Drugs X Allergies

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When we added the second egg albumin the response was smaller when compared to the first one. It happened because of the small time between the egg albumin’s exposures. In the entire body, the immune response takes hours to be created and the autacoids released, that is why the response was smaller. The tissue did not have time to produce a new allergic response.

Preparation 2

About the results of preparation 2 we can observe that the vehicle group had the same response in both additions of Ach and Histamine. That is expected once this group works as the control group and has normal functions.

The Mepyramine group had a much bigger response in the Ach addition than in the Histamine. It is expected because the Mepyramine treatment acts in the H1 histamine receptor. Once it is linked to H1’s receptors, histamine cannot connect with them and the response is very low. This response confirms that Mepyramine is traditionally classified as histamine H1 receptor antagonist. The bigger response to Ach as well can be explained by looking the S.E.M that was very high, and may explain it. Is not what we expect once Ach is not related to the hypersensitivity reaction.

Indomethacin is a non-steroidal anti-inflammatory. Its pharmacological effect is thought to be mediated through inhibition of the enzyme cyclooxygenase (COX), the enzyme responsible for catalyzes the rate-limiting step in prostaglandin synthesis via the arachidonic acid pathway. In this practical the response to the addition of histamine and Ach was not significant different because this treatment does not influence in any action of the autacoid but in the production of prostaglandins.

The Mepyramine + Indomathacin group had a lower response to the addition of Histamine, it happened because of the mepyramine action on H1 receptor and the non-influence of the indomethacin on this autacoids.

In hypersensitivity reaction an antigen is presented to CD4+ cells specific to the antigen that stimulate the production of IgE antibodies also specific to the antigen. During sensitisation, the IgE antibodies bind to receptors on the surface of tissue. Mast cells and basophils are "sensitised." In a second exposure to the antigen allergen cross-links the bound IgE on sensitised cells, resulting in degranulation and the secretion of pharmacologically active mediators such as histamine and prostaglandin that act on the surrounding tissues.

By having the vehicle as control, we can see that the Mepyramine group had a lower response in grams and a bigger maximal response in seconds when compared to indomethacin group and Vehicle group. We can learn that because Mepyramine links to Histamine receptors, this autacoid is the main one in hypersensitivity reaction. In addition to that, by analyzing the Indomethacin response, we can see that it is smaller in grams but bigger in second to maximal response. It means that the prostaglandins are “less released” when compared to histamine, but because the way they are produced, it is faster than anti-histamine reaction.

The group Mepyramine+Indomethacin had a decrease in the reaction in grams and an increase in time as seconds, it means that however we have the indomethacin that does not act in the histamine receptor, the response was similar to the mepyramine group, meaning that it is still there acting in the allergic response.

By analyzing the data we can assume that anti-histamines helps in the physical reactions of hypersensitivity, once they can decrease the histamine involved in the allergies like showed in graphs.

Another conclusion that we can take from the practical is that prostaglandins are released during allergic reaction because when we analyze the Indomethacin group we can see a lower reaction in grams and a bigger reaction in seconds but it still significant, showing us the block of production of prostaglandins.