Structural and functional remodeling of the female Apoe-/- mouse aorta due to chronic cigarette smoke exposure

2021 ◽  
Author(s):  
Yasmeen M. Farra ◽  
Jacqueline Matz ◽  
Bhama Ramkhelawon ◽  
Jessica M. Oakes ◽  
Chiara Bellini
Keyword(s):  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Cross Sectional ◽  
Fibrous Cap ◽  
Cardiovascular Morbidity And Mortality ◽  
Chronic Smoking ◽  
And Function ◽  
Thoracic And Abdominal

Despite a decline in popularity over the last several decades, cigarette smoking remains a leading cause of cardiovascular morbidity and mortality. Yet, the effects of cigarette smoking on vascular structure and function are largely unknown. To evaluate changes in the mechanical properties of the aorta that occur with chronic smoking, we exposed female Apolipoprotein E-deficient mice to mainstream cigarette smoke daily for 24 weeks, with room air as control. By the time of sacrifice, cigarette-exposed mice had lower body mass, but experienced larger systolic/diastolic blood pressure when compared to controls. Smoking was associated with significant wall thickening, reduced axial stretch, and circumferential material softening of the aorta. While this contributed to maintaining intrinsic tissue stiffness at control levels despite larger pressure loads, the structural stiffness became significantly larger. Furthermore, the aorta from cigarette-exposed mice exhibited decreased ability to store elastic energy and augment diastolic blood flow. Histological analysis revealed a region-dependent increase in the cross-sectional area due to smoking. Increased smooth muscle and extracellular matrix content led to medial thickening in the ascending aorta, while collagen deposition increased the thickness of the descending thoracic and abdominal aorta. Atherosclerotic lesions were larger in exposed vessels and featured a necrotic core overlaid by a thinned fibrous cap and macrophage infiltration, consistent with a vulnerable phenotype. Collectively, our data indicate that cigarette smoking decreases the mechanical functionality of the aorta, inflicts morphometric alterations to distinct segments of the aorta, and accelerates the progression of atherosclerosis.

Effects of lung volume, bronchoconstriction, and cigarette smoke on morphometric airway dimensions

1988 ◽  
Vol 64 (3) ◽  
pp. 913-919 ◽  
Author(s):  
A. L. James ◽  
P. D. Pare ◽  
J. C. Hogg
Keyword(s):  
Smooth Muscle ◽  
Cigarette Smoke ◽  
Lung Volume ◽  
Muscle Tone ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Airway Wall ◽  
Lung Inflation ◽  
Wall Area ◽  
Airway Dimensions

To examine the role of airway wall thickening in the bronchial hyperresponsiveness observed after exposure to cigarette smoke, we compared the airway dimensions of guinea pigs exposed to smoke (n = 7) or air (n = 7). After exposure the animals were anesthetized with urethan, pulmonary resistance was measured, and the lungs were removed, distended with Formalin, and fixed near functional residual capacity. The effects of lung inflation and bronchoconstriction on airway dimensions were studied separately by distending and fixing lungs with Formalin at total lung capacity (TLC) (n = 3), 50% TLC (n = 3), and 25% TLC (n = 3) or near residual volume after bronchoconstriction (n = 3). On transverse sections of extraparenchymal and intraparenchymal airways the following dimensions were measured: the internal area (Ai) and internal perimeter (Pi), defined by the epithelium, and the external area (Ae) and external perimeter (Pe), defined by the outer border of smooth muscle. Airway wall area (WA) was then calculated, WA = Ae - Ai. Ai, Pe, and Ae decreased with decreasing lung volume and after bronchoconstriction. However, WA and Pi did not change significantly with lung volume or after bronchoconstriction. After cigarette smoke exposure airway resistance was increased (P less than 0.05); however, there was no difference in WA between the smoke- and air-exposed groups when the airways were matched by Pi. We conclude that Pi and WA are constant despite changes in lung volume and smooth muscle tone and that airway hyperresponsiveness induced by cigarette smoke is not mediated by increased airway wall thickness.

scholarly journals Smoking-Induced Inhibition of Number and Activity of Endothelial Progenitor Cells and Nitric Oxide in Males Were Reversed by Estradiol in Premenopausal Females

