Effect of captopril on serum TNF-α level in acute lung injury rats induced by HCL

Liu, Hongmei; Guo, Yong

doi:10.1016/s1995-7645(14)60158-9

Cited by 7 publications

(8 citation statements)

References 10 publications

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“…Apart from our experimental setting, well-established substances like the ACE inhibitor captopril and the angiotensin II receptor antagonist telmisartan also have been tested in experimental ALI. For example, captopril has been shown to attenuate ALI in rats [18] and Liu and Guo observed decreased TNF-levels and an increased PaO2 after captopril in rats subjected to hydrochloric acid-induced ALI [19]. In meconium-or LPS-treated piglets, lisinopril or telmisartan led to severe hemodynamic instability requiring high doses of catecholamines.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-Converting Enzyme 2 Improves Arterial Hypoxemia in Meconium-Induced Acute Lung Injury in Piglets

Treml

Loeckinger

Kleinsasser

et al. 2015

Advances in Critical Care

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Objective.Meconium aspiration induces acute lung injury (ALI) in neonates born through meconium-stained amniotic fluid. As yet, there is no specific therapy for improving the outcome. Recently, angiotensin-converting enzyme 2 (ACE2), which inactivates angiotensin II (Ang II), has been shown to ameliorate murine ALI.Design.To evaluate the therapeutic potential of this substance, we studied ACE2 in a piglet model of ALI induced by meconium aspiration.Subjects.Twelve anesthetized piglets were subjected in an animal research laboratory. ALI was induced by tracheal meconium instillation. Thereafter, six animals were randomly assigned to the ACE2 group, while another 6 served as control.Measurements.Systemic, pulmonary hemodynamic, and blood gas exchange parameters and Ang II levels were examined before ALI induction and at various time points after administering ACE2 or saline. In addition, ventilation-perfusion distribution of the lung was assessed by the multiple inert gas elimination technique (MIGET).Main Results.Animals treated with ACE2 maintained significantly higher arterial partial pressures of oxygen (Pao2) and lower arterial partial pressures of carbon dioxide (Paco2), respectively. Furthermore, Ang II, which was substantially increased, returned to basal values.Conclusion.In summary, ACE2 improves blood gas exchange in meconium-induced ALI in piglets.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-Converting Enzyme 2 Improves Arterial Hypoxemia in Meconium-Induced Acute Lung Injury in Piglets

Treml

Loeckinger

Kleinsasser

et al. 2015

Advances in Critical Care

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“…Captopril has been reported to decrease the level of TNFα , reduce alveolar wall thickening and neutrophil infiltration in rats with induced acute lung injury [33].…”

Section: Discussionmentioning

confidence: 99%

“…Captopril has been reported to decrease the level of TNFα [ 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 ], reduce alveolar wall thickening and neutrophil infiltration in rats with induced acute lung injury [ 33 ]. Our research supports the results of other studies on the reduction of TNFα by ACEI.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Activities of Captopril and Diuretics on Macrophage Activity in Mouse Humoral Immune Response

Bryniarski

Nazimek

Marcinkiewicz

2021

IJMS

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Hypertension is accompanied by the over-activation of macrophages. Diuretics administered alone or in combination with hypotensive drugs may have immunomodulatory effects. Thus, the influence of tested drugs on mouse macrophage-mediated humoral immunity was investigated. Mice were treated intraperitoneally with captopril (5 mg/kg) with or without hydrochlorothiazide (10 mg/kg) or furosemide (5 mg/kg) by 8 days. Mineral oil-induced peritoneal macrophages were harvested to assess the generation of cytokines in ELISA, and the expression of surface markers was analyzed cytometrically. Macrophages were also pulsed with sheep red blood cells (SRBC) and transferred to naive mice for evaluation of their ability to induce a humoral immune response. Tested drugs increase the expression of surface markers important for the antigen phagocytosis and presentation. SRBC-pulsed macrophages from mice treated with captopril combined with diuretics increased the secretion of antigen-specific antibodies by recipient B cells, while macrophages of mice treated with hydrochlorothiazide or furosemide with captopril increased the number of antigen-specific B cells. Tested drugs alter the macrophage secretory profile in favor of anti-inflammatory cytokines. Our results showed that diuretics with or without captopril modulate the humoral response by affecting the function of macrophages, which has significant translational potential in assessing the safety of antihypertensive therapy.

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“…Captopril is an orally active inhibitor of ACE which is widely used as an anti-hypertensive agent but it is known to modulate the neurohormonal system to reduce inflammation and preventing tissue fibrosis. However, the role of ACE inhibitor in the lungs is not well-understood (13). We, therefore, conducted this study to elucidate the severity of pulmonary involvement of oleic acid induced ARDS rats treated with captopril according to Berlin pathological criteria.…”

Section: Discussionmentioning

confidence: 99%

Investigating the effect of captopril on reducing the severity of symptoms of acute respiratory distress syndrome in rats

2021

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Introduction: Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in the lungs. Objectives: This study aimed to investigate the effect of captopril in reducing the symptoms of ARDS induced by oleic acid in experimental rats. Materials and Methods: This experimental study was conducted on 14 Wistar male rats of 6-7 weeks weighing 200-250 g. In the first group, they received 1.25 mg/kg of captopril daily in glucose solution for one week, but the second group did not. After one week, these rats were anesthetized by 5% isoflurane respiration and oleic acid (0.1 mg/kg) was injected intraperitoneal for ARDS induction. During the first 6 hours after starting ARDS, the rats were randomly selected and after anesthesia with ether and autopsy, they were cut and the lung histology was conducted. Results: Intensity of lung tissue edema in the group receiving captopril (Cap) was 2.83 ± 0.41 and in the captopril group with oleic acid (Cap+OA) was 2.50±0.55. Additionally, 83.3% of the rats had severe pulmonary edema in the OA group which was statistically significant (P=0.003). The "severity of inflammation and bleeding" in the OA+Cap group was significantly less than OA group (P=0.026). Conclusion: Captopril can play a significant role in reducing the damage of the lung tissue and severity of tissue edema and inflammation and bleeding. Therefore, it may be possible to use this drug in human samples with acute respiratory distress syndrome to prevent further damage.

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Effect of captopril on serum TNF-α level in acute lung injury rats induced by HCL

Abstract: Captopril can significantly reduce serum TNF-α level, elevate PaO2 and reduce PaCO2 in rats with ALI. It has a protective effect on ALI rats.

Cited by 7 publications

References 10 publications

Angiotensin-Converting Enzyme 2 Improves Arterial Hypoxemia in Meconium-Induced Acute Lung Injury in Piglets

Angiotensin-Converting Enzyme 2 Improves Arterial Hypoxemia in Meconium-Induced Acute Lung Injury in Piglets

Anti-Inflammatory Activities of Captopril and Diuretics on Macrophage Activity in Mouse Humoral Immune Response

Investigating the effect of captopril on reducing the severity of symptoms of acute respiratory distress syndrome in rats

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