ORIGINAL�ARTICLE

ABSTRACT
Objective : To observe how loud noise affects the growth of new blood vessels in rat skin wounds. 
Study Design :QUASI experimental study. 

th
Place and Duration of Study: The study was conducted at National Institute of Health Islamabad from 28   June 

th 
2017 to 28 February 2018.
Materials and Methods: Thirty male Sprague Dawley rats were split into control and experimental groups by 
convenient sampling, with 15 animals belonging to each leading group. On the dorsum of each rat, a 2 cm 
incision was created. While experimental subgroups endured 4h/d intermittent noise exposure of 85-95db five 
days a week for two consecutive weeks, control subgroup rats were left to heal with routine background noise 
exposure. On days 3, 7, and 14, five rats from each group were slaughtered. Wounds were excised, repaired, 
and prepared for H&E stain before being able to see and count the freshly grown blood vessels. 
Results: Although difference in mean number of newly formed blood vessels among both control and 
experimental group was found with more numbers in control group but it was not statistically significant.
Conclusion: Intermittent noise exposure has tendency to impair the process of angiogenesis thus delaying 
wound healing.

Key Words: Angiogenesis, Noise, Skin Wound, Stimulator, Inhibitor.

exposure between 70 and 100 dB is believed to cause 
structural alterations in the vasculature as well as 
morphological changes due to an increase in stress 

3
hormone and lipid peroxidation.  The sympathetic 
nervous system is activated as a result of elevated 
levels of epinephrine and norepinephrine, 

4
angiotensin II.  Angiotensin ii in turn activates 
NADPH oxidase, which is responsible for oxidation 
stress in vasculature. Angiogenesis is integral to 
successful wound repair involves, budding from 

5
capillaries of wound edge.  Soon after the invasion 
into damaged site newly formed vessels appear as a 
network to nourish the tissue and helps in formation 

6
of granulation tissue.  Formation of granulation 
tissue from the wound edge involves immigration of 

7
local fibroblast and lying down of fibrin network.  
Sprouting of capillaries initiates neovascularization 

8
and angiogenesis  Previously noise exposed .
subjects showed more pronounced association 

9
between noise and endothelial functions.  Although 
significant efforts have been made in the past to 

10
address the issue of delayed wound healing , further 
research on the angiogenesis process is still required 
to identify all the factors that contribute to the delay. 
Present study by demonstrating  all stressors that 
harm the physical environment will aid in effective 
wound healing and, more specifically, by shedding 
light on noise-induced poor vascular regeneration. 

Introduction
Restoration of skin integrity following injury is 
dependent on cell and ECM interaction and it can be 
hindered at any point during the process of wound 

1
healing.  Multiple research models concluded that 
psychological stress may affect wound healing.  It is 
evident from experimental work done in the past 
that aircraft noise is linked to stress-induced vascular 
damage, which is mediated by inflammatory cells 
infiltrating the blood vessels, endothelial nitric oxide 
synthetase being uncoupled, and NADPH oxidase 

2
being oxidized.  Transcriptome research has also 
revealed alterations in the expression of genes 
involved in controlling vascular function, re 
modelling, and cell death in the aortic tissues of 
animals exposed to noise. This explains how noise-
induced vascular damage works. White noise 

Loud Noise; Wound Angiogenic Stimulator or Inhibitor?
1 2 3 4 5

Khalida Moeed , Jamshed Khan , Anum Usman , Fauzia Siraj , Waseem Kausar

Correspondence:
Dr. Khalida Moeed
Department of Anatomy
Loralai Medical College, Loralai
E-mail: dr.khalidamoeed@gmail.com  

1,2 5
Department of Anatomy/Biochemistry

Loralai Medical College, Loralai
3
Department of Histopathology

AlNafees Medical College, Islamabad
4
Department of Anatomy

Wah Medical College, Wah

Received: September 23, 2022; Revised: January 31, 2023
Accepted: 16, February 2023

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The objective of my study was to know how noise 
affects the growth of new blood vessels in rat skin 
wound.