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yijia Shao ◽  
Liang Luo ◽  
Zi Ren ◽  
Jiayi Guo ◽  
Xingxing Xiao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cigarette Smoking ◽  
Premenopausal Women ◽  
Cross Sectional Study ◽  
Favorable Effect ◽  
No Production ◽  
Vascular Protection ◽  
Cross Sectional ◽  
And Function ◽  
Flow Mediated Vasodilation

Objectives. The number and activity of circulating EPCs were enhanced in premenopausal women contrast to postmenopausal females and age-matched males. Here, we investigated whether this favorable effect exists in premenopausal women and age-matched men with cigarette smoking. Methods. In a cross-sectional study, the number and activity of circulating EPCs and nitric oxide production (NO) as well as flow-mediated vasodilation (FMD) in both premenopausal women and age-matched men with or without cigarette smoking were studied. Results. Compared with age-matched men with or without smoking, the number and function of circulating EPCs as well as NO level in premenopausal women were obviously higher than that in the former and not affected by smoking. The number and function of circulating EPCs as well as NO level in male smokers were shown to be the most strongly inhibited. Furthermore, there was significant correlation between EPC number and activity, plasma NO level, and NO secretion by EPCs and FMD. Conclusions. Estradiol was deemed to play an important role in enhancing the number and activity of EPCs and NO production in premenopausal women even when affected by smoking, which may be the important mechanisms underlying vascular protection of estradiol in premenopausal women, but not in age-matched men.

scholarly journals Impact of acute exposure to cigarette smoke on airway gene expression

2018 ◽  
Vol 50 (9) ◽  
pp. 705-713 ◽  
Author(s):  
E. Billatos ◽  
A. Faiz ◽  
Y. Gesthalter ◽  
A. LeClerc ◽  
Y. O. Alekseyev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lung Cancer ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Acute Exposure ◽  
Cigarette Smoke Exposure ◽  
Airway Epithelial ◽  
Long Term Effects ◽  
Chronic Smoking

Background: Understanding effects of acute smoke exposure (ASE) on airway epithelial gene expression and their relationship with the effects of chronic smoke exposure may provide biological insights into the development of smoking-related respiratory diseases. Methods: Bronchial airway epithelial cell brushings were collected from 63 individuals without recent cigarette smoke exposure and before and 24 h after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Results: We identified 91 genes differentially expressed 24 h after ASE (false discovery rate < 0.25). ASE induced genes involved in xenobiotic metabolism, oxidative stress, and inflammation and repressed genes related to cilium morphogenesis and cell cycle. While many genes altered by ASE are altered similarly in chronic smokers, metallothionein genes are induced by ASE and suppressed in chronic smokers. Metallothioneins are also suppressed in current and former smokers with lung cancer relative to those without lung cancer. Conclusions: Acute exposure to as little as three cigarettes and chronic smoking induce largely concordant changes in airway epithelial gene expression. Differences in short-term and long-term effects of smoking on metallothionein expression and their relationship to lung cancer requires further study given these enzymes’ role in the oxidative stress response.

Smoking-Related “Interstitial” Lung Disease

2014 ◽  
Vol 139 (8) ◽  
pp. 974-977 ◽  
Author(s):  
Teri J. Franks ◽  
Jeffrey R. Galvin
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Cigarette Smoke Exposure ◽  
Wall Thickening ◽  
Alveolar Wall ◽  
Cigarette Smokers ◽  
Pulmonary Langerhans Cell Histiocytosis ◽  
Airway Injury ◽  
Wide Range ◽  
Arteriolar Wall

Context Emphysema, respiratory bronchiolitis, desquamative interstitial pneumonia, pulmonary Langerhans' cell histiocytosis, small-airway injury including submucosal and adventitial fibrosis, increased bronchus-associated lymphoid tissue, and small artery/arteriolar wall thickening are recognized histologic findings in cigarette smokers. It has only recently been acknowledged that the range of lung injury from cigarette smoke is wider than generally accepted, in particular, there is increasing recognition that fibrosis of alveolar walls occurs in smokers. Objectives To review the literature that describes the range of histologic findings in cigarette smokers and that links cigarette smoke exposure to the development of alveolar wall fibrosis. Data Sources Relevant peer-reviewed literature indexed in PubMed (National Library of Medicine) form the basis of this review. Conclusions Smokers demonstrate a wide range of lung injury at biopsy that defies simple placement within single categories, and the current categories do not adequately take into account the importance of alveolar wall and airway fibrosis.

