Low-dose PGI2 prevents monocrotaline-induced thromboxane production and lung injury

1986 ◽  
Vol 60 (2) ◽  
pp. 464-471 ◽  
Author(s):  
G. T. Czer ◽  
J. Marsh ◽  
R. Konopka ◽  
K. M. Moser
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Platelet Activation ◽  
Endothelial Damage ◽  
Base Line ◽  
Lung Water ◽  
Platelet Deposition ◽  
Thromboxane Production

In animals, monocrotaline induces an acute lung injury secondary to capillary endothelial damage. To date, no reports have appeared dealing with the role of prostaglandins in monocrotaline-induced injury. Our studies, in dogs, revealed that monocrotaline (30 mg/kg iv) caused an acute and persistent thrombocytopenia, lung platelet deposition, pulmonary hypertension, and increased extravascular lung water (EVLW). The pulmonary hypertensive response was biphasic. Thromboxane B2 levels were similarly biphasic, peaking at 5 min and 2 h. The levels of 6-keto-PGF1 alpha peaked at 30 min and returned to base line at 3 h. Pulmonary vascular resistance paralleled thromboxane levels. Infusion of prostacyclin (PGI2) at 50 ng X kg-1 X min-1 effectively prevented the thrombocytopenia, lung platelet deposition, pulmonary hypertension, and increased EVLW; and it decreased excess thromboxane production by 79%. These results suggest that platelet activation and lung sequestration play a role in acute lung injury due to monocrotaline, and that the resultant thromboxane production may contribute to the pulmonary hypertension. PGI2 ameliorates monocrotaline-induced injury, perhaps by preventing platelet activation.

scholarly journals Acute lung injury in TBI patients with SIRS: role of vascular endothelial damage

Critical Care ◽  
2010 ◽  
Vol 14 (Suppl 1) ◽  
pp. P191 ◽  
Author(s):  
T Saito ◽  
H Kushi ◽  
T Miki ◽  
J Sato ◽  
A Yoshino ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Endothelial Damage ◽  
Vascular Endothelial

scholarly journals Vasopressin Receptor Expression Reveals Role of Endogenous Vasopressin in Ameliorating Acute Lung Injury in Pig Models of Pulmonary Hypertension

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Catherine F T Uyehara ◽  
Lee‐Ann M Murata ◽  
Jauchia W Blythe ◽  
Dao H Ho ◽  
Wayne M Ichimura ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Receptor Expression ◽  
Vasopressin Receptor

Effect of intravenous catalase on the pulmonary vascular response to endotoxemia in goats

1988 ◽  
Vol 64 (2) ◽  
pp. 697-704 ◽  
Author(s):  
R. J. Maunder ◽  
R. K. Winn ◽  
J. M. Gleisner ◽  
J. Hildebrandt ◽  
J. M. Harlan
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Endothelial Damage ◽  
In Vivo Model ◽  
Lung Edema ◽  
Experimental Sepsis ◽  
Base Line ◽  
In Vitro Systems

Neutrophils have been implicated in the pathogenesis of acute lung injury associated with clinical and experimental sepsis. Data from in vitro systems and experimental animals have suggested that neutrophil-derived oxidants, particularly H2O2, may be primarily responsible for endothelial damage, vasoconstriction, and lung edema. With the use of endotoxin infusion as an in vivo model of sepsis we tested the hypothesis that pretreatment with catalase, a peroxide scavenger, would ameliorate the resultant changes in pulmonary vasoconstriction and lung fluid balance. Paired experiments were performed in 16 goats with chronic lung lymph fistulas. One group of animals (n = 7) received endotoxin first alone and then again, several days later, after pretreatment with Ficoll-linked catalase. As a control, identical experiments were performed in a separate group (n = 6) with Ficoll-linked albumin substituted for Ficoll-catalase. A third group (n = 3) was given endotoxin alone and then again during a continuous infusion of catalase. Plasma and lymph levels of catalase were comparable to or exceeded those previously shown to be completely protective in isolated perfused lung preparations and in vitro systems. Endotoxin caused neutropenia, pulmonary arterial hypertension, decreased cardiac output, and increases in lymph flow to approximately three times base line, with a return of all variables toward control values by 6 h. Catalase pretreatment produced no significant differences in any of these variables. These experiments do not support a role for H2O2 as a mediator of acute lung injury due to endotoxemia.

