European International Journal of Multidisciplinary Research
and Management Studies
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TYPE
Original Research
PAGE NO.
39-47
DOI
OPEN ACCESS
SUBMITED
12 December 2024
ACCEPTED
14 January 2025
PUBLISHED
16 February 2025
VOLUME
Vol.05 Issue02 2025
COPYRIGHT
© 2025 Original content from this work may be used under the terms
of the creative commons attributes 4.0 License.
Morphofunctional Analysis
of The State of The
Rectum Under Stress
(Literature Review)
Xomidchonova Sh.X.
Ferghana Medical Institute of Public Health, Ferghana State University,
Uzbekistan
Karimov V.A.
Ferghana Medical Institute of Public Health, Ferghana State University,
Uzbekistan
Abdulxakimov A.R.
Ferghana Medical Institute of Public Health, Ferghana State University,
Uzbekistan
Ganizhonov P.X.
Ferghana Medical Institute of Public Health, Ferghana State University,
Uzbekistan
Abstract:
Stress-induced changes in the rectum involve
structural and functional alterations affecting its
integrity and physiological role. This study examines
histological modifications in the rectal wall under
immobilization stress, emphasizing epithelial integrity,
vascular reactions, and connective tissue remodeling.
Morphometric analysis reveals mucosal atrophy,
increased
inflammatory
infiltration,
and
microcirculatory disturbances. Functional assessments
indicate impaired motility and altered mucus secretion,
potentially predisposing to chronic pathologies. These
findings highlight the significance of stress as a factor in
colorectal dysfunction and emphasize the necessity of
preventive measures to mi.
Keywords:
Stress, rectum, morphofunctional analysis,
histological changes, microcirculation, inflammatory
infiltration, mucosal atrophy, motility, mucus secretion,
colorectal dysfunction.
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European International Journal of Multidisciplinary Research and Management Studies
Introduction:
The modern rhythm of life is
characterized by a high stress load, which leads to an
increase in the prevalence of stress-associated
diseases, including pathologies of the gastrointestinal
tract [60, 50]. The rectum, being the final part of the
digestive system, is highly sensitive to neurohumoral
influences and changes in the functional state of the
div under stress. It is known that stress factors can
lead to impaired motility, microcirculation, and the
integrity of the intestinal mucosa, contributing to the
development of inflammatory, degenerative, and
functional changes. However, the morphofunctional
mechanisms of stress-induced disorders in the rectum
have not been sufficiently studied, which makes it
difficult to develop effective methods for the
prevention and correction of these conditions.
The purpose and objectives of the literary review
. The
purpose of this literature review is to analyze current
data on morphofunctional changes in the rectum
during stress, their pathogenetic mechanisms and
possible consequences.
METHODS
This literature review is based on an analysis of modern
scientific data on morphofunctional changes in the
rectum under the influence of stress factors. The
search and selection of sources were carried out using:
Information resources: international and national
databases (PubMed, Scopus, Web of Science, Google
Scholar, eLibrary, etc.), analysis of publications over
the past 10-15 years with the inclusion of key historical
works on the topic, the use of original scientific articles,
reviews, monographs and dissertations. Inclusion
criteria: publications containing data on morphological
and functional changes in the rectum under stress.
Exclusion criteria: works with insufficient evidence
base, duplicate results without new contribution to
science.
RESULTS AND DISCUSSION
The rectum is the distal part of the large intestine that
performs the final stages of digestion, accumulation,
and evacuation of fecal matter. Its length in an adult is
on average 12-15 cm, and the diameter varies
depending on the condition of the filling. Anatomically,
the rectum is divided into two main parts: ampullary
and anal.
The wall of the rectum consists of several layers [38,
51]:
• The mucous membrane (tunica mucosa) is
represented by a single
—
layered prismatic epithelium
with goblet-shaped cells producing mucus necessary to
facilitate the transit of intestinal contents. In the anal
region, the epithelium is replaced by a multilayered flat
keratinizing one.
• The submucosa base (tunica submucosa) contains a
dense plexus of blood vessels and nerve endings, which
makes this part of the intestine highly sensitive to
various influences.
