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.

The adenosine 2A receptor agonist GW328267C improves lung function after acute lung injury in rats

2012 ◽  
Vol 303 (3) ◽  
pp. L259-L271 ◽  
Author(s):  
Hans G. Folkesson ◽  
Stephanie R. Kuzenko ◽  
David A. Lipson ◽  
Michael A. Matthay ◽  
Mark A. Simmons
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Fluid Transport ◽  
Unmet Need ◽  
Alveolar Epithelium ◽  
Experimental Models ◽  
Adrenergic Stimulation ◽  
Edema Formation ◽  
Beneficial Effects

There is a significant unmet need for treatments of patients with acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). The primary mechanism that leads to resolution of alveolar and pulmonary edema is active vectorial Na+ and Cl− transport across the alveolar epithelium. Several studies have suggested a role for adenosine receptors in regulating this fluid transport in the lung. Furthermore, these studies point to the A2A subtype of adenosine receptor (A2AR) as playing a role to enhance fluid transport, suggesting that activation of the A2AR may enhance alveolar fluid clearance (AFC). The current studies test the potential therapeutic value of the A2AR agonist GW328267C to accelerate resolution of alveolar edema and ALI/ARDS in rats. GW328267C, at concentrations of 10−5 M to 10−3 M, instilled into the airspaces, increased AFC in control animals. GW328267C did not increase AFC beyond that produced by maximal β-adrenergic stimulation. The effect of GW328267C was inhibited by amiloride but was not affected by cystic fibrosis transmembrane conductance regulator inhibition. The drug was tested in three models of ALI, HCl instillation 1 h, LPS instillation 16 h, and live Escherichia coli instillation 2 h before GW328267C instillation. After either type of injury, GW328267C (10−4 M) decreased pulmonary edema formation and restored AFC, measured 1 h after GW328267C instillation. These findings show that GW328267C has beneficial effects in experimental models of ALI and may be a useful agent for treating patients with ALI or prophylactically to prevent ALI.

scholarly journals Neurogenic Pulmonary Edema

2018 ◽  
Vol 21 (1) ◽  
pp. 49-52
Author(s):  
Carlos Eduardo Romeu De Almeida ◽  
Eberval Gadelha Figueiredo ◽  
Bernardo Assumpção De Monaco ◽  
Arthur Maynart Pereira Oliveira ◽  
Manoel Jacobsen Teixeira
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Subarachnoid Hemorrhage ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Patient Management ◽  
Acute Onset ◽  
Neurogenic Pulmonary Edema ◽  
Alveolar Space ◽  
Pulmonary Vasoconstriction

Neurogenic Pulmonary Edema (NPE) is defined as the acute onset of dyspnea or a decrease in PaO2/FiO2 ratio, following an acute central nervous system (CNS) insult, in the absence of other obvious causes of lung injury. The most important cause of NPE is subarachnoid hemorrhage (SAH), followed by cerebraltrauma and epilepsy. The incidence of NPE after SAH in the literature may vary from 4 to 23% in greater studies, with SAH accounting for 43-73% of cases of NPE. It is postulated that an excessive adrenergic discharge would lead to pulmonary vasoconstriction and a rapid increase in pulmonary capillaryhydrostatic pressure, thus promoting fluid leakage to the alveolar space. NPE is generally treated in a supportive and conservative fashion, and patient management should be focused in the primary insult.

scholarly journals Mechanisms of neurogenic pulmonary edema development

2008 ◽  
pp. 499-506
Author(s):  
J Šedý ◽  
J Zicha ◽  
J Kuneš ◽  
P Jendelová ◽  
E Syková
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Pulmonary Edema ◽  
Current Knowledge ◽  
Experimental Models ◽  
Neurogenic Pulmonary Edema ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Sympathetic Discharge

Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia in the etiopathogenesis of neurogenic pulmonary edema are considered in detail. The management of the patient and experimental models of neurogenic pulmonary edema are also discussed.

Selected Contribution: Mechanisms that may stimulate the resolution of alveolar edema in the transplanted human lung

2002 ◽  
Vol 93 (5) ◽  
pp. 1869-1874 ◽  
Author(s):  
Lorraine B. Ware ◽  
Xiohui Fang ◽  
Yibing Wang ◽  
Tsutomu Sakuma ◽  
Timothy S. Hall ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Organ Donor ◽  
Dry Weight ◽  
Organ Donors ◽  
Alveolar Fluid Clearance ◽  
Adrenergic Stimulation ◽  
Lung Water ◽  
Human Donor ◽  
Pharmacological Agents ◽  
Alveolar Edema