scholarly journals p19Arf Exacerbates Cigarette Smoke-Induced Pulmonary Dysfunction

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 462
Author(s):  
Ryuta Mikawa ◽  
Tadashi Sato ◽  
Yohei Suzuki ◽  
Hario Baskoro ◽  
Koichiro Kawaguchi ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cellular Senescence ◽  
Cigarette Smoke Extract ◽  
Senescent Cell ◽  
Cigarette Smoke Exposure ◽  
Pulmonary Dysfunction ◽  
Potential Therapeutic Target ◽  
Tissue Compliance

Senescent cells accumulate in tissues during aging or pathological settings. The semi-genetic or pharmacological targeting of senescent cells revealed that cellular senescence underlies many aspects of the aging-associated phenotype and diseases. We previously reported that cellular senescence contributes to aging- and disease-associated pulmonary dysfunction. We herein report that the elimination of Arf-expressing cells ameliorates cigarette smoke-induced lung pathologies in mice. Cigarette smoke induced the expression of Ink4a and Arf in lung tissue with concomitant increases in lung tissue compliance and alveolar airspace. The elimination of Arf-expressing cells prior to cigarette smoke exposure protected against these changes. Furthermore, the administration of cigarette smoke extract lead to pulmonary dysfunction, which was ameliorated by subsequent senescent cell elimination. Collectively, these results suggest that senescent cells are a potential therapeutic target for cigarette smoking-associated lung disease.

scholarly journals Cigarette smoke exposure and alveolar macrophages: mechanisms for lung disease

Thorax ◽  
2021 ◽  
pp. thoraxjnl-2020-216296
Author(s):  
Sebastian T Lugg ◽  
Aaron Scott ◽  
Dhruv Parekh ◽  
Babu Naidu ◽  
David R Thickett
Keyword(s):  
Cigarette Smoking ◽  
Lung Injury ◽  
Lung Disease ◽  
Alveolar Macrophage ◽  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Iron Homeostasis ◽  
Cigarette Smoke Exposure ◽  
Bacterial Killing ◽  
Macrophage Populations

Cigarette smoking is the leading cause of preventable death worldwide. It causes chronic lung disease and predisposes individuals to acute lung injury and pulmonary infection. Alveolar macrophages are sentinel cells strategically positioned in the interface between the airway lumen and the alveolar spaces. These are the most abundant immune cells and are the first line of defence against inhaled particulates and pathogens. Recently, there has been a better understanding about the ontogeny, phenotype and function of alveolar macrophages and their role, not only in phagocytosis, but also in initiating and resolving immune response. Many of the functions of the alveolar macrophage have been shown to be dysregulated following exposure to cigarette smoke. While the mechanisms for these changes remain poorly understood, they are important in the understanding of cigarette smoking-induced lung disease. We review the mechanisms by which smoking influences alveolar macrophage: (1) recruitment, (2) phenotype, (3) immune function (bacterial killing, phagocytosis, proteinase/anti-proteinase release and reactive oxygen species production) and (4) homeostasis (surfactant/lipid processing, iron homeostasis and efferocytosis). Further understanding of the mechanisms of cigarette smoking on alveolar macrophages and other lung monocyte/macrophage populations may allow novel ways of restoring cellular function in those patients who have stopped smoking in order to reduce the risk of subsequent infection or further lung injury.

