scholarly journals Never Change a Flowing System? The Effects of Retrograde Flow on Isolated Perfused Lungs and Vessels

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1210
Author(s):  
Hanif Krabbe ◽  
Sergej Klassen ◽  
Johannes Bleidorn ◽  
Michael J. Jacobs ◽  
Julia Krabbe ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Perfusion Pressure ◽  
Lavage Fluid ◽  
Flow Reversal ◽  
Edema Formation ◽  
Retrograde Perfusion ◽  
Cytokine Levels ◽  
Sense And Respond ◽  
Flowing System

Retrograde perfusion may occur during disease, surgery or extracorporeal circulation. While it is clear that endothelial cells sense and respond to changes in blood flow, the consequences of retrograde perfusion are only poorly defined. Similar to shear stress or disturbed flow, retrograde perfusion might result in vasomotor responses, edema formation or inflammation in and around vessels. In this study we investigated in rats the effects of retrograde perfusion in isolated systemic vessels (IPV) and in pulmonary vessels of isolated perfused lungs (IPL). Anterograde and retrograde perfusion was performed for 480 min in IPV and for 180 min in the IPL. Perfusion pressure, cytokine levels in perfusate and bronchoalveolar lavage fluid (BALF), edema formation and mRNA expression were studied. In IPV, an increased perfusion pressure and initially also increased cytokine levels were observed during retrograde perfusion. In the IPL, increased edema formation occurred, while cytokine levels were not increased, though dilution of cytokines in BALF due to pulmonary edema cannot be excluded. In conclusion, effects of flow reversal were visible immediately after initiation of retrograde perfusion. Pulmonary edema formation was the only effect of the 3 h retrograde perfusion. Therefore, further research should focus on identification of possible long-term complications of flow reversal.

scholarly journals Selective inhibition of COX-2 improves early survival in murine endotoxemia but not in bacterial peritonitis

2001 ◽  
Vol 281 (3) ◽  
pp. L537-L543 ◽  
Author(s):  
Raju C. Reddy ◽  
Gina H. Chen ◽  
Kazuhiro Tateda ◽  
Wan C. Tsai ◽  
Susan M. Phare ◽  
...  
Keyword(s):  
Cecal Ligation ◽  
Selective Inhibition ◽  
Lavage Fluid ◽  
Neutrophil Sequestration ◽  
Bacterial Peritonitis ◽  
Cytokine Levels ◽  
Cox 2 ◽  
And Control ◽  
Late Survival

Prostaglandins of the E series are believed to act as important mediators of several pathophysiological events that occur in sepsis. Studies were performed to evaluate the effect of cyclooxygenase (COX)-2-specific inhibition on the outcome in murine endotoxemia and cecal ligation and puncture (CLP). We observed a significant time-dependent upregulation of PGE2production in both blood and lung homogenates of mice administered lipopolysaccharide intraperitoneally, which was nearly completely suppressed by the administration of the COX-2 inhibitor NS-398. Treatment with NS-398 significantly improved early but not late survival in lipopolysaccharide-challenged mice. On the contrary, elevated PGE2levels were found in bronchoalveolar lavage fluid but not in plasma of mice subjected to CLP (21 gauge). Pretreatment with NS-398 failed to significantly improve survival in CLP mice. No significant differences were noted in plasma or lung homogenate proinflammatory cytokine levels or lung neutrophil sequestration between the NS-398-treated and control groups. These results demonstrate that selective COX-2 inhibition confers early but not long-term benefits without affecting the expression of proinflammatory cytokines or the development of lung inflammation.

scholarly journals Role and Regulation of Adipokines during Zymosan-Induced Peritoneal Inflammation in Mice

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4080-4085 ◽  
Author(s):  
Maria Pini ◽  
Melissa E. Gove ◽  
Joseph A. Sennello ◽  
Jantine W. P. M. van Baal ◽  
Lawrence Chan ◽  
...  
Keyword(s):  
Inflammatory Infiltrate ◽  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Wild Type ◽  
Cellular Infiltrate ◽  
Peritoneal Lavage Fluid ◽  
Peritoneal Inflammation ◽  
Leptin Deficiency ◽  
Cytokine Levels