Pulmonary edema is common in organ donors and lung transplant recipients. Therefore, we assessed the responsiveness of human donor lungs to pharmacological agents that stimulate clearance of alveolar edema. Organ donors whose lungs were rejected for transplantation were studied. After resection, transport (4°C), and rewarming (37°C) of lungs, alveolar fluid clearance was measured with ( n = 8 donors) or without ( n = 23 donors) β-adrenergic stimulation. Terbutaline-stimulated clearance (10−4M) was higher than unstimulated clearance (7.1 ± 1.3 vs. 4.8 ± 2.4%/h, P < 0.01). Second, we determined whether medications given to the organ donor were associated with the extent of pulmonary edema or the rate of alveolar fluid clearance in the harvested lung. Preharvest administration of dopamine in low to moderate doses was associated with faster alveolar fluid clearance ( r = 0.62, P < 0.01). Preharvest administration of diuretics was associated with lower extravascular lung water-to-dry weight ratios. This study provides the first evidence that a β2-adrenergic agonist stimulates alveolar fluid clearance in the human donor lung. Aerosolized β2-adrenergic agonists may have therapeutic value for hastening the resolution of alveolar edema during the management of donors before resection of lungs for transplantation or in the posttransplant setting.

Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits

1987 ◽  
Vol 63 (1) ◽  
pp. 335-341 ◽  
Author(s):  
F. L. Minnear ◽  
C. Kite ◽  
L. A. Hill ◽  
H. van der Zee
Keyword(s):  
Pulmonary Edema ◽  
Sodium Citrate ◽  
Endothelial Injury ◽  
Saline Control ◽  
Neurogenic Pulmonary Edema ◽  
Pulmonary Congestion ◽  
Microvascular Endothelium ◽  
Lung Weight ◽  
Protein Rich ◽  
Pulmonary Vascular Hypertension

The objectives of the present study were to determine whether an intracisternal injection of fibrinogen-sodium citrate, a model of neurogenic pulmonary edema (NPE), produces protein-rich or protein-poor pulmonary edema, and to determine whether the edema is associated with pulmonary vascular hypertension and pulmonary congestion. Fibrinogen (6–10 mg/ml) dissolved in 0.055 M sodium citrate was injected into the cisterna magna of six New Zealand White rabbits. Six additional rabbits were injected with saline to control for the effects of intracranial hypertension and pulmonary vascular hypertension. The fibrinogen-sodium citrate solution or sodium citrate alone, as opposed to saline, produced systemic and pulmonary vascular hypertension, pulmonary edema, hypoxemia, hypercapnia, and acidosis. The lungs from fibrinogen-injected rabbits were edematous, congested, and liverlike in appearance. Tracheal froth that was blood tinged and protein rich was present in five of the six rabbits. Microscopic examination of lung biopsies revealed erythrocytes and plasma in the alveoli and focal injury to the pulmonary microvascular endothelium. Fibrinogen-sodium citrate increased (P less than 0.05) the extravascular lung water (EVLW) (10.3 +/- 2.0 vs. 5.5 +/- 0.6 g, means +/- SE), lung blood weight (9.7 +/- 1.3 vs. 3.8 +/- 0.6 g), total dry lung weight (3.2 +/- 0.4 vs. 2.0 +/- 0.1 g), and the EVLW-to-blood-free dry lung weight ratio (7.0 +/- 0.8 vs. 4.0 +/- 0.3 g) from saline-control values. There was no difference in the blood-fre dry lung weight (1.4 +/- 0.1 vs. 1.3 +/- 0.1 g) between the two groups. These findings demonstrate that pulmonary congestion, pulmonary vascular hypertension, and focal endothelial injury contribute to the development of NPE.

Sudden Death in Toddlers with Viral Meningitis, Massive Cerebral Edema, and Neurogenic Pulmonary Edema and Hemorrhage: Report of Two Cases

2006 ◽  
Vol preprint (2007) ◽  
pp. 1
Author(s):  
Henry Krous ◽  
Amy Chadwick ◽  
Douglas Miller ◽  
Laura Crandall ◽  
Hannah Kinney
Keyword(s):  
Sudden Death ◽  
Pulmonary Edema ◽  
Cerebral Edema ◽  
Viral Meningitis ◽  
Neurogenic Pulmonary Edema

METHODS FOR SIMULATION OF ACUTE BRAIN ISCHEMIA: PATHOPHYSIOLOGICAL SUBSTANTIATION OF SELECTION AND IMPORTANCE FOR CLINICAL PRACTICE

2019 ◽  
pp. 142-152
Author(s):  
Б.И. Гельцер ◽  
Э.В. Слабенко ◽  
Ю.В. Заяц ◽  
В.Н. Котельников
Keyword(s):  
Clinical Practice ◽  
Experimental Studies ◽  
Cerebrovascular Diseases ◽  
Experimental Models ◽  
Pathological Process ◽  
Ischemic Brain ◽  
Actual Clinical Practice ◽  
Acute Cerebral Ischemia ◽  
Different Types ◽  
Acute Brain Ischemia

