Evidence for angiotensin mediation of the late histopathological effects of pulmonary fat embolism: Protection by losartan in a rat model

Poisner, Alan M.; Bass, Devin; Fletcher, Amanda N.; Jain, Ashwin; England, Janessa Pennington; Davis, M.; Arif, Dauod; Molteni, Agostino

doi:10.1080/01902148.2018.1552339

Cited by 8 publications

(6 citation statements)

References 13 publications

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“…In one, we gave the AT1 blocker losartan 6 weeks after the triolein injection and examined the rats 4 weeks later. In this experiment the protective effect of losartan was still demonstrated at this late stage, supporting the view of continued activation of the RAS [96]. In another study we found that 24 and 48 hours after triolein there was an increase in renin staining in lungs that diminished but was still present at 3 and 6 weeks [97].…”

Section: Effect Of Ras Drugs On Pulmonary Fat Embolismsupporting

confidence: 82%

From Angiotensin to Renin to Prorenin and from the Adrenal to the Kidney to the Placenta and the Lungs: An Historical Journey

Poisner¹

2020

Selected Chapters From the Renin-Angiotensin System

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In 1966 I carried out a study on the role of calcium on angiotensin's stimulant effects on the adrenal medulla. Since then I have been studying the reninangiotensin system (RAS) for over a half-century in a wide variety of biological preparations, while awareness of its complexity has exploded. My journey has involved studies on genes, proteins, organelles, cells, tissues, glands, organs and whole animals. This chapter reviews what my colleagues and I have learned from these different levels of organization and is not meant to be an update on all features of the RAS. My studies have included experiments on: perfused cat adrenal glands; genetic and second messenger control of catecholamine synthesis and secretion from cultured bovine chromaffin cells and from rats in vivo; renin storage and release in the rat kidney and secretory granules; properties of isolated renin, prorenin and renin-like proteins; hormonal and second messenger control of prorenin secretion from human utero-placental tissues; renin/prorenin in a variety of tumors; and the effect of RAS drugs in a rodent model of pulmonary fat embolism. This most recent study has direct clinical application. I conclude with what I have learned about biomedical research and lessons for the future.

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Section: Effect Of Ras Drugs On Pulmonary Fat Embolismsupporting

confidence: 82%

From Angiotensin to Renin to Prorenin and from the Adrenal to the Kidney to the Placenta and the Lungs: An Historical Journey

Poisner¹

2020

Selected Chapters From the Renin-Angiotensin System

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“…In both studies, the interference of RAS reduced the inflammatory, vasoconstrictor and profibrotic effects at 48 hours in the lungs for fat embolism (FE) syndrome besides the vascular lumen remaining patent, and the reduction in size and number of fat droplets [ 21 ]. The ARB losartan was also shown to block the late phase of fat embolism beyond six weeks indicating involvement of RAS in late as well as early stages of histopathological changes following fat embolism [ 40 ]. The pulmonary pathology in this animal model was found to be parallel to that found in a fatal case of fat embolism syndrome in a patient who developed respiratory failure after caesarean delivery [ 41 - 42 ].…”

Section: Discussionmentioning

confidence: 99%

Renin-Angiotensin Blockade Reduces Readmission for Acute Chest Syndrome in Sickle Cell Disease