Adipokines, cytokines mainly produced by adipocytes, are active participants in the regulation of inflammation. Administration of zymosan (ZY) was used to investigate the regulation and role of adipokines during peritonitis in mice. Injection of ZY led to a significant increase in leptin levels in both serum and peritoneal lavage fluid, whereas a differential trend in local vs. systemic levels was observed for both resistin and adiponectin. The role of leptin in ZY-induced peritonitis was investigated using leptin-deficient ob/ob mice, with and without reconstitution with exogenous leptin. Leptin deficiency was associated with delayed resolution of peritoneal inflammation induced by ZY, because ob/ob mice had a more pronounced cellular infiltrate in the peritoneum as well as higher and prolonged local and systemic levels of IL-6, TNFα, IL-10, and chemokine (C-X-C motif) ligand 2 compared with wild-type mice. Reconstitution with exogenous leptin exacerbated the inflammatory infiltrate and systemic IL-6 levels in ob/ob mice while inhibiting production of TNFα, IL-10, and chemokine (C-X-C motif) ligand 2. In contrast with the important role of leptin in regulating each aspect of ZY-induced peritonitis, adiponectin deficiency was associated only with a decreased inflammatory infiltrate, without affecting cytokine levels. These findings point to a complex role for adipokines in ZY-induced peritonitis and further emphasize the interplay between obesity and inflammation.

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

scholarly journals Long-Term Survival and Quality of Life After Transfusion-Associated Pulmonary Edema in Critically III Medical Patients

CHEST Journal ◽  
2010 ◽  
Vol 137 (4) ◽  
pp. 783-789 ◽  
Author(s):  
Guangxi Li ◽  
Marija Kojicic ◽  
Martin K. Reriani ◽  
Evans R. Fernández Pérez ◽  
Lokendra Thakur ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Pulmonary Edema ◽  
Medical Patients ◽  
Term Survival ◽  
Long Term Survival

Acute and specific collagen type I degradation increases diastolic and developed tension in perfused rat papillary muscle

2004 ◽  
Vol 286 (3) ◽  
pp. H889-H894 ◽  
Author(s):  
Regis R. Lamberts ◽  
Maurice J. J. M. F. Willemsen ◽  
Néstor G. Pérez ◽  
Pieter Sipkema ◽  
Nico Westerhof
Keyword(s):  
Papillary Muscle ◽  
Collagen Type ◽  
Perfusion Pressure ◽  
Collagen Type I ◽  
Type I ◽  
Collagenase Treatment ◽  
Before And After ◽  
Diastolic Coronary Flow ◽  
Rat Papillary Muscle

Collagen degradation is suggested to be responsible for long-term contractile dysfunction in different cardiomyopathies, but the effects of acute and specific collagen type I removal (main type in the heart muscle) on tension have not been studied. We determined the diastolic and developed tension length relations in isometric contracting perfused rat papillary muscles (perfusion pressure 60 cmH2O) before and after acute and specific removal of small collagen struts with the use of purified collagenase type I. At 95% of the maximal length (95% Lmax), diastolic tension increased 20.4 ± 8.1% ( P < 0.05, n = 6) and developed tension increased 15.0 ± 6.7% after collagenase treatment compared with time controls. Treatment increased the diastolic muscle diameter by 7.1 ± 3.4% at 95% Lmax, whereas the change in diameter due to contraction was not changed. Diastolic coronary flow and normalized coronary arterial flow impediment did not change after collagenase treatment. Electron microscopy revealed that the number of small collagen struts, interconnecting myocytes, and capillaries was reduced to ∼32% after treatment. We conclude that removal of the small collagen struts by acute and specific collagen type I degradation increases diastolic and developed tension in perfused papillary muscle. We suggest that diastolic tension is increased due to edema, whereas developed tension is increased because the removal of the struts poses a lower lateral load on the cardiac myocytes, allowing more myocyte thickening.

