Platelet activating factor inhibition reduces lung injury after cardiopulmonary bypass

Zehr, Kenton J.; Poston, Robert; Lee, Paul C.; Uthoff, K; Kumar, Pankaj; Cho, Peter W.; Gillinov, A. Marc; Redmond, John M.; Winkelstein, Jerry A.; Herskowitz, Ahvie; Cameron, Duke E.

doi:10.1016/0003-4975(94)00725-m

Cited by 41 publications

(13 citation statements)

References 36 publications

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“…PMN sequestration could also be caused by other endogenous mediators such as platelet-activating factor (PAF). PAF is a potent PMN priming agent and CPB has been shown to increase PAF up to 350% [26]. Another possibility is that endotoxin or inflammatory mediators released secondary to endotoxin exposure cause cytoskeletal changes in neutrophils that result in increased stiffness and a decreased PMN deformability [27].…”

Section: Discussionmentioning

confidence: 99%

Soluble Tumor Necrosis Factor Receptor Prevents Post-pump Syndrome

Carney

Lutz

Picone

et al. 1999

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Soluble Tumor Necrosis Factor Receptor Prevents Post-pump Syndrome

Carney

Lutz

Picone

et al. 1999

Journal of Surgical Research

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“…This is manifested by increased arterio‐venous oxygen difference, increased vascular resistance, leakage of fluid into the interstitial space, reduced pulmonary compliance (53, 78) and surfactant activity (79). Ischaemia/reperfusion injury, including washout of retained cells in the vascular bed during the bypass period and sequestered PMNs during the reperfusion period, is likely to be responsible for the tissue damage (80, 81). Only one study concerning paediatric cardiac surgery with CPB found any correlation between respiratory index and inflammatory markers (24), while other studies could not confirm this association (18, 20, 34, 82).…”

Section: Inflammatory Events At the Organ Levelmentioning

confidence: 99%

The systemic inflammatory response after cardiac surgery with cardiopulmonary bypass in children

Christensen¹

2001

Acta Anaesthesiol Scand

140

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Paediatric cardiac surgery often requires cardiopulmonary bypass (CPB) during the surgical intervention. CPB is known to elicit a systemic inflammatory response with activation of the complement and coagulation systems, stimulation of cytokine production, cellular entrapment in organs, neutrophil activation with degranulation, platelet activation, and endothelial dysfunction. These changes are associated with a risk of postoperative organ dysfunction and increased morbidity and mortality in the postoperative period. Clinical studies have concentrated on measurement of inflammatory markers and mediators in peripheral blood, where the systemic inflammatory response in the paediatric cardiac patient seems to be different from the adult case. Looking at the organ level, experimental studies have the advantage of providing information contributing to a better understanding of the pathological events that may lead to the deteriorated organ function. This review focuses on the systemic inflammatory response after cardiac surgery with CPB in children and experimental CPB models.

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“…There are several studies pertaining to the prevention of CPB-induced lung injury: elimination of leukocytes in bypass circuit by anti-leukocyte agents (mustine hydrochloride) or a leukocyte filter (7), prevention of leukocyte adhesion to pulmonary endothelium (8), addition of oxygen free radical scavengers (vitamin E, coenzyme Q, vitamin C, glutathione) (9), utilization of cyclooxygenase antagonists (indomethacin), thromboxane A1 synthetase antagonist (dazmegral) (10), platelet activation factor inhibitors (11), and steroid administration (12, 13). Although these methods may help to protect the pulmonary vascular bed to some extent, the clinical application of these agents is limited due to unproven safety and cost-effectiveness.…”

Section: Introductionmentioning

confidence: 99%

Aprotinin Attenuates the Elevation of Pulmonary Vascular Resistance After Cardiopulmonary Bypass

Yun

Rho

2006

J Korean Med Sci

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Pulmonary vascular resistance (PVR) is generally believed to be elevated after cardiopulmonary bypass (CPB) due to whole body inflammation. Aprotinin has an anti-inflammatory action, and it was hypothesized that aprotinin would attenuate the PVR increase induced by CPB. Ten mongrel dogs were placed under moderately hypothermic CPB for 2 hr. The experimental animals were divided into a control group (n=5, group I) and an aprotinin group (n=5, group II). In group II, aprotinin was administered during pre-bypass (50,000 KIU/kg) and post-bypass (10,000 KIU/kg) periods. Additional aprotinin (50,000 KIU/kg) was mixed in CPB priming solution. PVRs at pre-bypass and post-bypass 0, 1, 2, 3 hr were calculated, and lung tissue was obtained after the experiment. Post-bypass PVRs were significantly higher than prebypass levels in all animals (n=10, p<0.001). PVR elevation in group II was less than in group I at 3 hr post-bypass (p=0.0047). Water content of the lung was lower in group II (74±9.4%) compared to that of group I (83±9.5%), but the difference did not reach significance (p=0.076). Pathological examination showed a near normal lung structure in group II, whereas various inflammatory reactions were observed in group I. We concluded that aprotinin may attenuate CPB-induced PVR elevation through its anti-inflammatory effect.

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Platelet activating factor inhibition reduces lung injury after cardiopulmonary bypass

Cited by 41 publications

References 36 publications

Soluble Tumor Necrosis Factor Receptor Prevents Post-pump Syndrome

Soluble Tumor Necrosis Factor Receptor Prevents Post-pump Syndrome

The systemic inflammatory response after cardiac surgery with cardiopulmonary bypass in children

Aprotinin Attenuates the Elevation of Pulmonary Vascular Resistance After Cardiopulmonary Bypass

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