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HAINAN MEDICAL UNIVERSITY

DEPARTMENT OF PATHOPHYSIOLOGY

TITLE OF THE EXPERIMENT


HEMORRHAGIC SHOCK IN RABBIIT

PREPARED BY
SARPONG KWADWO
ROLL NO. 913905004

PARTNERS
EVANS YAW PEPRAH
ERIC KOBBY ANKOMAH
MIRRIAM NAKAMBA NAWALE
ARIANE MAELLE FEUKENG

INSTRUCTOR
PROF. SHIMIN CHEN

CLASS
2014 INTERNATIONAL CLASS

DATE OF EXPERIMENT
2016/06/8

ABSTRACT
The main focus of this experiment is to observe the major changes and
compensatory mechanisms that occur during hemorrhagic shock. With
rabbit used as experimental model, blood was drawn from the rabbit and
the major changes during shock were seen. From increasing in the blood
pressure as a compensatory mechanism, cold temperature in the
periphery to blood pressure starting to decrease as more blood was drawn
from the circulatory system.

INTRODUCTION
Shock refers to a dangerous systemic pathologic process under the effect
of various drastic etiological factors characterized by acute circulatory
blood volume, inadequate tissue perfusion, cell damage and dysfunction of
multiple organs. Shock can occur with normal blood pressure and
hypotension can occur without shock. Shock can be classified into
hypovolemic, anaphylactic, neurogenic and obstructive shock. In this
experiment, using rabbit as a model, hypovolemic shock i.e. hemorrhagic,
was performed to observe the major changes that occur during shock.
MATERIALS AND METHODS
Animals

One rabbits

Instrument and Reagents

Trachea cannula

Stethoscope

Arterial and venous catheterization

A set of operation instrument

2 set of venous conduct and venous transfusion

Silk thread

Cotton thread

Cotton ball

Filter paper

Tee pipe coupling

100ml syringe

6 needles

50 ml beaker

Balance

Central venous pressure measurement

Thermometer

1% procaine

0.5% heparin in 0.9% NaCl

3% pentobarbital sodium

PROCEDURES

BL-420 experimental biological function system was turned on and


connected to pressotransducer to the system. Pressotransducer and
arterial catheterization were filled with 0.5% heparin in 0.9% NaCl for
recording arterial blood pressure. Venous catheterization for venous
transfusion and central venous pressure were prepared.

Experimental biological function system was turned


on.
1. Surgical procedures

Rabbit was weighed and fastened on the operation platform in a


supine position. Fur was removed from the operation field

1% procaine was injected in the subcutaneous on the neck as


infiltration anesthetize.

Anterior neck skin was cut longitudinally to isolate the trachea and
right vena jugularis externa.

Trachea cannula was performed and linked to the respiratory


recording system.

External jugular vein catheterization was performed and connected


to venous transfusion devices. 5cm of the catheter was implanted in

the vein close to the right atrium and connected to water


manometer for monitoring CVP. 2ml of 0.5% heparin in 0.9% NaCl
into the vein from the tee pipe coupling.

Left common carotid catheterization to record the blood pressure

2. Observation and record.

BEFORE
DRAWING
BLOOD

AFTER
DRAWING
BLOOD
(10MINS)

AFTER
RESETTING
BLOOD
PRESSURE

BLOOD PRESSURE

42.89mmHg

43.08mmHg

72.61mmHg

CVP

-2.5

-4

-0.5

HEART RATE

72 bpm

60 bpm

92 bpm

TEMPERATURE

38.4C

38C

37.6C

BREATHING RATE

76/min

57/mins

74/mins

DISCUSSION
From the table able above, stages of shock can be clearly seen. Just
before the blood was drawn, the blood pressure and other parameters
were normal. 10 minutes after the blood was drawn from the aorta, the
blood pressure increased, due to the activation of the sympathetic
nervous system, this increase the heart rate and constricts peripheral
arterioles to redistribute blood to the vital organs. Constriction of the
peripheral arterioles caused the fall in temperature in periphery. There
is also activation of renin angiotensin aldosterone system. This leads to
conversion of angiotensin I to angiotensin II, which is a strong
vasoconstrictor. This also helps in maintaining the blood pressure.

20 minutes later, there was further increase in the blood pressure but
the intravascular volume was decreased. The breathing rate was
increase compared to just after the blood was drawn from the aorta.
Decrease in perfusion leads to hypoxia, the endothelia cells produce NO
with dilates the vessels. Also less oxygen delivery cause decrease in
aerobic glycolysis, hence producing more lactic acid. The NO and the
lactic acid are strong vasodilators, causing stagnant hypoxia. As a result
of this blood is pulled to the periphery, decreasing venous return.
Pulling of blood can lead hypercoagulability.
After 35% of blood volume is drawn, the condition may progress to
refractory stage. This stage is mostly resistant to treatment, but can be
reversed. Blood begins to coagulate in the microcirculation, which can
cause DIC. Lactic acid accumulates around the cells, this destroys the
cell membrane. Decrease in aerobic glycolysis reduces the production
of ATPs, which is used to provide energy for Na-K, ATPases, hence
accumulation of Na in the cells. Na being highly osmotic draws water
into the cells causing the cells to burst.
At this stage, if there is not proper treatment, the shock can lead to
Multiple Organs Dysfunction, then death.

CONCLUSION
From the discussion it can be concluded that progressive decrease in
intravascular volume with immediate and effective treatment can cause
severe damage from cellular level to the organ level and can be fatal too
REFERENCE

RAPID REVIEW PATHOLOGY

CLINICAL PATHOPHYSIOLOGY MADE SIMPLE

PROF. SHIMIN CHEN SHOCK LECTURE NOTE