Abstract

Prof. D. K. Awasthi* and Gyanendra Awasthi

ABSTRACT

Autacoids or "autocoids" are biological factors which act like local hormones, have a brief duration, and act near the site of synthesis. The word autacoid comes from the Greek "Autos" and "Acos". The effects of autacoids are mostly localized but large amounts can be produced and moved into circulation. Autacoids may thus have systemic effect by being transported via circulation. These regulating molecules are also metabolized locally. So the compounds are produced locally, they act locally and are metabolised locally. Autacoids can have many different biological actions including modulation of the activity of smooth muscles, glands, nerves, platelets and other tissues. Some other autacoids are primarily characterized by the effect they have upon different tissues, such as smooth muscle. With respect to vascular smooth muscle, there are both vasoconstrictor and vasodilator autacoids. Vasodilator autacoids can be released during periods of exercise. Their main effect is seen in the skin, allowing for heat loss. These are local hormones and therefore have a paracrine effect. Autacoids are chemical mediators that are synthesized and function in a localized tissue or area and participate in physiologic or pathophysiologic responses to injury. They act only locally and therefore also termed ?local hormone.? Autacoids normally do not function as the classical blood-borne hormones. Typically, autacoids are short-lived and rapidly degraded. Autacoid modulators interfere with the synthesis, inhibit the release or the receptors upon which they act. Autocoids are biological factors synthesized and released locally that play a role in vasoconstriction, vasodilation, and inflammation. These include serotonin,bradykinin, histamine, andeicosanoids. Vertebrates have evolved remarkable mechanisms for the repair and maintenance of their own tissues (i.e., ?host? tissues) that simultaneously preclude the invasion and growth of non-host cells and viruses. The front line of host defense relies on the skin, mucosal surfaces, and cornea, where epithelial tissues provide not only the critical physical barrier to a constant exposure to pathogens, but also an interface with commensal microbes.[1.2] Inflammation is a major component of host defense, and a fundamental feature of this vital response is the recruitment of leukocytes to sites of injury.[3,4] Polymorphonuclear leukocytes (PMN) and macrophages in particular are essential for preventing infection and the concomitant threat of life-threatening sepsis. Indeed, in humans, vulnerability to infection is an inevitable consequence of all known genetic or acquired defects in leukocyte function, including defects in adhesion, microbial killing, and phagocytosis; deficiencies in the generation of leukocytes in the bone marrow increase rates of infection and also other illnesses and raise mortality rates.[1] In fact, any injury that compromises the external epithelial barrier triggers a robust inflammatory response.