Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress

Said, Mona A.; El-Gohary, Ola A

doi:10.4149/gpb_2016003

Cited by 66 publications

(52 citation statements)

References 32 publications

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“…Overall, the present systematic review found clear evidence of a relationship between occupational noise exposure and the risk of hypertension. We assess the causality between exposure to occupational noise and the development of hypertension according to Hill [ 76 ], as follows: Mechanistic studies demonstrate an increased excretion of blood pressure-increasing hormones, such as adrenaline and noradrenaline in noise-exposed workers [ 26 , 27 ], and animal studies [ 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ] support the biological plausibility of the link. Further evidence of a dose-response relationship between the level of occupational noise exposure and risk of hypertension supports the association.…”

Section: Discussionmentioning

confidence: 99%

“…Various animal studies report correlations between acute [ 6 , 7 , 8 , 9 ] or chronic noise exposures [ 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ] and an increase of blood pressure. On the other hand, four experimental studies found no association between noise and blood pressure increase [ 21 , 22 , 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

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Occupational Noise and Hypertension Risk: A Systematic Review and Meta-Analysis

Bolm‐Audorff

Hegewald

Pretzsch

et al. 2020

IJERPH

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A number of epidemiological studies report an association between occupational noise exposure and arterial hypertension. Existing systematic reviews report conflicting results, so we conducted an updated systematic review with meta-analysis. We registered the review protocol with PROSPERO (registration no.: CRD 42019147923) and searched for observational epidemiological studies in literature databases (Medline, Embase, Scopus, Web of Science). Two independent reviewers screened the titles/abstracts and full texts of the studies. Two reviewers also did the quality assessment and data extraction. Studies without adequate information on recruitment, response, or without a comparison group that was exposed to occupational noise under 80 dB(A) were excluded. The literature search yielded 4583 studies, and 58 studies were found through hand searching. Twenty-four studies were included in the review. The meta-analysis found a pooled effect size (ES) for hypertension (systolic/diastolic blood pressure ≥140/90 mmHg) due to noise exposures ≥80 dB(A) of 1.81 (95% CI 1.51–2.18). There is no substantial risk difference between men and women, but data concerning this question are limited. We found a positive dose-response-relationship: ES = 1.21 (95% CI 0.78–1.87) ≤ 80 dB(A), ES = 1.77 (95% CI 1.36–2.29) > 80–≤85 dB(A), and ES = 3.50 (95% CI 1.56–7.86) > 85–≤90 dB(A). We found high quality of evidence that occupational noise exposure increases the risk of hypertension.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Occupational Noise and Hypertension Risk: A Systematic Review and Meta-Analysis

Bolm‐Audorff

Hegewald

Pretzsch

et al. 2020

IJERPH

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“…Increased release of stress hormones, activation of sympathetic nervous system, increased reactive oxygen species production, endothelial dysfunction, peripheral vasoconstriction, increased peripheral vascular resistance, and increased blood viscosity are among the proposed mechanisms elicited by acute or chronic noise stress leading to detrimental outcomes on the cardiovascular system [7,9,38]. Following this line of investigation, Said and El-Gohary studied the effect of noise in the 80-100-dB range on heart rate and mean systemic arterial blood pressure in adult male albino rats and explored possible underlying mechanisms [39]. They concluded that noise stress has many adverse effects on cardiovascular system through increasing plasma levels of stress hormones, oxidative stress, and endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Infrasound induces coronary perivascular fibrosis in rats

Lousinha

Oliveira

Borrecho

et al. 2018

Cardiovascular Pathology

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Background: Chronic exposure to industrial noise is known to affect biological systems, namely, by inducing fibrosis in the absence of inflammatory cells. In rat hearts exposed to this environmental hazard, we have previously found myocardial and perivascular fibrosis. The acoustic spectrum of industrial environments is particularly rich in high-intensity infrasound (b20 Hz), whose effects on the heart are unknown. We evaluated the morphological changes induced by IFS in rat coronaries in the presence and absence of dexamethasone. Methods: Adult Wistar rats were divided into three groups: group A (GA)-IFS (b20 Hz, 120 dB)-exposed rats for 28 days treated with dexamethasone; group B (GB)-IFS-exposed rats; group C (GC)-age-matched controls. The midventricle was prepared for observation with an optical microscope using 100× magnification. Thirty-one arterial vessels were selected (GA 8, GB 10, GC 13). The vessel caliber, thickness of the wall, and perivascular dimensions were quantified using image J software. Mann-Whitney and Kruskal-Wallis tests were used to compare the groups for lumen-to-vessel wall (L/W) and vessel wall-to-perivascular tissue (W/P) ratios. Results: IFS-exposed rats exhibited a prominent perivascular tissue. The median L/W and median W/P ratios were 0.54 and 0.48, 0.66 and 0.49, and 0.71 and 0.68, respectively, in GA, GB, and GC. The W/P ratio was significantly higher in GC compared with IFS-exposed animals (P=.001). The difference was significant between GC and GB (P=.008) but not between GC and GA. Conclusion: IFS induces coronary perivascular fibrosis that differs under treatment with corticosteroid.

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“…150 In animal models, chronic exposure to continuous noise (80–100 dB) has been reported to increase heart rate and mean systemic arterial blood pressure, functional changes that were associated with an increase in plasma corticosterone, adrenaline and endothelin-1. 151 Therefore, it is not surprising that exposure to environmental noise has been found to be associated with increased CVD risk in several epidemiological studies. In a recent meta-analysis of 14 studies on the association between road traffic noise and CHD, the pooled estimate of RR was found to be 1.08.…”

Section: The Social Environmentmentioning

confidence: 99%

Environmental Determinants of Cardiovascular Disease

Bhatnagar

2017

Circulation Research

432

268

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Many features of the environment have been found to exert an important influence on cardiovascular disease (CVD) risk, progression, and severity. Changes in the environment due to migration to different geographic locations, modifications in lifestyle choices, and shifts in social policies and cultural practices alter CVD risk, even in the absence of genetic changes. Nevertheless, the cumulative impact of the environment on CVD risk has been difficult to assess and the mechanisms by which some environment factors influence CVD remain obscure. Human environments are complex; and their natural, social and personal domains are highly variable due to diversity in human ecosystems, evolutionary histories, social structures, and individual choices. Accumulating evidence supports the notion that ecological features such as the diurnal cycles of light and day, sunlight exposure, seasons, and geographic characteristics of the natural environment such altitude, latitude and greenspaces are important determinants of cardiovascular health and CVD risk. In highly developed societies, the influence of the natural environment is moderated by the physical characteristics of the social environments such as the built environment and pollution, as well as by socioeconomic status and social networks. These attributes of the social environment shape lifestyle choices that significantly modify CVD risk. An understanding of how different domains of the environment, individually and collectively, affect CVD risk could lead to a better appraisal of CVD, and aid in the development of new preventive and therapeutic strategies to limit the increasingly high global burden of heart disease and stroke.

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Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress

Cited by 66 publications

References 32 publications

Occupational Noise and Hypertension Risk: A Systematic Review and Meta-Analysis

Occupational Noise and Hypertension Risk: A Systematic Review and Meta-Analysis

Infrasound induces coronary perivascular fibrosis in rats

Environmental Determinants of Cardiovascular Disease

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