• The tunica muscularis is represented by two layers of
smooth muscle fibers: the inner circular and the outer
longitudinal. In the anorectal region, the circular layer
thickens, forming the internal sphincter of the rectum.
• Serous and adventitious membranes —
cover
different parts of the intestine, depending on their
location in the abdominal or pelvic cavity.
The rectum performs several key physiological
functions:
1. Reservoir function
—
accumulation of fecal matter
before defecation.
2. Evacuation function
—
participation in defecation due
to the coordinated work of the muscles of the pelvic
floor, abdominal press and anal sphincter.
3. The barrier function is to ensure the involuntary
retention of intestinal contents between bowel
movements due to the operation of the sphincter
apparatus.
4. Reflex regulation
—
the susceptibility of mucosal
receptors to mechanical and chemical stimuli affecting
intestinal motility.
The role of the mucous membrane, nervous and
vascular structures in ensuring its functioning
The mucous membrane of the rectum plays a central
role in its function, providing:
• Mucus production to protect the epithelium from
mechanical and chemical damage.
• Absorption of water and some electrolytes
, which
regulates the consistency of intestinal contents.
• Immune protection due to lymphoid elements in its
own mucosal plate.
Nervous regulation is represented by a complex system:
•
Autonomic
innervation
(sympathetic
and
parasympathetic) regulates muscle tone and secretion.
• Somatic innervation (via pudendal nerve) controls
arbitrary components of bowel movements.
The vascular network provides an intensive blood
supply:
Arterial nutrition is provided by the upper, middle and
lower rectal arteries.
• V
enous outflow through the rectal veins is associated
with the portal vein system and the caval system, which
predisposes to the development of hemorrhoids in
hemodynamic disorders.
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European International Journal of Multidisciplinary Research and Management Studies
Mechanisms of stress and its effect on the div
Stress is a non
—
specific reaction of the div to the
effects of various factors that disrupt homeostasis.
Stressors can be classified according to their nature
and mechanism of action. [16, 27, 1, 64, 68, 69, 2]:
1. Physical stressors are the effects of external factors
affecting the div at the level of tissues and organs:
o Temperature changes (hypothermia, hyperthermia).
o Injuries, surgical procedures.
o Prolonged hypoxia or ischemia.
o Dehydration, electrolyte imbalance.
o Increased physical activity.
2. Emotional stressors are psychoemotional factors
that lead to changes in the nervous and endocrine
systems.:
o Social and interpersonal conflicts.
o Chronic anxiety, depression.
o Information overload, stress at work.
3. Physiological stressors
–
internal processes that
cause a stress reaction:
o Diseases, inflammatory processes.
o Hormonal disorders.
o Prolonged starvation, lack of nutrients.
o Disturbance of sleep and circadian rhythms.
Each of these factors can trigger complex adaptive
mechanisms, leading to changes in various organs,
including the gastrointestinal tract and rectum.
The key mechanism of the stress response is the
activation of the hypothalamic-pituitary-adrenal (HPA)
axis, the endocrine system that regulates the div's
adaptation to adverse effects [66, 67, 48, 61, 13, 57,
71].
1. Initiation of a stress response
In response to stressful factors, the hypothalamus
produces corticotropin-releasing hormone (CRH),
which stimulates the anterior pituitary gland.
The pituitary gland secretes adrenocorticotropic
hormone (ACTH), which activates the adrenal cortex.
The adrenal glands secrete glucocorticoids (cortisol),
which regulate metabolism, immune response, and
adaptive mechanisms.
2. Long-term exposure to glucocorticoids
Increased cortisol levels lead to immunosuppression,
catabolic
processes,
and
dysregulation
of
inflammatory responses.
In the gastrointestinal tract, this contributes to
atrophic changes in the mucous membrane, increased
epithelial
permeability,
and
microcirculation
dysfunction.
Stimulation of the sympathetic nervous system
increases peristalsis and secretion, which can cause
hypermotor or, conversely, intestinal hypotension.