Materials and Methods
Study period of this Quasi experiment was from 28th 

th
June 2017 to 28  February 2018.  Institutional Ethical 

Review Committee  approved  the research proposal 

via registration no,F.2/IUIC-ANMC /EC 64/2025 on 

June 23,2015. 30 Sprague dawley male rats  

purchased from  NIH Islamabad were included in the 

study aged between three and five months, they 

weighed between 250 and 300 grams, and  rats with 

any skin conditions discovered during or after the 

trial were eliminated. The control and experimental 

groups of rats were housed in separate cages. Each 

cage had five rats. The normal settings for 

temperature, light, and humidity were given to both 

groups. The animals were kept in 12-hour cycles of 

light and darkness, with lights on at 8 a.m. and off at 8 

p.m, at a temperature of 23–27 °C, 30–40% humidity, 

and a normal pelleted feed with unlimited access to 

tap water. The animals were acclimatized to the 

surroundings for a week prior to the experiment to 

reduce handling and habitat-like stressors. Two 

groups of thirty rats were created: control A (incised 

but not exposed to loud noise)  .H&E stain was used 

to see the newly formed blood vessels.They were 

counted three times in incisional space in control 

A(incised but not exposed to white noise) and 

experimental B (incised and exposed to white noise). 

There were fifteen rats in each group (Table i). The 

control and experimental groups were then 

separated into three subgroups, each with five rats 

(A1, A2, A3, and B1, B2, and B3). Their days of 

exposure to noise (3, 7 and 14)—which consisted of 

white noise for the experimental groups and routine 

noise for the control groups—formed the basis for 

the grouping (Table-i). The rats were put to sleep 

using intramuscular injections of Xylazine and 

ketamine. The predicted dose for rats was 

0.1ml/100g body weight and was created by mixing 

5ml of ketamine and 0.5ml of xylazine. After shaving 

the back to produce a single 2 cm wound parallel to 

the right side of the vertebral column, a full-

thickness incision was created. Metallic clips were 

used to close wounds with a disposable skin stapler. 

Five rats were housed in each cage, they were kept in 

a quiet environment, and they were only exposed to 

typical background noise at a volume of 40 to 50 dB. 

After three days of exposure to noise, seven days for 

group A2 and fourteen days for group A3, rats were 

slaughtered. All rats in the test groups were 

subjected to white noise (85-95db). The exposure 

period began in the morning and lasted from 8 am 

until 4 am. The noise exposure was 4 hours per day 

with hourly breaks, followed by 5 days per week for 

two weeks straight (sub-acute stress) occasionally to 

prevent adaption. A sound player amplified and 

recorded the sound of pressure horns by an amplifier 

that was mounted 30 cm from the cages and 

connected to two 15 w loudspeakers. B1for three 

days, B2 seven days, and B3 fourteen days, the 

subgroup was exposed to loud noise. Rats from 

group B1 were sacrificed on day 3, group B2 on day 7, 

and group B3 on day 14 after being exposed to noise 

(table - i). Wounds were repaired, histologically 

e x a m i n e d , i n  p r e  c a l i b r a t e d  u n i t  a r e a  a t  

x100magnification.Mean value of these readings 

was calculated. Unit area was calculated by 

calibrating the stage and ocular micrometers.    

Statistical analysis was performed according to 

standard methods (SPSS version 20).  Result was 

expressed as mean standard deviation (mean ± SD). 

Mean of the two groups was compared using 

independent student's t test. p-value of ≤ 0.05 was 

considered statistically significant.

Table I: Group Distribution of Rats 

Results
New blood vessels were counted at wound site for all 
three days of noise exposure.

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Blood vessels count per unit area in incisional space 
in control group. Three days of white noise exposure 
to A1 resulted in (12%,1.20  ±0.44). (Table ii ). In the 
experimental sub-group B1 exposed to white noise 
for three days, blood vessels were discovered to be 
present with a mean number (08%,0.80 ± 0.83). 
(Table ii). Process of angiogenesis was slower in noise 
exposed group than routine noise exposed group. 
Comparison of mean number of blood vessels 
present per unit area showed insignificant p value 
(p=0.37) (Table ii) on day three. Mean number of 
newly formed blood vessels counted in group A2 on 
day seven was (16%,1.60 ± 0.89) and  blood vessels in  
experimental group B2 were seen in number 
(14%,1.40 ± 0.89) (Table ii). Difference in mean 
number of newly formed blood vessels among both 
groups on day seven was not significant (p value= 
0.73) (Table ii). Newly formed blood vessels were 
counted in control group (A3) on fourteenth day 
showed mean number (20%,2.00 ± 0.00) (Table ii) 
while Mean number of blood vessel in experimental 
group B3 was counted as (16%,0.70 ±.18) (Table ii) 
per unit area, difference in mean number of blood 
vessels was not significant (p value= 0.14) (Table ii).

