Rat akciğerlerinde künt torasik travma modeli: deneysel bir çalışma

PDF Dosyası: 

arastirmax_1647_pp_249-252.pdf

Introduction
Thoracic trauma accounts for a quarter of deaths due
to multiple injuries according to the U.S. Government
Statistical Institute records (1,2). The vast majority of
chest traumas occur due to blunt injuries (1,2). The
incidence of isolated blunt thoracic injury among the
multiple injuries was 16% (3). Endothelial cell injury
occurs directly proportional to the intensity of trauma after the blunt chest trauma (BCT). We aimed to
investigate the effects of BCT on lung by using a new
BCT model in rats.
Material and Methods
This study was performed on the Animal Research
Laboratory of the Gulhane Military Medical Academy.
Ethics committee’s permission of the Gulhane
Military Medical Academy was obtained before the
study. Fifty adult rats Norvecus weighing between
120 and 160 grams were used. All rats were fed with
rat feed including 25% protein (4).
We developed a new and easy way of doing trauma
model for occurring BCT (Figure 1) (5). Our new model essentially was made up from three components.
First component is 90 cm long pipe and pipe stabilization part, second support table and third metal
weights including of 40, 70, 100 grams.
The rats were separated into five groups and all
groups contained ten rats. Group I was control group.
The control group was subjected to the same experimental protocol, but no blust trauma was delivered.
The second group was mild intensity BCT, third was
moderate intensity BCT and the fourth was severe
intensity trauma groups. The last one was the fifth
group; we called this group survivor group. A light
blast trauma, like Group II, was applied to the survival group. Test subject groups and intensity of trauma applied onto subjects are shown in Table I. The
rats were anesthetized with intraperitoneal xylazine
10 mg/kg and ketamine 90 mg/kg. Three different
* Department of Thoracic Surgery, Gulhane Military Medical Faculty
** Department of Pathology, Gulhane Military Medical Faculty
Reprint request: Dr. Orhan Yücel, Department of Thoracic Surgery, Gulhane
Military Medical Faculty, Etlik-06018, Ankara, Turkey
E-mail: orhanycl@gmail.com
Date submitted: December 10, 2007 • Date accepted: November 25, 2008250 • December 2008 • Gulhane Med J Yücel et al.
intensity traumas were applied onto rats. Rats were
placed in lateral decubitis position over the trauma
model’s support part. All rats were heated by using
tungsten electric bulb (100W/220V) and oxygen supply was obtained. Metal weights were dropped from 1
m height onto rats through the plastic pipe for gaining mild, moderate and severe trauma. Analgesia was
obtained by using buterfenol (0.5 mg/kg, sc).
Cardiac rates, breath rates, and SpO2
values of rats
were recorded in 1st, 5th, 10th, 30th, 60th, 90th, and
120th minutes. All the rats were sacrificed except for
the Group V by giving lethal dose of xylazine and
ketamine after 120th minutes. The survivor group
was followed for 10 days and was sacrificed. The lungs
of sacrificed rats were examined microscopically and
macroscopically. Statistical analysis was done with
Kruskal-Wallis, Mann-Whitney U, and Chi-Square
tests.
Results
BCT caused initially a significant decrease in the
heart rate. Then, the cardiovascular response to injury was bradycardia in the light injury group and
tachycardia in the moderate injury group. Heart
rate of selected time points for comparison among
different trauma intensities is presented in Figure 2.
Respiratory rate was calculated at 120 min after injury. Respiratory rate was recorded after trauma. This
study showed that a bradypne occurred during the
first minute after trauma in all trauma groups. Then,
the respiratory rate response was an increasing mode
in the moderate injury group. Respiratory rate never reached the levels measured before chest trauma
(Figure 2). SpO2
values were relatively increased one
hour after anesthesia in Group I. The same increase
was not seen in the trauma groups (Groups II and
III). While the trauma intensity resulted in significant
heart rate differences, there were no changes related
with time. There were significant increases on heart
rate, on 10th, 20th, 30th, 40th, and 50th minutes after trauma in Group III, and then it turned to normal
rate (p<0.05). The pulmonary response was the decreasing SpO2
for all trauma groups (Figure 2).
Table I. Intensity of trauma according to the test subject groups
Group Applied weight (g) Intensity of trauma (joule)
Group I (Control) 40 0.04
Group II (Light) 40 0.04
Group III (Moderate) 70 0.07
Group IV (Severe) 100 0.10
Group V (Survivor) 40 0.04
Figure 2. Heart rate (2a), respiratory rate (2b) and SpO2
(2c)
of selected time points for comparison among different trauma
intensities are presented
Figure 1. Our blunt trauma model
Metal weights
Pipe
Subject
Support table
Metal weights
Pipe stabilization part
Figure 3. Distribution of the incidence of lung pathology
Contusion (10) Laceration (7) Hematoma (5) Hemorrhage (3)
A few minutes after the trauma, 2 in Group II, and 9
in Group IV, a total of 11 rats, were dead due to trauma. Autopsy examination showed pulmonary contusion (90%), pulmonary laceration (63%), pulmonary
hematoma (45%) and pulmonary hemorrhage (20%).
The most frequent pulmonary lesion was pulmonary
contusion (90%) (p<0.05) (Figure 3).Volume 50 • Issue 4 Trauma model • 251
The lung contusion was the most common pathology in all trauma groups (p<0.05). In this study, other
important macroscopic findings were non-pulmonary lesions including pericardial hematoma in two
