The process of follicle rupture has been described as an inflammatory reaction in which prostaglandins (PGs) and/or histamine may be involved. With an in vitro perfused rabbit ovary preparation, experiments were carried out for determination of whether a relationship exists among PGs, histamine, and ovulation. PGF2 alpha alone was capable of inducing ovulation when added to the perfusion fluid at 1, 10, and 100 ng/ ml. Effectiveness in achieving ovulation varied directly with the dosage; however, the ovulatory efficiency of PGF2 alpha-treated ovaries was lower than that of ovaries exposed to human chorionic gonadotropin (hCG, 100 IU). PGF2 alpha-induced ovulation could not be blocked by the H2 receptor antagonist, cimetidine. The PG synthesis inhibitor, indomethacin, did not prevent histamine-induced ovulation. Ovulation induced by hCG was partially blocked by the administration of indomethacin; however, the concomitant administration of cimetidine was not associated with further reduction in ovulation. In all but one experimental group, the majority of ovulated ova did not progress beyond the intact germinal vesicle stage unless the ovaries had been exposed to hCG. On the basis of these experiments, PGs and histamine do not appear to be interdependent in their effects on the ovulatory process in vitro.
Source: http://www.ncbi.nlm.nih.gov/pubmed/3857188
There are many, many substances released when tissues are injured, but one of the interesting ones would be prostaglandins. Some other substances of interest that are released would be histamine, antibodies, clotting factors, and a host of others.
Stool (poo) is the chemical substance produced by the body that is associated with the pain of inflammation, as inflammation is pain in your backside.
Kinins and prostaglandins are both key cells in the process of inflammation. Active complement or tissue damage can trigger these mast cells. The Kinins trigger pain in the nerve endings. Prostaglandins are like histamine and increase permiability and vasodilation in the capillary vessel. Which is the most important part of the inflammation process.
It doesn't atropine only acts on muscarinic receptors (it's a competitive antagonist here for ACh), but histamine acts on different receptors (histamine receptors). There is no direct interaction between atropine and histamine receptors
They have completely different functions in the body; histamine stimulates certain kinds of immune responses, and serotonin is a neuro-transmitter.
When your body is invaded by any virus, bacteria or even a splinter, it will respond with general inflammatory response chemicals These chemicals include histamine (mostly secreted by basophils, white blood cells found in connective tissue), kinins, prostaglandins (PGs), and complement.Vasodilation (dilation of blood vessels), stimulated by histamine and other chemicals, increases blood supply to the damaged area. This causes redness and an increase in local temperature. All of these responses are harmful to the pathogens causing the infection.
Yes, prostaglandins are made in the renal medulla.
difference between relation sehema and relation instance in dbms
Histamine and heparin
Non steroidal anti inflammatory drugs inhibit prostaglandin production
no
relation between telsa and gauss