that as a normal phenomenon in intact tissue 
delivery of oxygen and nutrients equalizes the 
removal of waste products , hence maintaining the 

13
vascular homeostasis.  While in injured tissue 
disrupted microvasculature leads to inflammation 
and hypoxia which in turn activates endothelial 

14,15
cells. Thereafter; the new vessels differentiate 
into arteries and venules. The difference between 
capillaries and arterioles was made by the presence 
or absence of smooth muscles in their walls. When 
all control groups A1, A2 & A3 were compared with 
experimental groups B1, B2 & B3, on days three, 
seven, and fourteen. The difference was found to be 
insignificant (p >0.05) . These findings don't match 
with previous studies which said that most probable 
factor responsible for process of angiogenesis, were 
a protein called hypoxia inducible factor I (HIF-1), 

Table II: Number of Blood Vessels/Unit Area at Different 
Days of Sacrifice

Figure 1: Photomicrograph of Specimen Number 1's 
Third Day Skin Wound(Group experiment B1). The arrow 
indicates how granulation tissue is growing and bridging 
the wound space. the H&E stain 10X10.

Figure 2: Photomicrograph showing newly formed blood 
vessels at base of wound in specimen number 5 (control 
group A2). H&E stain.40X10

Discussion
Non-healing of wounds drives patient morbidity and 
increases healthcare cost, became a major medical 

11
problem.  Reduced vascular growth by the process 
of angiogenesis is found to be one among the key 

12
factors of chronic non healing wounds.  We 
observed and counted newly formed blood vessels at 
wound site in both control and experimental groups 
and found the fact mentioned previously, to be true 

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16
thought to be inhibited by noise stress.  This has 
been shown by another researcher that ''HIF'' has a 

17 
key role in wound healing. Another study done in 
past has also supported the above-mentioned 
conclusion that at the site of wound, pro-
inflammatory cytokines were affected by stress, that 
might be a possible mechanism of inadequately 
formed blood vessels, resulted in delayed wound 

18
healing in noise exposed group.  Another study 
showed not only difference in inflammatory cell 
count but significant inhibition of epidermal 

19
regeneration in experimental rats too.  In addition 
to count the proliferation and migration 0f fibroblast 

20
and number of new vessels was also decelerated.  
Underlying mechanism is explained by another 
author in terms of correlation of reduced number of 
inflammatory cytokines and enzymes involved in 
tissue repair with inhibition of regeneration of 
endothelial cells consequent on delayed wound 

21
healing.  Any study in favor of our conclusion 
regarding formation of new blood vessels in 
experimental groups subjected to noise stress for 
fourteen days doesn't exist as per my knowledge. 
The matter of conflict might be the alternative 
exposure of noise, with (one hour exposure followed 
by one hour rest) as mentioned in ''subject and 
method'' in our study was quite different from 
previous above-mentioned studies. Present study 
adopted the said pattern of noise exposure based 
upon the fact that prolonged repeated stress can be 
extremely harmful to auditory apparatus of rats as 
they are more sensitive to auditory stimuli than 

22
humans.  It is also a fact that harmfulness of noise to 
hearing or even healing depends not only on the 
sound level only, but there are some other factors 
like sensitivity of the exposed person or 

23
experimental animal and the duration of exposure.

Conclusion
Intermittent noise exposure has tendency to impair 
the process of angiogenesis  thus delaying wound 
healing.

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CONFLICT OF INTEREST
Authors declared no conflicts of Interest.

GRANT SUPPORT AND FINANCIAL DISCLOSURE
Authors have declared no specific grant for this 
research from any funding agency in public, 
commercial or nonprofit sector.

DATA SHARING STATMENT
The data that support the findings of this study 
are available from the corresponding author 
upon request.

This is an Open Access article distributed under the terms of the Creative Commons Attribution- Non-
Commercial 2.0 Generic License.

Loud Noise Affects AngiogenesisJIIMC 2023 Vol. 18, No.1

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