rats (one in Group II and one in Group III), one left
ventricle laceration, one left ventricle contusion and
two cardiac lacerations in Group IV.
Intraparenchymal hemorrhage, including intraalveolar, intrabronchial and subpleural hemorrhage
was the microscopic findings in all trauma groups.
Intraparenchymal hemorrhage was divided into four
groups due to histopathological findings (Figure 4).
The distribution of pulmonary collapse according
to the lobe is shown in Table II.
A survival study was carried out to test the long
term effects of BCT. No death occurred during the
10-day observation period.
Discussion
BCT is one of the most important leading causes
of morbidity and mortality around the world (2,3).
Main causes of BCT contain motor-vehicle crash,
strike, earthquake and falling from height (6). The
mortality rate of BCT is around 25% (1). The understanding of physiopathology and the relationship between time and physiopathology will decrease morbidity and mortality and clarify diagnosis and treatment process.
In this study we easily constituted a BCT model useful on small animals (5). We used rats because it is easy
to obtain, reproduce and maintain for long follow-up.
We aimed to investigate the effects of BCT on the cardiopulmonary parameters and microscopic and macroscopic level of lung by using this trauma model.
The BCT is always associated with cardiac changes.
Forces applied to the chest wall may cause cardiac
rhythm disorders and also may result in a sudden
death. We performed right sided trauma on the rats
in order to decrease the incidence of heart injury. In
mild intensity trauma group, bradycardia was seen
from beginning to the 120th minute of trauma. We
thought that vagal response was the cause of bradycardia. Bradycardia, hypotension and apnea after trauma
were also reported in two studies (7,8). In Group III,
heart rate was significantly higher. We realized that
tachycardia occurred due to intrathoracic hemorrhage. Compared with other studies, the cause of low
incidence of cardiac injury depends on the localizations of applied trauma. We preferred right sided trauma instead of left sided or anterior trauma to avoid
cardiac injury. A significant decrease was seen in SpO2
after trauma due to deteriorated ventilation and perfusion (V/Q) value. Deterioration in V/Q occurred at
the beginning of trauma and got worsen during the
next period. It is very important in clinical practice for
the patients with chronic obstructive pulmonary disease and children whose defense mechanism has not
developed yet.
Pulmonary contusion was seen in 70% in Group II,
100% in Group III, and 80% in Group IV. It was proved
that pulmonary contusion is the major pathology in
BCT patients. Mirua et al. have found pulmonary
contusion of 49% in their study with BCT in their
series containing 161 patients (9). We found pulmonary contusion in light traumatized rats; pulmonary
laceration, pulmonary hematoma, and hemorrhage
increased with the intensity of trauma. We made auFigure 4. Microscopic findings of the lung: (a) Mild hemorrhage, (b) Moderate hemorrhage, (c) Severe hemorrhage, (d) Pulmonary collapse
Table II. Distribution of the incidence of lung collapse
according to the lobe
Location Group
Collapse
All (n)
(+), n (%)
Right upper lobe
Group I 0 (0) 10
Group II 1 (10) 10
Group III 1 (10) 10
Group IV 1 (10) 10
Right middle lobe
Group I 0 (0) 10
Group II 3 (30) 10
Group III 2 (20) 10
Group IV 2 (20) 10
Right inferior lobe
Group I 0 (0) 10
Group II 4 (40) 10
Group III 2 (20) 10
Group IV 0 (0) 10
Left upper lobe
Group I 0 (0) 10
Group II 1 (10) 10
Group III 2 (20) 10
Group IV 2 (20) 10
Left inferior lobe
Group I 0 (0) 10
Group II 5 (50) 10
Group III 5 (50) 10
Group IV 1 (10) 10252 • December 2008 • Gulhane Med J Yücel et al.
topsies on 11 rats which died within 5 minutes after
trauma to evaluate the mortality associated with lung
injury. We found that pulmonary contusion (90%)
was the most common complication, but pulmonary
laceration was the most mortal complication (63%).
Peclet et al. reported a rate of pulmonary laceration
of 43% in their series containing 2086 patients (10).
Hemothorax increasing with the intensity of trauma
may also be seen in all groups. From this point, we
can conclude that all patients who were exposed to
trauma should be examined for hemothorax (1,11).
We have studied the effects of different trauma intensities in lung lobes. This is the unique side of our study.
In the study of Knoferl et al., trauma was applied to the
left hemitorax and intraparenchymal hemorrhage was
reported in both hemitoraces (about 53%) (12).
We had also important dates about the long-term
outcomes of contusion and collapse by using the survival group, which the same intensity of trauma was
applied with Group II. The rate of contusion was the
same with Group II, and it showed that contusion
did not recover in early period. The rate of collapse
was 50% and it was higher in Group V than in Group
II. The increasing collapse in Group V was due to the
parenchymal injury and obstruction of bronchial air
way caused by secretion and hemorrhage. This finding is very important in clinical practice for the mucolitic treatment and pulmonary rehabilitation in
patients with BCT.
As a result this study has established a useful model
for the study of blunt trauma in small animals (5).
Lung contusion is always more obvious than other
pathologies and some forms of ventilation and perfusion mismatch accompanied blunt trauma in each
case. The associated injuries are strictly related with
high mortality rates.