia, on platelet life-span and site of sequestration. 11 indium oxine platelet survivals with scintigraphic imaging were performed in newborn and adult rabbits exposed to room air (normoxia) or following exposure to a 15 minute, severe hypoxic insult (FjOa = 0.05). Platelet survivals in normoxic adults (n = 27) and newborn rabbits (n = 11) were similar (60 ± 3.9 hr vs 64 ± 8.0 hr, m ± SEM). Inhalation of 5% oxygen for 15 minutes was not associated with an acidemia and did not produce thrombocytopenia but significantly shortened the platelet survival to 34 ± 3 hr in the adult (n = 18) and 38 ± 3 hr in the newborn rabbit (n = 7). Postmortem measurement of the sites of mIn-platelet accumulation showed that under normoxic conditions the platelets accumulated in the liver and spleen (23 ±4.3% and 8 ± 1.0% of the total body counts) in the adult with even greater accumulation in the liver (58 ± 6.8%) and spleen (19 ± 4.9%) of the newborn (p <0.001). The latter observation was likely due to the relatively increased size of the liver and spleen in the newborn compared to the adult. Hypoxia did not alter the site of platelet sequestration in adults or newborns. Our results suggest that the newborn has the same platelet survival as the adult and that acute, severe hypoxia significantly shortens the survival of platelets in both groups. Although the sites of sequestration are qualitatively the same in the newborn, there is greater sequestration in the liver and spleen when compared to the adult.

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Section: Discussionmentioning

confidence: 99%

The Effect of Hypoxia on Platelet Survival and Site of Sequestration in the Newborn Rabbit

et al. 1988

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“…We therefore studied the effects of acute high‐dose and sustained low‐dose endotoxemia on arterial levels of tPA as well as pulmonary, mesenteric and hepatic tPA fluxes in pigs. All animals were fluid‐resuscitated to maintain a normodynamic circulation, because the cardiovascular response to endotoxemia can influence the release of tPA through changes in the plasma levels of adrenergic vasoconstrictors (7), endothelial shear forces (8) and oxygenation (9).…”

mentioning

confidence: 99%

Time‐ and dose‐related regional fluxes of tissue‐type plasminogen activator in anesthetized endotoxemic pigs

Nyberg

Jakob

Seeman-Lodding

et al. 2007

Acta Anaesthesiol Scand

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“…Increase of fibrin Increase levels of plasminogen activator inhibitor Induction of local inflammatory response Hypoxia and reactive oxygen species (ROS) release leading to inflammation and activation of coagulation cascade Surgical hypoxia may decrease fibrinolysis [16,23,[26][27][28][30][31][32][33][34] Extracellular Matrix Components Fibronectin, hyaluronic acid, glycosaminoglycans, proteoglycans Matrix for proliferation of cellular components Secreted by fibroblasts [35,36] Cellular Mediators [37,38]…”

Section: Surgical Traumamentioning

confidence: 99%

Prevention of Post-Operative Adhesions: A Comprehensive Review of Present and Emerging Strategies

et al. 2021

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Post-operative adhesions affect patients undergoing all types of surgeries. They are associated with serious complications, including higher risk of morbidity and mortality. Given increased hospitalization, longer operative times, and longer length of hospital stay, post-surgical adhesions also pose a great financial burden. Although our knowledge of some of the underlying mechanisms driving adhesion formation has significantly improved over the past two decades, literature has yet to fully explain the pathogenesis and etiology of post-surgical adhesions. As a result, finding an ideal preventative strategy and leveraging appropriate tissue engineering strategies has proven to be difficult. Different products have been developed and enjoyed various levels of success along the translational tissue engineering research spectrum, but their clinical translation has been limited. Herein, we comprehensively review the agents and products that have been developed to mitigate post-operative adhesion formation. We also assess emerging strategies that aid in facilitating precision and personalized medicine to improve outcomes for patients and our healthcare system.

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Modulation of tissue fibrinolysis from hypoxia and hyperoxia

Cited by 18 publications

References 17 publications

The Effect of Hypoxia on Platelet Survival and Site of Sequestration in the Newborn Rabbit

The Effect of Hypoxia on Platelet Survival and Site of Sequestration in the Newborn Rabbit

Time‐ and dose‐related regional fluxes of tissue‐type plasminogen activator in anesthetized endotoxemic pigs

Prevention of Post-Operative Adhesions: A Comprehensive Review of Present and Emerging Strategies

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