All of the following are true regarding vasodilation in acute inflammation, except:
Transient vasoconstriction of aerioles at the site of injury is the earliest vascular response in acute inflammation. This process is mediated by both neurogenic and chemical mediator systems and usually resolves within seconds to minutes. Followed by, Vasodilation first involves the aerioles and then leads to the opening of new capillary beds in the area. There is increased permeability of the microvasculature, with the outpouring of protein-rich fluid into the extravascular tissues. Engorgement of small vessels with slowly moving red cells, results in stasis. Vasodilation is induced by the action of several mediators, notably histamine, on vascular smooth muscle. Vasodilation is responsible for heat (calor) and redness (rubor) at the site of inflammation.
Caused by release of histamine
First affects capillaries and followed by opening of aerioles
Vasodilation leads to extravasation of fluid from microvasculature, leading to edema
Vasodilation occurs notably due to the action of histamine on vascular smooth muscle
Basic Concepts and Vascular changes of Acute Inflammation