The HGH axis plays a central role in the pathogenesis of
stress-induced lesions of the gastrointestinal tract,
including the formation of morphofunctional changes in
the rectum.
Stress can be acute (short-term exposure to a stressor)
or chronic (prolonged exposure to adverse factors) [33,
17, 23, 5, 34, 65].
1. Acute stress
- Activation of the sympatho-
adrenal system → releas
e
of adrenaline and norepinephrine.
Increased blood circulation, increased blood pressure.
- Intestinal hyperperistalsis, possible cramps, diarrhea.
- Accelerated metabolism, mobilization of energy
reserves.
2. Chronic stress
Prolonged exposure to glucocorticoids causes atrophic
and inflammatory processes in the gastrointestinal
mucosa.
- Microcirculation disorders lead to tissue ischemia,
which contributes to the development of ulcers and
erosions.
Changes in neurohumoral regulation lead to dysfunction
of intestinal motility, which can manifest as irritable
bowel syndrome (IBS).
An imbalance of the autonomic nervous system
(hyperactivation of sympathetic or parasympathetic
regulation) can lead to persistent functional disorders of
the gastrointestinal tract.
Thus, stress is a powerful trigger contributing to the
development of morphofunctional changes in the
rectum, and its mechanisms should be taken into
account when developing preventive and therapeutic
strategies.
Stress has a pronounced effect on the mucous
membrane of the rectum, causing morphological and
functional disorders. Studies show that under the
influence of chronic stress, there is a thinning of the
epithelium, a violation of the integrity of the mucous
barrier and the development of erosive and ulcerative
processes. Degenerative changes are accompanied by a
decrease in the number of goblet cells producing
protective mucus, which makes the mucosa more
vulnerable to aggressive factors. [19, 21, 31, 42].
Inflammatory processes in response to stress are
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mediated by the activation of immune cells and the
release of pro-inflammatory cytokines such as
interleukin-1b (IL-1b), tumor necrosis factor-alpha
(TNF-
α) and interleukin
-6 (IL-6). These mediators
contribute to infiltration of the mucosa by leukocytes,
increased epithelial permeability and destruction of
intercellular
contacts,
which
exacerbates
inflammatory reactions and increases the risk of
secondary infectious complications. [18, 22, 55, 49].
One of the key mechanisms of stress-induced changes
in the rectum is a violation of microcirculation. Under
the influence of stress factors, the sympathoadrenal
system is activated, which leads to vascular spasm and
decreased blood flow in the intestinal wall. Tissue
hypoxia caused by prolonged ischemia contributes to
the accumulation of reactive oxygen species (ROS),
which triggers the processes of oxidative damage to
cells. [14, 28, 39, 43].
Increased vascular permeability is accompanied by
extravasation of plasma and shaped blood elements
into the interstitial space, which leads to edema and
disruption of the structural integrity of tissues.
Prolonged hypoperfusion exacerbates inflammatory
processes by activating the transendothelial migration
of leukocytes and enhancing the damaging effects of
free radicals.
Stress has a significant effect on the nervous regulation
of the motor function of the rectum. Dysfunction of the
enteric nervous system leads to disruption of
coordinated peristaltic contractions, which manifests
itself in the form of hyper- or hypomotor disorders [3,
15, 29]. Hyperactivity of the sympathetic nervous
system under stress causes inhibition of intestinal
motility, which contributes to stagnation of intestinal
contents, impaired bowel movements and the
development of constipation. At the same time, a
number of patients have the opposite reaction
–
increased parasympathetic activity, which leads to
hypermotor activity, increased bowel movements and
diarrhea.
In addition, stress affects the sensitive nerve endings in
the mucous membrane, which can lead to visceral
hypersensitivity and pain in the rectum.
At the cellular level, stress effects activate the
processes of programmed cell death (apoptosis),
which is accompanied by loss of epithelial cells and
impaired barrier function of the mucosa. The
proapoptotic proteins of the Bcl-2 family, as well as the
activation of the caspase cascade, play an important
role in this process.
