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Research Article Open access CC BY 4.0

Five Different Noise Intensities Robustly Affects Corticosterone, Gastrin and Endothelin-1 Responses and Initiated Gastric Tissue Damage in Wistar Rats

Ravinder Kumar Mehra, Mahesh Prashad, Dinesh Kumar Sharma, Prevesh Kumar

Journal of Pharmaceutical Research International · pp. 54–69 · Published 8 Dec 2021

10.9734/jpri/2021/v33i54A33719

Abstract

Likewise other stress response noise stress is also affects the homeostasis of the biological systems and produce stress response in the form of Corticosterone to prevent the damage but if the exposure is longer with higher magnitude it may disrupt the robust ability of the homeostasis and could produce the damage to the biological systems. The goal of our study was to see how five different noise intensities affected stomach tissue damage. 42 healthy rats were divided into five different stress exposure group, normal control (NC) and sham control (SC) groups. Noise stress exposure was delivered for 1 hour per day continued for 30 days in all five noise exposed groups by specially designed noise chamber whereas sham control group of animals kept in noise chamber for 1 hour per day continued for 30 days without noise stress exposure and control group of animals neither exposed to noise stress of any intensities and nor kept in noise chamber without noise but remain in the same experimental room in their homecage for 30 days respectively. Results of the study showed that animals exposed to 60 and 80 dB noise give habituated and not significant Corticosterone, Gastrin and Endothelin-1 responses compared to NC and SC groups while animals exposed to 100, 120 and 140 dB had significantly higher Corticosterone, Gastrin and Endothelin-1 response and also chronic gastric damage was observed compared to later two noise exposed groups respectively. Study concluded that not only higher but also lower noise intensities also initiated the gastric damage even after the adaptation.

Noise stress noise exposure homeostasis corticosterone gastrin endothelin-1

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