2. 2
Inflamation
Is part of the complex biological response of vascular tissues to harmful
stimuli, such as pathogens, damaged cells, or irritants, The classical signs
of acute inflammation are pain, heat, redness, swelling, and loss of
function.
Inflammation is a protective attempt by the organism to remove the
injurious stimuli and to initiate the healing process. Inflammation is not a
synonym for infection, even in cases where inflammation is caused by
infection. Although infection is caused by a microorganism,
inflammation is one of the responses of the organism to the pathogen.
However, inflammation is a stereotyped response, and therefore it is
considered as a mechanism of innate immunity, as compared to adaptive
immunity, which is specific for each pathogen…
Causes
Burns
Chemical irritants
Frostbite
Toxins
Infection by pathogens
Physical injury, blunt or penetrating
Immune reactions due to hypersensitivity
Ionizing radiation
Foreign bodies, including splinters, dirt and debris
Stress
Trauma
Alcohol
Type of Inflamation
1-Acute inflammation is a short-term process, usually appearing
within a few minutes or hours and ceasing upon the removal of the
injurious stimulus.
3. 3
It is characterized by five cardinal signs :
1-Dolor (pain)
2- Calor (heat)
3-Rubor (redness)
4- Tumor (swelling)
(loss of function)of function)Functio laesa-5
2-Chronic Inflamation
If the condition causing acute inflammation is not resolved, the
inflammation may pass to a longer term chronic phase. Also, some
pathogies by their nature tend to directly provoke chronic rather than
acute inflammation. Many of the features of acute inflammation continue
as the inflammation becomes chronic, including increased blood flow and
increased capillary permeability. Accumulation of white blood cells also
continues, but the composition of the cells changes.
inflammatory mediators
Molecules that are released by immune cells during times when harmful
agents invade our body.
4. 4
Procedure:
1- injection of anti-inflammatory drug. ( unknown 4 )
2- wait 30 mins.
3- measure the thichness of the paw. ( 0.3 cm )
4- injection of albumine. ( 1 unit )
5- wait 30 mins. (20 mins )
6- measure the thickness of the paw. ( 0.4 cm )
7- wait 30 mins. (20 mins )
8- measure the thickness of the paw. ( 0.32 cm )
Results:
G1 / 0.15 → 0.5 Acetaminophen
G2 /0.3 → 0.4 → 0.3 ASA ( Acetyl Salicylic Acid )
G3 /0.3 → 0.5 → 0.3 Dexamethasone
G4 /0.3 → 0.4 → 0.32 Piroxicam
5. 5
Discussion
The aim of this experiment is to Know the effect of {Dexamethasone
,piroxicam , ASA , Acetaminophen} in inflamation & to determin which
one of them is more potent.
We inject those drug to the paw of the rat and as the drug become more
potent the paw of the rat become thinner acording to that the potensy of
drug in which we use it is like that
Dexamethasone piroxicam ASA Acetaminophen
Dexamethasoneis a potent synthetic member of the glucocorticoid
class of steroid drugs. It acts as an anti-inflammatory
andimmunosuppressant,
When injected in to the paw of the rat the sickness of paw was (0.3)&
after (30 min.) the sickness was (0.5)& after another (20min.) the
sickness of paw was (0.3) ,In comparision with other NSAIDs in wich we
use it Dexamethason was the most potent .
Mechanism of action
Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone
crosses cell membranes and binds with high affinity to specific
cytoplasmic glucocorticoid receptors. This complex binds to DNA
elements (glucocorticoid response elements) which results in a
modification of transcription and, hence, protein synthesis in order to
achieve inhibition of leukocyte infiltration at the site of inflammation,
interference in the function of mediators of inflammatory response,
suppression of humoral immune responses, and reduction in edema or
scar tissue. The antiinflammatory actions of dexamethasone are thought
to involve phospholipase A2 inhibitory proteins, lipocortins, which
control the biosynthesis of potent mediators of inflammation such as
prostaglandins and leukotrienes.
*Piroxicamis a non-steroidal anti-inflammatory drug of the oxicam
class used to relieve the symptoms of rheumatoid and osteoarthritis,
6. 6
primary dysmenorrhoea, postoperative pain; and act as an analgesic,
especially where there is an inflammatory component,
When injected in to the paw of the rat the sickness of paw was (0.3)&
after (30 min.) the sickness was (0.4)& after another (20min.) the
sickness of paw was (0.32), It is less potent than Dexomethasone.
Mechanism of action is a non-selective COX inhibitor possessing
both analgesic and antipyretic properties. It undergoes enterohepatic
circulation.
*Acetyl Salicylic Acid (Asprin) is a salicylate drug, often used
as an analgesic to relieve minor aches and pains, as an antipyretic to
reduce fever, and as an anti-inflammatory medication.
When injected in to the paw of the rat the sickness of paw was (0.3)&
after (30 min.) the sickness was (0.4)& after another (20min.) the
sickness of paw was (0.3).
It is less potent than Dexomethasone & Paroxicam,The result Here is
error this is may be because of the unaccuracy of measuring the thickness
of the paw of the rat.
Mechanism of action
Aspirin's effects and respective mechanisms of action vary with dose:
*Low doses (typically 75 to 81 mg/day) are sufficient to irreversibly
acetylate serine 530 of cyclooxygenase (COX)-1, This effect inhibits
platelet generation of thromboxane A2, resulting in an antithrombotic
effect.
*Intermediate doses (650 mg to 4 g/day) inhibit cyclooxygenase (COX)-
1 and COX-2, blocking prostaglandin (PG) production, and have
analgesic and antipyretic effects.
7. 7
*High doses (between 4 and 8 g/day) are effective as antiinflammatory
agents in rheumatic disorders; the mechanism(s) of action at these high
doses may include both PG-dependent (particularly COX-2 dependent
PGE2) and independent effects ,However, the usefulness of aspirin at
these high doses is limited by toxicity, including tinnitus, hearing loss,
and gastric intolerance..
*Acetaminophen: is a widely used over-the-counter analgesic and
antipyretic ,Paracetamol is classified as a mild analgesic. It is commonly
used for the relief of headaches and other minor aches and pains.
When injected in to the paw of the rat the sickness of paw was (0.15)&
after (30 min.) the sickness was (0.5)& after another (20min.) the
sickness of paw was (0.5) Because has no anti-inflamatory effect so the
sickness of paw was not change..
Mechanism of action
Acetaminophen is thought to act primarily in the CNS, increasing the
pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1,
COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis.
Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in
peripheral tissues and, thus, has no peripheral anti-inflammatory affects.
While aspirin acts as an irreversible inhibitor of COX and directly blocks
the enzyme's active site, studies have found that acetaminophen indirectly
blocks COX, and that this blockade is ineffective in the presence of
peroxides. This might explain why acetaminophen is effective in the
central nervous system and in endothelial cells but not in platelets and
immune cells which have high levels of peroxides. Studies also report
data suggesting that acetaminophen selectively blocks a variant of the
COX enzyme that is different from the known variants COX-1 and COX-
2. This enzyme is now referred to as COX-3. Its exact mechanism of
action is still poorly understood, but future research may provide further
insight into how it works. The antipyretic properties of acetaminophen
are likely due to direct effects on the heat-regulating centres of the
hypothalamus resulting in peripheral vasodilation, sweating and hence
heat dissipation