Management of the Extubation Problem in the Premature Child

1980 ◽  
Vol 89 (6) ◽  
pp. 508-511 ◽  
Author(s):  
Robin T. Cotton ◽  
Allan B. Seid
Keyword(s):  
Endotracheal Tube ◽  
Ventilatory Support ◽  
Disease Process ◽  
Upper Respiratory Tract ◽  
Endoscopic Evaluation ◽  
Newborn Period ◽  
Edema Formation ◽  
Premature Child ◽  
Upper Respiratory

Long-term endotracheal intubation is a widely established means of giving ventilatory support in the newborn period. Though such long-term intubation is well tolerated by the premature infant, laryngeal complications do occur and extubation may be impossible even though the initial disease process for which the intubation was performed has resolved. In such a situation, careful endoscopic evaluation of the upper respiratory tract is advocated to identify the site of the problem. If subglottic edema or mucosal ulceration in the subglottic area is the site of the damage and if, during endoscopic evaluation immediately following removal of the endotracheal tube, the subglottic area starts to narrow because of edema formation or edema fluid filling up compressed granulation tissue, then a split of the cricoid in the midline anteriorly, leaving the endotracheal tube in as a stent, appears to be a preferable alternative to performing a tracheotomy. Of 12 consecutive patients, 9 have been successfully extubated.

scholarly journals Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

2019 ◽  
Vol 71 (2) ◽  
pp. 339-346
Author(s):  
Jing Liu ◽  
Yidong Mao
Keyword(s):  
Oxidative Stress ◽  
Concanavalin A ◽  
Hepatoprotective Activity ◽  
Antioxidant Enzyme Activities ◽  
Mitochondrial Oxidative Stress ◽  
Immune Mediated ◽  
Wide Range ◽  
Cytokine Levels ◽  
Glucose 6 Phosphate Dehydrogenase

Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

scholarly journals Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammed M. Almutairi ◽  
Farzane Sivandzade ◽  
Thamer H. Albekairi ◽  
Faleh Alqahtani ◽  
Luca Cucullo
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Immune Cell ◽  
Clinical Manifestations ◽  
Cell Infiltration ◽  
Cellular Mechanisms ◽  
Cytokine Levels

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.

Alpha-thrombin-induced pulmonary vasoconstriction

1987 ◽  
Vol 63 (5) ◽  
pp. 1993-2000 ◽  
Author(s):  
M. J. Horgan ◽  
J. W. Fenton ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Base Line ◽  
Thrombin Injection ◽  
Weight Changes ◽  
Lung Weight ◽  
Edema Formation ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Hemodynamic ◽  
Proteolytic Site ◽  
Synthase Inhibitor

We examined the direct effects of thrombin on pulmonary vasomotor tone in isolated guinea pig lungs perfused with Ringer albumin (0.5% g/100 ml). The injection of alpha-thrombin (the native enzyme) resulted in rapid dose-dependent increases in pulmonary arterial pressure (Ppa) and pulmonary capillary pressure (Ppc), which were associated with an increase in the lung effluent thromboxane B2 concentration. The Ppa and Ppc responses decreased with time but then increased again within 40 min after thrombin injection. The increases in Ppc were primarily the result of postcapillary vasoconstriction. Pulmonary edema as evidenced by marked increases (60% from base line) in lung weight occurred within 90 min after thrombin injection. Injection of modified thrombins (i.e., gamma-thrombin lacking the fibrinogen recognition site or i-Pr2P-alpha-thrombin lacking the serine proteolytic site) was not associated with pulmonary hemodynamic or weight changes nor did they block the effects of alpha-thrombin. Indomethacin (a cyclooxygenase inhibitor), dazoxiben (a thromboxane synthase inhibitor), or hirudin (a thrombin antagonist) inhibited the thrombin-induced pulmonary vasoconstriction, as well as the pulmonary edema. We conclude that thrombin-induced pulmonary vasoconstriction is primarily the result of constriction of postcapillary vessels, and the response is mediated by generation of cyclooxygenase-derived metabolites. The edema formation is also dependent on activation of the cyclooxygenase pathway. The proteolytic site of alpha-thrombin is required for the pulmonary vasoconstrictor and edemogenic responses.

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