Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chemically and enzymatically generated oxidants alter endothelial cell shape, increase macromolecular permeability across endothelial cell monolayers, and increase lung microvascular permeability. We examined the effect of ANP (atrial natriuretic peptide) on oxidant-induced injuries to bovine aortic endothelial cell monolayers and to isolated, perfused rabbit lungs. Treatment of cultured endothelial monolayers with glucose oxidase (1.4 U/ml) caused changes in cell shape characterized by a retraction of cells and the formation of numerous intercellular gaps. Glucose oxidase treatment also caused a reduction in F-actin stress fibers visualized by rhodamine-phalloidin fluorescence. Pretreatment (5 min) of the endothelial monolayers with ANP (10(-7) M) attenuated the oxidant-induced changes in cell shape and reduction in F-actin staining. In addition, ANP significantly (P less than 0.05) reduced increases in endothelial monolayer permeability to albumin resulting from glucose oxidase treatment. Oxidant-induced injury of isolated, perfused rabbit lungs produced pulmonary edema measured as an increase in lung weight. This increase in weight was significantly (P less than 0.05) inhibited by pretreatment of lungs with ANP (10(-7) M). Collectively, these results suggest that ANP may act to preserve endothelial barrier function and reduce edema formation caused by oxidant injury.
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PMID:Atrial natriuretic peptide inhibits oxidant-induced increases in endothelial permeability. 171 22

Acute, diffuse lung injury, the principal lesion in ARDS, is often refractory to treatment. Recently, pretreatment with several pulmonary vasodilators that increase cAMP levels: isoproterenol, terbutaline, theophylline, and prostacyclin, was found to reduce the severity of lung injury in animal models. We have investigated the possible modulation of HCl-induced pulmonary edema in rats by VIP, a lung neuropeptide with potent vasodilator and cAMP-producing properties. The lungs of rats were perfused in situ at 10 ml/min with Krebs-4% albumin solution, and ventilated at constant tidal volume (6.5 ml/kg). Peak airway pressure (PAW), mean pulmonary arterial pressure (PPA) were measured throughout the experiment, and wet to dry lung weight ratio (W/D), afterwards. All animals were observed for one hour. In 6 rats receiving HCl only, 0.2 N-HCl was instilled intratracheally at 2 ml/kg. Four rats received 2 ml/kg of physiological saline intratracheally as control. In 6 other animals, VIP was infused into the pulmonary artery at 1 micrograms/kg/min, beginning 10 minutes before HCl and for the rest of the experiment. Another 6 rats were pretreated with atrial natriuretic peptide (ANP, atriopeptin II) just like the VIP group. Lungs of saline control animals showed little or no chage in PAW or PPA. With HCl alone, PAW increased immediately and continued to rise for the rest of the hour, reaching 500% of basal value at 30 minutes. PPA increased by 68% and W/D by 74% compared to saline-instilled lungs. In the VIP + HCl group, all abnormalities were significantly reduced relative to the HCl group. The rise in PAW was attenuated by 79% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Vasoactive intestinal peptide (VIP) protects against acid-induced acute lung injury in isolated perfused rat lungs]. 281 Sep 67

Protective effect of alpha-human atrial natriuretic peptide (alpha-hANP) on pulmonary edema was investigated using an isolated perfused lung model. Infusion of alpha-hANP (1.7 to 22 ng/ml or 0.56 to 7.3 nM) prevented the edema induced in isolated lung from guinea pig by repeated treatment of 50 micrograms of arachidonic acid at 30 min intervals via the pulmonary artery. The antiedematic action of alpha-hANP was considered to be receptor mediated because the effective concentration was close to the Kd value of the binding of the ANP receptors in the lung homogenate.
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PMID:Alpha-human atrial natriuretic peptide (alpha-hANP) prevents pulmonary edema induced by arachidonic acid treatment in isolated perfused lung from guinea pig. 295 47

