Ultrastructural aspects of pulmonary edema

Bachofen, H; Bachofen, M; Er, Weibel

doi:10.1097/00005382-198807000-00005

Cited by 33 publications

(16 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Bachofen et al (9) reported that in patients with chronic CHF, there is an increase in the number of alveolar type II cells. Notably, this finding might contribute to increased AFR.…”

Section: Discussionmentioning

confidence: 99%

Alveolar fluid reabsorption is increased in rats with compensated heart failure

Azzam

Adir

Welch³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

) is important in keeping the air spaces free of edema. This process is accomplished via active transport of Na ϩ across the alveolo-capillary barrier mostly by apical Na ϩ channels and basolateral Na ϩ -K ϩ -ATPases. Recently, we have reported that acute elevation of left atrial pressures is associated with decreased AFR in isolated rat lungs. However, the effect of chronic elevation of pulmonary capillary pressure, such as seen in patients with congestive heart failure (CHF), on AFR is unknown. CHF was induced by creating an aorto-caval fistula (ACF) in Sprague-Dawley male rats. Seven days after the placement of the fistula, AFR was studied in the isolated perfused rat lung model. AFR in control rats was 0.49 Ϯ 0.02 ml/h (all values are means Ϯ SE) and increased by ϳ40% (0.69 Ϯ 0.03 ml/h) in rats with chronic CHF (P Ͻ 0.001). The albumin flux from the pulmonary circulation into the air spaces did not increase in the experimental groups, indicating that lung permeability for large solutes was not increased. Na ϩ -K ϩ -ATPase activity and protein abundance at the plasma membrane of distal alveolar epithelial tissue were significantly increased in CHF rats compared with controls. These changes were associated with increased plasma norepinephrine levels in CHF rats compared with controls. We provide evidence that in a rat model of chronic compensated CHF, AFR is increased, possibly due to increased endogenous norepinephrine upregulating active sodium transport and protecting against alveolar flooding. edema; alveolar epithelium; Na ϩ -K ϩ -ATPase PULMONARY EDEMA DEVELOPS when fluid movement into the air space exceeds the ability of the lung to clear it (20, 37). Many in vivo and ex vivo models of normal and injured lungs have been used to determine the mechanisms by which excess air space fluid is cleared (8,13,26,29,34, 38). These studies have used models where fluid was either directly instilled into the lung or rapidly accumulated in the air space. However, there are no data regarding how the lung adapts to chronic imbalance of Starling forces as occurs in congestive heart failure (CHF). Tandon and Kasturi (40) reported that in patients with mitral stenosis, the pulmonary tissue remodels in response to chronically elevated left atrial pressure; the arterioles were muscularized with pronounced intimal proliferation. Other changes included medial hypertrophy in the veins and occasional muscularization and dilatation of the lymphatics. Patients with CHF have chronically elevated pulmonary capillary pressures, yet they develop frank pulmonary edema only occasionally and intermittently. These clinical features thus suggest that the lung must have mechanisms to compensate for chronic elevation of pulmonary hydrostatic pressures leading to lung edema. These mechanisms have not been previously defined.Recently, several studies have shown that exposure to acute elevation in left atrial pressures impairs alveolar fluid reabsorption (AFR) in rat lungs; however, exogenous administration of catecholamines and overexpressi...

show abstract

“…Bachofen et al (9) reported that in patients with chronic CHF, there is an increase in the number of alveolar type II cells. Notably, this finding might contribute to increased AFR.…”

Section: Discussionmentioning

confidence: 99%

Alveolar fluid reabsorption is increased in rats with compensated heart failure

Azzam

Adir

Welch³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…Although we did not directly measure the transcriptional rate, reductions in both steady-state mRNA and protein levels by prior HS or SA treatment can be accounted for at least in part by the transcriptional regulation of HSPs. Because the release of pro-inflammatory mediators is associated with injury to the endothelial and epithelial cells of the lung (18,19), an attenuation of pro-inflammatory cytokine expression by prior HSP induction means that HSPs may exert a cytoprotective effect to respiratory epithelial cells by blocking the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

“…During stress, cells undergo a prioritization of gene expression characterized by the rapid expression of stress proteins, whereas the expression of various nonstress proteins is transiently inhibited (17). Because the release of pro-inflammatory mediators is associated with injury to the endothelial and epithelial cells of the lung (18,19), it can be assumed that the cytoprotective effect of HSPs may be related to the inhibition of pro-inflammatory cytokine gene expression. Actually, it is well documented that HSP induction inhibits pro-inflammatory cytokine gene expression in mononuclear cells (20,21).…”

mentioning

confidence: 99%

Anti-Inflammatory Effect of Heat Shock Protein Induction Is Related to Stabilization of IκBα Through Preventing IκB Kinase Activation in Respiratory Epithelial Cells

