Abstract
Morphological changes induced by industrial noise (IN) have been experimentally observed in several organs. Histological observations of the coronary arteries showed prominent perivascular tissue and fibrosis among IN-exposed rats. The effects on the small arteries are unknown. Objective: To evaluate the histomorphometric changes induced by IN on rat heart small arteries. Methods: Twenty Wistar rats exposed to IN during a maximum period of seven months and 20 age-matched controls were studied. Hearts were transversely sectioned from ventricular apex to atria and a mid-ventricular fragment was selected for analysis. The histological images were obtained with an optical microscope using 400× magnifications. A total of 634 arterial vessels (298 IN-exposed and 336 controls) were selected. The mean lumen-to-vessel wall (L/W) and mean vessel wall-to-perivascular tissue (W/P) ratios were calculated using image J software. Results: There were no differences between exposed and control animals in their L/W ratios (p = 0.687) and time variations in this ratio were non-significant (p = 0.110). In contrast, exposed animals showed lower W/P ratios than control animals (p < 0.001), with significant time variations (p = 0.004). Conclusions: Industrial noise induced an increase in the perivascular tissue of rat small coronary arteries, with significant development of periarterial fibrosis.
Highlights
Industrial noise (IN) is characterized by high intensity and a wide spectrum of wavelengths that includes low-frequency noise (LFN), this last characterized by large pressure amplitude ≥90 dB and low-frequency bands of ≤500 Hz [1]
We previously reported that coronary artery vessels showed prominent perivascular tissue and fibrotic development among IN-exposed rats [2] and a significant fibrotic development in ventricular myocardium of rats exposed to LFN [3]
We found no differences in the lumen-to-vessel wall (L/W) ratio between exposed and non-exposed animals
Summary
Industrial noise (IN) is characterized by high intensity and a wide spectrum of wavelengths that includes low-frequency noise (LFN), this last characterized by large pressure amplitude ≥90 dB and low-frequency bands of ≤500 Hz [1]. Considering the epidemiological evidence relating noise to ischemic heart disease and hypertension [8] and the effects of LFN on the extracellular matrix between the cardiomyocytes and around the cardiac vessels, which lead to myocardial stiffness and left ventricular disfunction and possibly to cardiac heart failure and arrhythmias [9,10], additional studies were performed. These showed a reduction of cardiac connexin 43 and a significant increase of cardiac collagen I and III after LFN exposure [4,5], reinforcing the hypothesis of an inducible morphological arrhythmogenic substrate.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
