Application of α 2 ‐adrenergic agonists combined with anesthetics and their implication in pulmonary intravascular macrophages‐insulted pulmonary edema and hypoxemia in ruminants

2021 ◽  
Author(s):  
Mahmoud M. Abouelfetouh ◽  
Eman Salah ◽  
Mingxing Ding ◽  
Yi Ding
Keyword(s):  
Pulmonary Edema ◽  
Adrenergic Agonists ◽  
Pulmonary Intravascular Macrophages

456 BETA 2 ADRENERGIC AGONISTS DECREASE PULMONARY EDEMA IN EXPERIMENTAL LUNG INJURY BY UPREGULATING ALVEOLAR EPITHELIAL FLUID TRANSPORT.

2004 ◽  
Vol 52 (Suppl 1) ◽  
pp. S159.3-S159
Author(s):  
D. F. McAuley ◽  
J. A. Frank ◽  
X. Fang ◽  
M. A. Matthay
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Fluid Transport ◽  
Adrenergic Agonists ◽  
Alveolar Epithelial ◽  
Beta 2

scholarly journals Contribution ofα- andβ-Adrenergic Mechanisms to the Development of Pulmonary Edema

Scientifica ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Beate Rassler
Keyword(s):  
Pulmonary Edema ◽  
Experimental Models ◽  
Neurogenic Pulmonary Edema ◽  
Alveolar Fluid Clearance ◽  
Adrenergic Agonists ◽  
Alveolar Space ◽  
Adrenergic Stimulation ◽  
Abundant Protein ◽  
Different Types ◽  
Protein Rich

Endogenous or exogenous catecholamines can induce pulmonary edema (PE). This may occur in human pathologic conditions such as in pheochromocytoma or in neurogenic pulmonary edema (NPE) but can also be provoked after experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. With -adrenergic treatment, it develops more rapidly, is more severe with abundant protein-rich fluid in the alveolar space, and is accompanied by strong generalized inflammation in the lung. Similar detrimental effects of -adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Although -adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced by -adrenergic treatment as can be observed in tocolysis. In experimental models, infusion of -adrenergic agonists induces less severe PE than -adrenergic stimulation. The present paper addresses the current understanding of the possible contribution of - and -adrenergic pathways to the development of PE.

Aerosolized β2-adrenergic agonists achieve therapeutic levels in the pulmonary edema fluid of ventilated patients with acute respiratory failure

2002 ◽  
Vol 28 (6) ◽  
pp. 705-711 ◽  
Author(s):  
Kamran Atabai ◽  
Lorraine B. Ware ◽  
Mary E. Snider ◽  
Patrick Koch ◽  
Brian Daniel ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Acute Respiratory Failure ◽  
Pulmonary Edema ◽  
Adrenergic Agonists ◽  
Edema Fluid ◽  
Ventilated Patients

BETA 2 ADRENERGIC AGONISTS DECREASE PULMONARY EDEMA IN EXPERIMENTAL LUNG INJURY BY UPREGULATING ALVEOLAR EPITHELIAL FLUID TRANSPORT.

2004 ◽  
Vol 52 ◽  
pp. S159
Author(s):  
D. F. McAuley ◽  
J. A. Frank ◽  
X. Fang ◽  
M. A. Matthay
Keyword(s):  
Lung Injury ◽  
Pulmonary Edema ◽  
Fluid Transport ◽  
Adrenergic Agonists ◽  
Alveolar Epithelial ◽  
Beta 2

Dibutyryl cAMP, aminophylline, and beta-adrenergic agonists protect against pulmonary edema caused by phosgene

1989 ◽  
Vol 67 (6) ◽  
pp. 2542-2552 ◽  
Author(s):  
T. P. Kennedy ◽  
J. R. Michael ◽  
J. R. Hoidal ◽  
D. Hasty ◽  
A. M. Sciuto ◽  
...  
Keyword(s):  
Weight Gain ◽  
Respiratory Distress Syndrome ◽  
Pulmonary Edema ◽  
Distress Syndrome ◽  
Pulmonary Vasculature ◽  
Adrenergic Agonists ◽  
Dibutyryl Camp ◽  
Lung Weight ◽  
Beta Adrenergic Agonists ◽  
Exposed Workers

Phosgene is a toxic oxidant gas that causes the adult respiratory distress syndrome in exposed workers. Phosgene exposure markedly increased lung weight gain in buffer-perfused isolated rabbit lungs (31 +/- 5 g over 60 min after phosgene vs. 7.7 +/- 1.2 in control lungs, P less than 0.01) and markedly increased the lung leak index for 125I-albumin (0.28 +/- 0.03 after phosgene vs. 0.02 +/- 0.01 in control lungs, P less than 0.01). Pretreatment with dibutyryl adenosine 3′,5′ -cyclic monophosphate (DBcAMP), aminophylline, or terbutaline plus isoproterenol prevented the increase in lung weight caused by phosgene (31 +/- 5 g phosgene, 11.7 +/- 2.8 DBcAMP, 7.5 +/- 2.5 aminophylline, 6.1 +/- 1 terbutaline and isoproterenol, 6.1 +/- 1.2 control + aminophylline, and 7.7 +/- 1.2 control; all treatments were P less than 0.01 vs. the untreated phosgene group and not significantly different from control lungs). Pretreatment with aminophylline prevented the increase in lung leak index for 125I-albumin (0.28 +/- 0.03 after phosgene vs. 0.06 +/- 0.02 in aminophylline-treated lungs, P less than 0.01). Posttreatment with aminophylline and terbutaline also prevented the increase in lung weight caused by phosgene. These results indicate that phosgene dramatically increases the movement of fluid and protein across the pulmonary vasculature and that treatment with DBcAMP, aminophylline, terbutaline, or isoproterenol markedly reduces the pulmonary edema caused by phosgene.

Pulmonary Edema and Simultaneous Cardiac Dysfunction After Epileptic Seizures

2013 ◽  
Vol 40 (06) ◽  
pp. 896-897
Author(s):  
V. Pelliccia ◽  
C. Pizzanelli ◽  
S. Pini ◽  
P. Malacarne ◽  
U. Bonuccelli
Keyword(s):  
Pulmonary Edema ◽  
Cardiac Dysfunction ◽  
Epileptic Seizures

Effect of brefeldin A (BFA) on the unique surface coat of pulmonary intravascular macrophages (PIMs) of sheep: Ultrastructural and cytochemical study

1993 ◽  
Vol 51 ◽  
pp. 18-19
Author(s):  
Baljit Singh
Keyword(s):  
Brefeldin A ◽  
Ultrastructural Feature ◽  
Surface Coat ◽  
Anterograde Transport ◽  
Cytochemical Study ◽  
Active Involvement ◽  
Electron Lucent ◽  
Pulmonary Intravascular Macrophages ◽  
Unique Surface

The PIM of sheep, calf, goat and horse has a characteristic ultrastructural feature in the form of a unique, heparin sensitive, globular surface coat present around the plasma membrane with an intervening electron lucent space of 32-40 nm. We previously showed the active involvement of this surface coat in the phagocytosis of tracer material like monastral blue and cationized ferritin. The surface coat is capable of reconstitution in vivo following disruption with heparin. The present study was aimed to investigate whether PIM is the source of surface coat or not. In the recent years the BFA has been extensively used to understand the secretory pathways in the cells because of its ability to cause a rapid and reversible block to the anterograde transport of proteins from the endoplasmic reticulum to the Golgi.Sheep (n=6) were weighed, their plasma volume was calculated indirectly and based on which a sufficient single intravenous dose of BFA was given so as to reach a concentration of 4-5 microgram/ml of plasma.

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