Oxidative stress is one of the leading mechanisms of
cell damage during stress. Increased formation of
reactive oxygen species (ROS) and decreased activity of
antioxidant systems (superoxide dismutase, catalase,
glutathione peroxidase) leads to damage to lipids of cell
membranes, proteins and DNA.
Chronic stress is also accompanied by an imbalance of
inflammatory mediators, which contributes to the
maintenance of a long-term inflammatory process in the
mucous membrane and increases its vulnerability to
adverse factors. Thus, stress has a complex effect on the
morphofunctional state of the rectum, leading to
structural and functional changes that may be the
pathogenetic basis of various intestinal disorders.
The development of inflammatory bowel diseases
under stress
Stress has a significant impact on the gastrointestinal
tract, including the rectum. One of the key
consequences of chronic stress exposure is the
development of inflammatory diseases such as proctitis
and colitis. [46, 12, 19, 21].
Chronic stress causes activation of the hypothalamic-
pituitary-adrenal system (HPA), which leads to
hyperproduction
of
glucocorticoids
and
catecholamines. These hormones, in turn, contribute to:
• Dysfunction of the intestinal barrier, increasing its
permeability and facilitating the penetration of
pathogens.
• Disruption of the local immune response, which leads
to increased inflammatory processes.
• Activation of oxidative stress, which damages
epithelial cells and increases the production of
proinflammatory cytokines (TNF-
α, IL
-6, IL-1b).
Studies show that stress can provoke an exacerbation of
inflammatory bowel diseases, as well as play a
significant role in their pathogenesis, especially in the
presence of a genetic predisposition.
The role of stress in the pathogenesis of irritable bowel
syndrome (IBS)
Irritable bowel syndrome (IBS) is a functional disorder
characterized by impaired intestinal motility, abdominal
pain, and changes in stool patterns. Stress is considered
one of the key factors that initiates and supports the
symptoms of IBS. [58, 9, 11, 53].
The relationship between stress and IBS
• Imbalance of the autonomic nervous system.
Increased activity of the sympathetic nervous system
against the background of stress leads to hyperactivity
of the intestine or, conversely, its spasm.
• Changes in visceral sensitivity. Stress increases pain
perception
by
activating
central
perception
mechanisms, which increases pain in patients with IBS.
• Microbiome disorders. Changes in the composition of
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the intestinal microflora against the background of
stress contribute to the development of dysbiosis,
which worsens the intestinal barrier function and
promotes inflammation.
• Impaired serotonergic regulation. Serotonin plays a
key role in regulating intestinal motility, and stress
affects its metabolism, which can lead to diarrhea or
constipation.
Clinical studies confirm that patients with IBS are more
likely to experience stressful conditions, and
psychotherapeutic methods (cognitive behavioral
therapy, relaxation techniques) improve their
condition along with traditional medical approaches.
Long-term effects of stress damage to the rectal
mucosa
Chronic stress exposure leads to persistent structural
and functional changes in the rectal mucosa, which
may increase the risk of developing various pathologies
[20, 36].
The main consequences
1. Atrophic and degenerative changes
Prolonged activation of stress mechanisms leads to
depletion of the regenerative potential of the mucous
membrane.
- There is a decrease in the number of goblet cells
responsible for the production of protective mucus.
The development of microerosions and a decrease in
the height of the villi, which impairs the absorption
processes.
2. Increased permeability of the mucous membrane
Violation of the integrity of intercellular junctions leads
to an increase in the permeability of the intestinal
barrier, which contributes to the penetration of
bacterial toxins and the development of chronic
inflammation.
3. Fibrosis and decreased elasticity of the intestinal
wall
Prolonged inflammation and oxidative stress
contribute to active fibrosis.
This can lead to a violation of the motility of the
rectum, the formation of constipation and a decrease
in its functional activity.
4. The risk of precancerous changes
- Chronic inflammation, oxidative stress and
hyperproduction of proinflammatory cytokines create
conditions for malignant transformation of mucosal
cells.
- Studies show that prolonged stress exposure can
increase the risk of epithelial dysplasia and colorectal
cancer.