scholarly journals Extravascular Lung Water and Acute Lung Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ritesh Maharaj
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Extravascular Lung Water ◽  
Response To Treatment ◽  
Dilution Method ◽  
Lung Water ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Chest Auscultation

Acute lung injury carries a high burden of morbidity and mortality and is characterised by nonhydrostatic pulmonary oedema. The aim of this paper is to highlight the role of accurate quantification of extravascular lung water in diagnosis, management, and prognosis in “acute lung injury” and “acute respiratory distress syndrome”. Several studies have verified the accuracy of both the single and the double transpulmonary thermal indicator techniques. Both experimental and clinical studies were searched in PUBMED using the term “extravascular lung water” and “acute lung injury”. Extravascular lung water measurement offers information not otherwise available by other methods such as chest radiography, arterial blood gas, and chest auscultation at the bedside. Recent data have highlighted the role of extravascular lung water in response to treatment to guide fluid therapy and ventilator strategies. The quantification of extravascular lung water may predict mortality and multiorgan dysfunction. The limitations of the dilution method are also discussed.

ACUTE LUNG INJURY IN SIRS PATIENTS: ROLE OF VASCULAR ENDOTHELIAL DAMAGE.

2006 ◽  
Vol 34 ◽  
pp. A85
Author(s):  
Takeshi Saito ◽  
Hidehiko Kushi ◽  
Jun Sato ◽  
Katsuhisa Tanjo
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Endothelial Damage ◽  
Vascular Endothelial

scholarly journals Pulmonary Hypertension and Selective Pulmonary Vasodilators in Acute Lung Injury

1998 ◽  
Vol 26 (1) ◽  
pp. 26-39 ◽  
Author(s):  
D. Blythe ◽  
P. V. Van Heerden ◽  
B. M. Power
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Circulation ◽  
Management Options ◽  
Injury Management ◽  
Pulmonary Vasodilators ◽  
The Common

The pulmonary circulation and the mechanisms which generate pulmonary hypertension are reviewed. The role of these mechanisms in the common pulmonary hypertensive states are analysed, particularly those in acute lung injury. Management options are discussed, with particular emphasis on the use of selective pulmonary vasodilators.

scholarly journals Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Tao Qiu ◽  
Jiangqiao Zhou ◽  
Tianyu Wang ◽  
Zhongbao Chen ◽  
Xiaoxiong Ma ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Stromal Cells ◽  
Marrow Cell ◽  
Marrow Transplant ◽  
Cell Source ◽  
Transplant Model ◽  
Acute Inflammatory Disease

AbstractAcute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.

H2O2 inhibits alveolar epithelial wound repair in vitro by induction of apoptosis

2004 ◽  
Vol 287 (2) ◽  
pp. L448-L453 ◽  
Author(s):  
Thomas Geiser ◽  
Masanobu Ishigaki ◽  
Coretta van Leer ◽  
Michael A. Matthay ◽  
V. Courtney Broaddus
Keyword(s):  
Acute Lung Injury ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Cell Viability ◽  
Wound Repair ◽  
Wound Edge ◽  
Alveolar Epithelial ◽  
Induction Of Apoptosis

Reactive oxygen species (ROS) are released into the alveolar space and contribute to alveolar epithelial damage in patients with acute lung injury. However, the role of ROS in alveolar repair is not known. We studied the effect of ROS in our in vitro wound healing model using either human A549 alveolar epithelial cells or primary distal lung epithelial cells. We found that H2O2 inhibited alveolar epithelial repair in a concentration-dependent manner. At similar concentrations, H2O2 also induced apoptosis, an effect seen particularly at the edge of the wound, leading us to hypothesize that apoptosis contributes to H2O2-induced inhibition of wound repair. To learn the role of apoptosis, we blocked caspases with the pan-caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp (zVAD). In the presence of H2O2, zVAD inhibited apoptosis, particularly at the wound edge and, most importantly, maintained alveolar epithelial wound repair. In H2O2-exposed cells, zVAD also maintained cell viability as judged by improved cell spreading and/or migration at the wound edge and by a more normal mitochondrial potential difference compared with cells not treated with zVAD. In conclusion, H2O2 inhibits alveolar epithelial wound repair in large part by induction of apoptosis. Inhibition of apoptosis can maintain wound repair and cell viability in the face of ROS. Inhibiting apoptosis may be a promising new approach to improve repair of the alveolar epithelium in patients with acute lung injury.

Sign in / Sign up

Export Citation Format

Share Document