Одним из основных требований к разработке экспериментальных моделей цереброваскулярных заболеваний является их максимальная приближенность к реальной клинической практике. В работе систематизированы данные по основным методам моделирования острой ишемии головного мозга (ОИГМ), представлена их классификация, анализируются данные о преимуществах и недостатках той или иной модели. Обсуждаются результаты экспериментальных исследований по изучению патогенеза ОИГМ с использованием различных моделей (полной и неполной глобальной, локальной и мультифокальной ишемии) и способов их реализации (перевязка артерий, клипирование, коагуляция, эмболизация и др.). Особое внимание уделяется «стабильности» последствий острого нарушения мозгового кровообращения: необратимых ишемических повреждений головного мозга или обратимых с реперфузией заданной продолжительности. Отмечается, что важное значение в этих исследованиях должно принадлежать современным методам прижизненной визуализации очагов острого ишемического повреждения, что позволяет оценивать динамику патологического процесса. Предлагаемый метод отвечает требованиям гуманного обращения с животными. Подчеркивается, что выбор релевантной модели ОИГМ определяется задачами предстоящего исследования и технологическими ресурсами научной лаборатории. Development of experimental models for acute forms of cerebrovascular diseases is essential for implementation of methods for their prevention and treatment. One of the principal requirements to such models is their maximum approximation to actual clinical practice. This review systematized major models of acute cerebral ischemia (ACI), their classification, and presented information about their advantages and shortcomings. Also, the review presented results of experimental studies on pathophysiological mechanisms of different types of modeled ACI (complete and incomplete global, local, and multifocal ischemia) and methods for creating these models (arterial ligation, clipping, coagulation, embolization, etc.). Particular attention was paid to “stability” of the consequences of acutely impaired cerebral circulation - an irreversible ischemic brain injury or a reversible injury with reperfusion of a given duration. The authors emphasized that in such studies, a special significance should be given to intravital imaging of acute ischemic damage foci using modern methods, which allow assessing the dynamics of the pathological process and meet the requirements to humane treatment of animals. The choice of a relevant ACI model is determined by objectives of the planned study and the technological resources available at the research laboratory.

scholarly journals Experimental Methods to Simulate and Evaluate Postsurgical Peripheral Nerve Scarring

2021 ◽  
Vol 10 (8) ◽  
pp. 1613
Author(s):  
Alessandro Crosio ◽  
Giulia Ronchi ◽  
Benedetta Elena Fornasari ◽  
Simonetta Odella ◽  
Stefania Raimondo ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Peripheral Nerves ◽  
Experimental Methods ◽  
Scar Tissue ◽  
Experimental Models ◽  
Tissue Formation ◽  
Surgical Interventions ◽  
Pubmed Database ◽  
Different Types ◽  
Scar Tissue Formation

As a consequence of trauma or surgical interventions on peripheral nerves, scar tissue can form, interfering with the capacity of the nerve to regenerate properly. Scar tissue may also lead to traction neuropathies, with functional dysfunction and pain for the patient. The search for effective antiadhesion products to prevent scar tissue formation has, therefore, become an important clinical challenge. In this review, we perform extensive research on the PubMed database, retrieving experimental papers on the prevention of peripheral nerve scarring. Different parameters have been considered and discussed, including the animal and nerve models used and the experimental methods employed to simulate and evaluate scar formation. An overview of the different types of antiadhesion devices and strategies investigated in experimental models is also provided. To successfully evaluate the efficacy of new antiscarring agents, it is necessary to have reliable animal models mimicking the complications of peripheral nerve scarring and also standard and quantitative parameters to evaluate perineural scars. So far, there are no standardized methods used in experimental research, and it is, therefore, difficult to compare the results of the different antiadhesion devices.

ANTAGONISM BETWEEN INSULIN AND SELECTIVE ADRENERGIC AGONISTS ON THE GLYCOGEN SYNTHETASE AND PHOSPHORYLASE SYSTEMS OF THE ISOLATED RAT DIAPHRAGM

1975 ◽  
Vol 78 (2) ◽  
pp. 392-400
Author(s):  
Arne T. Hostmark ◽  
Ole Grønnerød ◽  
Robert S. Horn
Keyword(s):  
Glycogen Metabolism ◽  
Rat Diaphragm ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Insulin Effect ◽  
Glycogen Synthetase ◽  
Adrenergic Antagonists ◽  
Fasted Rats ◽  
Isolated Rat ◽  
Stimulation Of

ABSTRACT The antagonism between insulin and selective adrenergic stimulation on the converting systems for glycogen synthetase and phosphorylase has been investigated in the isolated rat diaphragm. Insulin significantly inhibited stimulation by terbutaline and noradrenaline of phosphorylase b to a conversion as well as stimulation of glycogen synthetase I to D conversion by these agents. The inhibition by insulin was stronger on the synthetase system than on the phosphorylase system. The insulin effect was not dependent upon the presence of glucose. In diaphragms from 24 h fasted rats the response of the phosphorylase system to both agonists decreased. Inhibition by insulin of terbutaline stimulated phosphorylase conversion was maintained upon fasting while no effect of insulin against stimulation by noradrenaline could be obtained in diaphragms from fasted rats. The effects of fasting and insulin were not influenced by beta adrenergic antagonists (practolol and butoxamine). The results indicate a difference in sensitivity of the synthetase and phosphorylase systems to insulin and suggest that noradrenaline and terbutaline influence glycogen metabolism by differing mechanisms.

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