The present work focuses on pulmonary gas exchange during repeated rowing to exhaustion and the recovery of pulmonary diffusion capacity for carbon monoxide (DL) after exercise in healthy young subjects. The components of DL are examined at rest using the single breath method at two different alveolar O2 tensions. Electrical impedance and 99mTechnetium labelled erythrocytes were used to evaluate the recovery of blood distribution. Special attention has been given to the role of the inspiratory muscles as a limiting factor for VO2max and performance. The documentation in this study of a reduced DL several hours after exercise conflicts with the prerequisites of optimal conditions for high metabolic rates in elite athletes. Even low intensity exercise induces a reduction in DL, and together with the fact that a diuretic does not attenuate this decrease, emphasises that the reduction in DM is not due to an interstitial pulmonary edema. The major part of the reduction is due to a decreased CBV reflected in a reduction of VC and a minor part is caused by an injury to the membrane component carried over from exercise. The ability in athletes to repeat exhaustive exercise within 2 h indicates that the slow recovery of DL is not combined with either impaired pulmonary gas exchange or performance. Thus, an acute diffusion limitation and a low pH cause the desaturation in some athletes during exhaustive exercise. Despite the inspiratory muscles having a slower response to endurance training compared with the cardiovascular system, selective training of the inspiratory muscles does not improve either VO2max or performance. This indicates that maximal inspiratory pressure is not a limiting factor for maximal exercise and that the stimuli to increase VA depends on an increased metabolic rate; stressing the role of the peripheral chemoreceptors. Together with the post-exercise decrease in ANP, the reduction in DL may be involved in the mechanism increasing the total blood volume in endurance trained athletes.
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PMID:Pulmonary function after exercise with special emphasis on diffusion capacity. 1091 85

High altitude pulmonary edema (HAPE) is associated with increases in pulmonary arterial and hydrostatic pressures and an increase in pulmonary vascular permeability. There is evidence to suggest that inflammatory mediators may cause some forms of HAPE, and Salmonella enteritidis endotoxin (ETX) is known to activate neutrophils and inflammatory mediators, such as TNF-alpha and IL1-beta. Since HAPE has been produced in rats primed with ETX, we hypothesized that ANP release and action may ameliorate HAPE and that ANP blockade may exacerbate HAPE in ETX-primed rats exposed to high altitude (HA). Plasma ANP, right atrial ANP mRNA, and indexes of lung injury were measured in rats primed with endotoxin (ETX) (0.1 mg/kg BW, i.p.) and exposed to simulated HA (4267 m; P(B) = 440 mmHg) for either 12 or 24 h. Catheters were chronically inserted into the right carotid artery, pulmonary artery, and jugular vein for assessment of hemodynamic parameters in response to ETX and/or HA. In addition, some rats were injected with an antibody against ANP (alphaANP) prior to normoxic (NX) or HA exposure. Pulmonary arterial pressure increased in the alphaANP group (50 +/- 20%; p < or = 0.05) and in the HA + alphaANP (51 +/- 15%; p < or = 0.05) group at 12 h compared to NX sham rats injected with normal rabbit serum. In addition, systemic arterial pressure was significantly lower in the HA + ETX rats compared to HA + ETX + alphaANP rats (p < or = 0.001). Plasma ANP levels were significantly higher at 12 and 24 h in ETX, HA, and HA + ETX groups (p <or = 0.05) compared to NX controls. There was an inverse relationship (p <or = 0.001) between plasma ANP levels and lung wet to dry (W/D) weight when data from NX, ETX, HA, and HA + ETX groups were pooled. The HA + alphaANP rats had significantly higher lung W/D ratios (p < 0.001) compared to sham rats. These results support the hypothesis that ANP, at physiological levels, modulates the development of pulmonary edema in HA-exposed ETX-primed rats.
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PMID:Atrial natriuretic peptide blockade exacerbates high altitude pulmonary edema in endotoxin-primed rats. 1168 14