Wamkpah¹,

Shrestha²,

Salzman³

et al. 2022

Cureus

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Rationale Acute chest syndrome (ACS) is a life-threatening complication of sickle cell disease (SCD). Current treatment is supportive-supplemental oxygen, transfusions, and antibiotics. Prevention of ACS may reduce morbidity and mortality in patients with SCD. Acute chest syndrome appears similar to pulmonary fat embolism (PFE), a complication of severe skeletal trauma or orthopedic procedures from pulmonary micro-vessel blockage by bone marrow fat. Vascular obstruction and bone marrow necrosis occur in PFE and ACS. Pulmonary fat embolism rat models have shown that angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) mitigate damage in PFE. These medications could work similarly in ACS. We hypothesize that time to readmission after one hospitalization for ACS will be reduced in patients taking ACEI or ARB compared to patients who are not. Methods This is a retrospective cohort study. Inclusion criteria are adults (18 to 100 years) with sickle cell anaemia (HbSS), hemoglobin SC (HbSC) disease, sickle cell thalassemia (HbSβThal), hospitalized with ACS over 16 years (January 1, 2000, to March 31, 2016); patients who take and don’t take ACEI or ARB. Children (<18 years old), elderly adults (>100 years old), pregnant patients, and patients with sickle cell trait were excluded. Data was collected from the Health Facts database, which contains de-identified information from the electronic medical records of hospitals in which Cerner© has a data use agreement. Kaplan-Meier estimates explored a time-to-event model of ACS readmission. Multivariable analysis (age, gender, smoking history) was conducted using Cox proportional hazards regression. Results were reported around a 95% confidence interval. Results There were 6972 patients in total. Of which, 9.6% (n = 667) reported taking ACEI or ARB. Results for the covariates were: average age of 38 years old; 63% female (n = 4366/6969); 16% smokers (n = 1132). Readmission rates were higher for patients not taking ACEI/ARB than those who did: 0.44 (95% CI 0.43, 0.46) versus 0.28 (95% CI 0.24, 0.31) at one year, and 0.56 (95% CI 0.55, 0.58) versus 0.33 (95% CI 0.29, 0.37) at two years. Age had the strongest effect on readmission rates for patients taking ACEI/ARB (adjusted hazards ratio 0.78 [95% CI 0.68, 0.91]). Conclusion Patients with SCD who reported taking ACEI or ARB had lower readmission rates for ACS; age was the strongest covariate. Our results may have a significant impact on the prevention of ACS. Prospective studies comparing ACEI or ARB therapy versus placebo are needed to confirm this preventative effect.

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“…sc-53142, Santa Cruz Biotechnology, Dallas, Texas) and 1:25 CD68 (Catalog No. sc-17832, Santa Cruz Biotechnology, Dallas, TX, USA) primary antibody at room temperature for half an hour [16,17] . Later, secondary antibody was added for 10 minutes.…”

Section: Alpha Smooth Muscle Actin (α-Sma) and Cluster Of Differentia...mentioning

confidence: 99%

The possible protective effect of magnolol on triolein-induced lung structural changes in rats: Histological and immunohistochemical study

Kandeel

Estfanous

2021

Egyptian Journal of Histology

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Introduction:Triolein is a neutral fat derives from an oleic acid. It has been used as a textile lubricant, a plasticizer and present in cocoa butter. Its occupational exposure lead to health hazards especially lung injury. Magnolol is a Chinese herbal complex with anti-inflammatory, antioxidant and antifibrotic actions. Aim: The present research aimed to evaluate the possible protective effect of magnolol on triolein-induced lung structural changes in rats using histological and immunohistochemical study. Materials and Methods: 45 male Wistar rats were used. Their weights were from 120 to 150 gm. They were divided into Group 1 (15 rats as control group); Group 2: 15 rats that received 0.2 ml triolein at the caudal vein then were sacrificed after 2, 4 and 21 days; Group 3: 15 rats that received 50 mg/kg oral dose of magnolol daily 60 minutes before giving triolein then were sacrificed after 2, 4 and 21 days. Results: Group 2 showed significant thickened inter-alveolar septa, inflammatory cellular infiltrations, congested blood vessels, luminal inflammatory exudates, disorganized sloughed epithelium and lost cilia at H&E stained sections. Group 2 also showed significantly increased deposition of collagen fibers, significantly increased expression of alpha -Smooth muscle actin (α-SMA) in the interalveolar septa, wall of the blood vessels and bronchioles and significant increase in the number of macrophages with positive CD68 (Cluster of Differentiation 68) immunohistochemical reaction. Group 3 showed improvements of the previous pathological findings. Conclusion: Magnolol could protect the lung from the injurious effect of triolein possibly due to its anti-inflammatory, antioxidant and antifibrotic actions. This may favor the use of magnolol for the treatment of lung injuries.

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Evidence for angiotensin mediation of the late histopathological effects of pulmonary fat embolism: Protection by losartan in a rat model

Cited by 8 publications

References 13 publications

From Angiotensin to Renin to Prorenin and from the Adrenal to the Kidney to the Placenta and the Lungs: An Historical Journey

From Angiotensin to Renin to Prorenin and from the Adrenal to the Kidney to the Placenta and the Lungs: An Historical Journey

Renin-Angiotensin Blockade Reduces Readmission for Acute Chest Syndrome in Sickle Cell Disease

The possible protective effect of magnolol on triolein-induced lung structural changes in rats: Histological and immunohistochemical study

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