Cigarette smoking delays ulcer healing: role of constitutive nitric oxide synthase in rat stomach

1999 ◽  
Vol 276 (1) ◽  
pp. G238-G248 ◽  
Author(s):  
Li Ma ◽  
Jimmy Yip Chuen Chow ◽  
Chi Hin Cho
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Ulcer Healing ◽  
Gastric Blood Flow ◽  
Cigarette Smoke Exposure ◽  
Ulcer Margin ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase

Epidemiological studies have shown that cigarette smoking is associated with peptic ulceration. This study aims to investigate the mechanisms by which cigarette smoking delays ulcer healing in rats. Gastric ulcers were induced by applying acetic acid to the luminal surfaces in rats. Twenty-four hours later, rats were exposed to different concentrations of cigarette smoke (0, 2, or 4%) for a 1-h period once daily for 3 or 6 days. Cigarette smoke exposure delayed ulcer healing and decreased gastric blood flow and angiogenesis at the ulcer margin. These changes were accompanied by a significant reduction of constitutive nitric oxide synthase (cNOS) activity but not PGE2 production and vascular endothelial growth factor levels. Administration ofl-arginine (10 mg/kg iv) completely reversed the adverse actions on ulcer healing, gastric blood flow, and angiogenesis in the mucosa at the ulcer margin but partially restored angiogenesis in granulation tissues. In conclusion, cigarette smoke exposure delays ulcer healing through depression of gastric blood flow and angiogenesis at the ulcer margin. Reduction of cNOS expression and activity is suggested to be involved in these ulcerogenic processes.

Hyperhomocysteinemia leads to pathological ventricular hypertrophy in normotensive rats

2003 ◽  
Vol 285 (2) ◽  
pp. H679-H686 ◽  
Author(s):  
Jacob Joseph ◽  
Lija Joseph ◽  
Nawal S. Shekhawat ◽  
Sulochana Devi ◽  
Junru Wang ◽  
...  
Keyword(s):  
Cardiac Remodeling ◽  
Ventricular Hypertrophy ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Left Ventricular ◽  
Lv Function ◽  
Wall Thickening ◽  
Cardiovascular Morbidity And Mortality ◽  
And Function

A recent report indicated that hyperhomocysteinemia (Hhe), in addition to its atherothrombotic effects, exacerbates the adverse cardiac remodeling seen in response to hypertension, a powerful stimulus for pathological ventricular hypertrophy. The present study was undertaken to determine whether Hhe has a direct effect on ventricular remodeling and function in the absence of other hypertrophic stimuli. Male Wistar-Kyoto rats were fed either an amino acid-defined control diet or an intermediate Hhe-inducing diet. After 10 wk of dietary treatment, rats were subjected to echocardiographic assessment of left ventricular (LV) dimensions and systolic function. Subsequently, blood was collected for plasma homocysteine measurements, and the rats were killed for histomorphometric and biochemical assessment of cardiac remodeling and for in vitro cardiac function studies. Significant LV hypertrophy was detected by echocardiographic measurements, and in vitro results showed hypertrophy with significantly increased myocyte size in the LV and right ventricle (RV). LV and RV remodeling was characterized by a disproportionate increase in perivascular and interstitial collagen, coronary arteriolar wall thickening, and myocardial mast cell infiltration. In vitro study of LV function demonstrated abnormal diastolic function secondary to decreased compliance because the rate of relaxation did not differ between groups. LV systolic function did not vary between groups in vitro. In summary, in the absence of other hypertrophic stimuli short-term intermediate Hhe caused pathological hypertrophy and remodeling of both ventricles with diastolic dysfunction of the LV. These results demonstrate that Hhe has direct adverse effects on cardiac structure and function, which may represent a novel direct link between Hhe and cardiovascular morbidity and mortality, independent of other risk factors.

scholarly journals Bacoside A: Role in Cigarette Smoking Induced Changes in Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
G. Vani ◽  
K. Anbarasi ◽  
C. S. Shyamaladevi
Keyword(s):  
Cigarette Smoking ◽  
Rat Brain ◽  
Cigarette Smoke ◽  
Passive Smoking ◽  
Experimental Studies ◽  
Smoke Exposure ◽  
Pharmacological Intervention ◽  
Cigarette Smoke Exposure ◽  
Bacoside A ◽  
Mitochondrial Functions

Cigarette smoking (CS) is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA) on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated fromBacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke.

Sign in / Sign up

Export Citation Format

Share Document