Yoo

Lee

et al. 2000

The Journal of Immunology

246

171

View full text Add to dashboard Cite

Heat shock protein (HSP) induction confers protection against diverse forms of cellular and tissue injury. However, the mechanism by which HSP exerts cytoprotective effects is unclear. Because HSP induction inhibits genetic expression of pro-inflammatory cytokines, the transcription of which is dependent on NF-κB activation, we explored the relationship between the anti-inflammatory effect of HSP induction and the NF-κB/IκBα pathway. Both HS and sodium arsenite treatment increased HSP70 expression time dependently at mRNA and protein levels. Prior induction of HSP suppressed cytokine-induced IL-8 and TNF-α expression at both mRNA and protein levels. Although HSP induction did not affect total cellular expression of NF-κB, TNF-α-induced increase in NF-κB-DNA binding activity and nuclear translocation of the p65 subunit of NF-κB were inhibited by prior HSP induction, suggesting that activation of NF-κB was blocked. Cytokine-induced IκBα phosphorylation and its degradation were blocked in HSP-induced cells. Immune complex kinase assays demonstrated that TNF-α induced increase in IκB kinase activity was suppressed by prior HSP induction. These results suggest that the anti-inflammatory effect of HSP induction in respiratory epithelial cells is related to stabilization of IκBα, possibly through the prevention of IκB kinase activation, which thereby inhibits activation of NF-κB.

show abstract

“…Other authors reported a significant bronchodilating response to the use of salbutamol and ipratropium bromide, indicating that chronic congestive heart failure may result in a mild obstructive ventilatory disorder. Experimental evidence associating peribronchial vascular congestion and increased airway resistance supports this finding 5 . Caruana et al 6 ruled out the diagnosis of diastolic heart failure in some of their patients because they had FEV1 results < 70% of the foretold value, which, according to the above reported, is unacceptable.…”

Section: Discussionmentioning

confidence: 80%

“…They consisted of intense proliferation of fibroblasts and histiocytes in the alveolar septa, resulting in dense deposits of collagen fibers that Bachofen et al 5 denominated congestive pulmonary fibrosis, which may lead to compression of the small adjacent airways. The pulmonary blood vessels of all dimensions undergo important changes, among which are the deposition of dense connective tissue in the intima and adventitia layers 2,5 . An intense proliferation of type II pneumocytes is still observed, translating into the presence of a reparative activity, as are alveolar macrophages phagocytizing proteins and red blood cells.…”

Section: Discussionmentioning

confidence: 99%

Insuficiência respiratória persistente secundária a insuficiência cardíaca diastólica

Neto¹,

Benchimol²,

Lima³

2004

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

This study assessed two 85-year-old The incidence and prevalence of congestive heart failure have progressively increased in industrialized countries, because of their population aging and the longer survival of individuals with coronary artery disease 1 . Consequently, an increasing number of clinical findings, as of yet unknown, may be present in elderly patients with congestive heart failure. This study assesses 2 elderly patients with diastolic heart failure, who developed severe and persistent respiratory impairment, which led to death. The possibility that the respiratory findings could be attributed to primary pulmonary disease was ruled out based on clinical data and complementary tests. These respiratory findings, characterized by the presence of severe obstructive ventilatory disorder and important and persistent gas exchange alterations, also differ from the respiratory manifestations already described in chronic congestive heart failure. Case reportCase 1 -The patient was an 85-year-old man, who sought medical care at the Hospital São Vicente de Paulo in August 1998 for the first time, when, reporting worsening of the dyspnea initiated months before, he was brought to the emergency unit and immediately referred to the ICU. The patient denied antecedents of smoking and of respiratory disease, but reported exposure to vegetal coal in an open environment during work.On physical examination, the patient was restless, objectively dyspneic, cyanotic, and had jugular venous distension at 90º. The use of the inspiratory musculature was markedly visible, and the respiratory sounds were intensely and diffusely reduced. His heart rate was 104 bpm with regular rhythm, and his blood pressure was 190/100 mmHg. His abdomen was distended and hypertympanic. The lower limbs were not edematous, but signs of chronic venous insufficiency existed. Previous chest X-rays performed during the 4 years preceding his first visit to our hospital showed alterations compatible with mild pulmonary edema ( fig. 1A and 1B).His first arterial blood gas analysis in the ICU showed PO 2 of 26.5 mmHg and PCO 2 of 67.4 mmHg. The diagnosis of respiratory insufficiency was established and a ventilatory prosthesis was installed. The echocardiogram showed preserved systolic function (this result was repeated in all tests performed later, the left ventricular ejection fraction being always above 70%), and pulmonary capillary pressure oscillating from 15 to 23 mmHg in the first 24 hours. The chest X-rays had alterations characteristic of pulmonary congestion. The pulmonary arteriography was negative for thromboembolic disease and showed an increase in the caliber of the pulmonary arteries. A pulmonary biopsy was performed, the result being negative for primary pulmonary disease and compatible with pulmonary edema. In the ICU, the patient received diuretics and vasodilators discontinuously. He improved progressively, which allowed ventilator weaning and discharge from the ICU.Signs of pulmonary congestion persisted on chest computed tomography ...

show abstract

Ultrastructural aspects of pulmonary edema

Cited by 33 publications

References 1 publication

Alveolar fluid reabsorption is increased in rats with compensated heart failure

Alveolar fluid reabsorption is increased in rats with compensated heart failure

Anti-Inflammatory Effect of Heat Shock Protein Induction Is Related to Stabilization of IκBα Through Preventing IκB Kinase Activation in Respiratory Epithelial Cells

Insuficiência respiratória persistente secundária a insuficiência cardíaca diastólica

Contact Info

Product

Resources

About