Thus, chronic stress not only provokes inflammatory
diseases of the rectum, but can also contribute to their
progression, as well as the formation of precancerous
conditions. This highlights the need for a comprehensive
approach to correcting stress-induced changes,
including both drug-based and non-drug prevention
methods.
Various morphological, histochemical, functional and
biochemical methods are used for a comprehensive
analysis of changes that occur in the rectum under the
influence of stress factors. Their combination makes it
possible to identify structural and functional disorders
at the cellular and molecular levels. [54, 70, 7, 10].
Histological examination is a key method for assessing
morphological changes in the tissues of the rectum.
Staining of sections with hematoxylin and eosin makes
it possible to detect epithelial damage, inflammatory
infiltrates, and vascular structure disorders. Special
colors (PAS-reaction, toluidine blue) make it possible to
analyze changes in mucin-producing cells and the
degree of degranulation of mast cells involved in stress-
associated inflammatory reactions.
Immunohistochemical analysis is used to detect specific
proteins associated with inflammation, apoptosis, and
stress-induced changes. Markers of inflammation (COX-
2, NF-kB), apoptosis (caspase-3, Bcl-2), oxidative stress
(SOD, iNOS), and mucosal barrier permeability
(Occludin, Claudin-1) are used.
Transmission and scanning electron microscopy
methods make it possible to study ultrastructural
changes in cells and intercellular contacts that occur
under the influence of stress. Examination at the
subcellular
level
reveals
the
destruction
of
mitochondria, the separation of dense contacts
between epithelial cells, damage to microvilli and the
accumulation of autophagic vacuoles. These changes
indicate a violation of the barrier function of the mucous
membrane and increased processes of cellular stress
and apoptosis.
Stress has a significant effect on motor activity and
secretion of the rectum, which can be assessed using
various functional tests. [8, 47, 30, 6, 25].
• Manometry is used to analyze intestinal motility,
detect peristalsis disorders and spasms characteristic of
stress-induced disorders.
• Electrogastroenterography is a method of recording
the bioelectric activity of the intestine, which makes it
possible to assess changes in the contractile function of
smooth muscle cells.
• Mucus secretion study —
quantitative analysis of
secreted mucins (MUC2, MUC4) to assess changes in the
barrier function of the mucous membrane.
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• Permeability of the intestinal barrier is determined
using tests with markers such as lactulose/mannitol
coefficient, which makes it possible to detect a
violation of the integrity of the epithelium under the
influence of stress.
Important information about the state of the rectum
under stress is provided by biochemical parameters
reflecting the level of inflammation and oxidative
tissue damage [62, 4, 56].
• Inflammatory marker enzymes: cyclooxygenase
-2
(COX-2), interleukins (IL-1b, IL-6), tumor necrosis
factor-
α (TNF
-
α), which are involved in stress
-induced
inflammatory reactions.
• Indicators of oxidative stress: activity of superoxide
dismutase (SOD), catalase (CAT), malondialdehyde
(MDA) level as an indicator of lipid peroxidation.
• Markers of apoptosis and cell damage: the level of
caspase-3, expression of proteins p53 and Bcl-2,
indicating the induction of programmed cell death.
• Intestinal microbiota and its metabolites: analysis of
changes in the composition of microflora and the
concentration of short-chain fatty acids (SCFA), which
play an important role in protecting the mucous
membrane from stress-induced damage.
The combined use of these methods makes it possible
to obtain an objective picture of morphofunctional
changes in the rectum under stress, identify key
pathogenetic mechanisms and identify possible
approaches to their correction.
Modern approaches to the prevention and correction
of stress-induced changes in the rectum
Pharmacological correction of stress-induced changes
in the rectum is aimed at stabilizing the functional state
of the mucous membrane, reducing inflammation, and
improving neurohumoral regulation [40, 45, 26].
• Neuroprotectors are drugs that affect the central and
autonomic nervous systems, reducing the effects of
stress on the regulation of intestinal motility and the
barrier function of the mucous membrane. These
include
adaptogens
(melatonin,
phenotropil),
anxiolytics (afobazole, grandaxin), and drugs that
regulate serotonergic transmission (trittico, selective
serotonin reuptake inhibitors).