Dilated cardiomyopathy (DCM) is the major cause of heart failure affecting both women and men. Limited clinical studies show conflicting data in sex-related differences in the progression of dilated cardiomyopathy and heart failure (HF) outcomes. We examined the comparative sex-related progression of cardiomyopathy and the development of HF (at 4, 7, 13 weeks of age) in a well-established, transgenic mouse model of DCM that recapitulates the progressive stages of human HF. By 13 weeks of age, female mice with DCM had more severe left ventricular systolic dysfunction, left ventricular dilation and wall thinning (P<0.001 for all) than age-matched male mice with DCM. Female mice also had greater lung edema (P<0.001), cardiac fibrosis (P<0.01) and pleural effusions, which were not rescued by ovariectomy. By comparison to DCM male mice at 13 weeks, these pathological changes in female mice with DCM, were associated with significant increases in plasma active renin (P<0.01), angiotensin II (P<0.01) and aldosterone levels (P<0.001). In comparison to DCM male mice, DCM female mice also showed differential expression of the natriuretic peptide system with lower corin and higher ANP, BNP and cGMP levels at 13 weeks of age. We conclude, that female mice with experimental DCM have an accelerated progression of cardiomyopathy and HF, which was not corrected by early ovariectomy. These alterations are associated with early renin activation with increased angiotensin II and aldosterone levels, and altered expression of the natriuretic peptide system.
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PMID:Enhanced heart failure, mortality and renin activation in female mice with experimental dilated cardiomyopathy. 2924 Jul 88

Congestive heart failure (CHF) often leads to progressive cardiac hypertrophy and salt/water retention as evident by peripheral and lung edema. Although the pathogenesis of CHF remains largely unclarified, it is widely accepted that neurohormonal changes and inflammatory processes are profoundly involved in structural and functional deterioration of vital organs including, heart, kidney and lungs. Corin, a cardiac serine protease, is responsible for converting pro-ANP and pro-BNP to biologically active natriuretic peptides (NPs). Although the involvement of corin in cardiac hypertrophy and heart failure was extensively studied, the alterations in corin and PCSK6, a key enzyme in the conversion of procorin to corin, have not been studied in the pulmonary tissue. Thus, this study aims at examining the status of PCSK6/Corin in the lung of rats with CHF induced by the creation of aorto-caval fistula (ACF) between the abdominal aorta and vena cava in SD rats. Rats with ACF were divided into 2 subgroups based on the pattern of their daily sodium excretion, compensated and decompensated CHF. Placement of ACF led to cardiac hypertrophy, pulmonary congestion, and renal dysfunction, which were more severe in the decompensated subgroup, despite remarkable elevation of circulatory ANP and BNP levels. Corin mRNA and immunoreactive peptide were detected in pulmonary tissue of all experimental groups. However, the expression and abundance of pulmonary corin significantly increased in the decompensated animals, but not in the compensated ones. Noteworthy, the expression of PCSK6 and ANP/BNP in the pulmonary tissue followed a similar pattern as corin. The upregulation of pulmonary Corin/PCSK6 and NPs were accompanied by local activation of cathepsin L and certain cytokines including IL-6. In light of the anti-inflammatory role of NPs, we postulate that the obtained upregulation of pulmonary PCSK6/Corin along NPs in rats with decompensated CHF may represent a counterbalance response to the inflammatory milieu characterizing CHF especially in severe cases.
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PMID:Natriuretic peptides system in the pulmonary tissue of rats with heart failure: potential involvement in lung edema and inflammation. 2977 97

Advanced age, underlying cardiovascular disease (including hypertension), and obesity are associated with a higher risk of progression to severe hypoxemia, acute respiratory distress syndrome (ARDS), and death in COVID-19-infected patients. African Americans have a higher degree of COVID-19 mortality. The incidence of salt-sensitive hypertension is higher in older individuals and African Americans. Lower circulating levels of natriuretic peptides, key regulators of vascular tone and kidney function, have been associated with salt-sensitive hypertension and obesity. Evidence has accumulated that ANP administered to pulmonary endothelial cells, isolated lungs, and patients suffering from ARDS reduces endothelial damage and preserves the endothelial barrier, thereby reducing pulmonary edema and inflammation. Epidemiologic and pharmacologic data suggest that deficiencies in the natriuretic peptide hormone system may contribute to the development of severe lung pathology in COVID-19 patients, and treatments that augment natriuretic peptide signaling may have potential to limit progression to ARDS.
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PMID:An Impaired Natriuretic Peptide Hormone System May Play a Role in COVID-19 Severity in Vulnerable Populations. 3283 15