Lousinha, A. et al. Histomorphometric Evaluation of the Small Coronary Arteries in Rats Exposed to Industrial Noise
International Journal of Molecular Sciences
Int. J. Mol. Sci. 2015, 16, 10095-10104; doi:10.3390/ijms160510095
Published: 4 May 2015
“It will be our challenge in the future to understand the clinical impact on cardiac diseases among humans exposed to industrial and low-frequency noise.”
Discussion
A number of animal studies found modifications in several tissues induced by low-frequency noise, characterized by abnormal deposition of collagen in the extracellular matrices.
In the present study we found an increase in the perivascular tissue around the small coronary arteries in rats exposed to IN [industrial noise]. This is in agreement with the previous findings of our group, concerning the histomorphometric evaluation of the coronary arterial vessels in rats exposed to industrial noise. In both studies we found the development of perivascular fibrosis in the absence of inflammatory cells and in the absence of obstructive coronary artery disease…
A previous review of epidemiological studies concerning environmental noise exposure (including road and aircraft noise sources) and cardiovascular risk reported increasing evidence relating noise and hypertension and ischemic heart disease, making pertinent to investigate the effects of IN on the heart.
Thus far, we documented that coronary artery vessels showed prominent perivascular tissue and fibrotic development among IN-exposed rats and also a significant fibrotic development in ventricular myocardium of rats exposed to LFN. Considering that these structural changes ultimately lead to myocardial stiffness and left ventricular disfunction and possibly to cardiac heart failure and arrhythmias, 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, reinforcing the hypothesis of an inducible morphological arrhythmogenic substrate. The present study allowed the documentation of structural changes induced by industrial noise on the rat heart small arteries, suggesting a general influence of industrial noise over the heart…
The changes in the structure of coronary resistance vessels, with quantitative characterization of small coronary arteries and arterioles in the myocardium, have been extensively studied under several experimental conditions and were already extended to humans. Cardiac hypertrophy in hypertension, with an increase in left ventricular mass, is characterised by increased wall thickness in arterioles and small arteries, increased lumen to wall ratio, and decreased number of capillary profiles per arteriole in cross section. Volume overload-induced cardiac hypertrophy is characterized by normal coronary reserve and maximal flow and there is evidence that both arteriolar and capillary growth is proportional to the magnitude of hypertrophy. Pathologic findings have described diabetic cardiomyopathy as a microvascular disease and previous studies have demonstrated that structural changes of coronary microvessels in diabetes include thickening of the vascular wall, perivascular fibrosis, capillary aneurysms, and decrease in capillary density. Several structural abnormalities of the heart are present in chronic renal failure, including arteriolar thickening, reduced capillary density, and interstitial fibrosis. These findings contribute to myocardial ischemia, left ventricular wall stiffness, diastolic dysfunction, and arrhythmogenicity in patients with renal failure.
It will be our challenge in the future to understand the clinical impact on cardiac diseases among humans exposed to industrial and low-frequency noise.
We are aware of several limitations of the study. We admit that interpretation of the results must be done cautiously because, for logistical reasons, the number of animals per group was limited. Additionally, small coronary arteries in biopsy samples were partially crushed during the procedure, which might have affected the quantitative analyses of lumen area and perivascular tissue. Furthermore, we acknowledge that at the present time there is not a well-defined morphological cardiac model induced by industrial noise. Thus far, we have limited our observations to the structural modifications induced by industrial noise or by low-frequency noise in the myocardium of rat heart and can only extrapolate these observations to humans, with all the existing limitations. The experimental conditions tried to simulate the schedule of industrial plant workers, characterized by 8 hours/day, 5 days/week of exposure to industrial noise. Once again, we reinforce the need of clinical investigations concerning the effects of industrial and low-frequency noise on the heart.