• Antioxidants –
reduce oxidative stress, which is one
of the key mechanisms of mucosal damage during
chronic stress. Preparations based on alpha-lipoic acid,
vitamin E, coenzyme Q10, as well as natural
antioxidants (curcumin, resveratrol) are used.
• Anti–
inflammatory drugs are aimed at suppressing
inflammatory processes that occur in response to
stress.
Nonsteroidal
anti-inflammatory
drugs
(ibuprofen, nimesulide) are used in limited doses, as
well as pro-inflammatory cytokine inhibitors (infliximab,
adalimumab) in case of pronounced pathological
changes.
Non-drug approaches
Alternative methods of correcting the effects of stress
have a complex effect, helping to restore the balance of
the microbiota, reduce inflammation and improve the
adaptive capabilities of the div. [52, 59, 44, 24].
• Diet Therapy –
dietary recommendations are aimed at
restoring the intestinal barrier and reducing
inflammation. Preference is given to foods rich in fiber
(vegetables, fruits, whole grains), polyunsaturated fatty
acids (fish, flaxseed oil) and probiotic cultures (yoghurts,
kefir). The consumption of simple carbohydrates,
refined foods and alcohol is limited.
• Probiotics and prebiotics –
contribute to the
normalization of intestinal microflora, which reduces
the negative effects of stress on intestinal permeability
and inflammation. The most effective strains are
Lactobacillus and Bifidobacterium, as well as prebiotics
(inulin, fructooligosaccharides) that stimulate the
growth of beneficial bacteria.
• Psychotherapy a
nd stress management - cognitive
behavioral therapy methods, meditation and breathing
practices can reduce the level of chronic stress by
reducing its effect on the intestines. Mindfulness,
biofeedback,
and
autotraining
techniques
are
considered effective.
Promising areas of research
Despite a significant amount of research, many aspects
of the effect of stress on the morphofunctional state of
the rectum remain insufficiently studied [41, 32, 63, 35].
• Genetic and epigenetic mechanisms of stress
-
associated changes
–
studying the expression of genes
regulating the inflammatory response and barrier
function of the mucosa will allow a deeper
understanding of the mechanisms of intestinal
adaptation to stress.
• The role of the microbiome in the formation of str
ess-
induced disorders
–
in-depth studies of the interaction
of intestinal microflora with the nervous and immune
systems will open up new opportunities for probiotic
and metabiotic correction.
• Development of new pharmacological drugs –
promising areas are selective neuroinflammation
modulators,
drugs
that
affect
the
intestinal
endocannabinoid system, as well as innovative
antioxidant complexes.
• Personalized prevention strategies –
the use of
multiomic technologies (metagenomics, metabolomics)
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to select individual treatment regimens and prevent
stress-induced disorders.
These areas of research will allow not only to better
understand the mechanisms of stress effects on the
rectum, but also to develop more effective methods of
protection and therapy.
CONCLUSION
An analysis of the literature data indicates a significant
effect of stress factors on the morphofunctional state
of the rectum. Stress induces disturbances in
microcirculation, leading to hypoxia and increased
vascular permeability, which contributes to the
development of inflammatory and destructive changes
in the mucous membrane. Morphological studies
confirm the presence of degenerative processes such
as epithelial atrophy, destabilization of intercellular
contacts and activation of apoptosis. Functional
disorders caused by stress include changes in the
motility of the rectum, manifested by discoordination
of peristalsis, cramps or hypomtility, which can
contribute to the development of proctogenic
constipation or diarrhea. An imbalance of autonomic
regulation, accompanied by changes in the secretion of
neurotransmitters
and
cytokines,
exacerbates
pathological processes, creating conditions for the
formation of chronic inflammatory bowel diseases.
Thus, stress has a complex effect on the morphological
and functional parameters of the rectum, involving
neuroendocrine, vascular and immune mechanisms.
These processes can contribute to the development of
stress-associated pathologies such as irritable bowel
syndrome, chronic proctitis and colitis.
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