Acute Heat Stress Damage And Its Pathogenesis In Heat-Stressed Broilers

The main objective of this paper is to investigate pathological tissue injury and its pathogenesis of broiler in acute heat stress. 100 AA broilers were randomly divided into five groups (20 broilers per group). After adaptive feeding for 30 days under the normal temperature, 80 conditioned broilers were suddenly stressed by increasing environment temperature from 2±21℃to 40±1℃. Clinical blood parameter, histopathological lesion and immunohistochemistry staining of timely killed heat stressed chickens were examined at 2 h, 3 h, 5 h and 10 h respectively. The activity of creatine kinase (CK), which implies myocardium damage, increased significantly from 2h to 5h (P < 0.01) and decreased at 10h. The activity of lutamic-oxaloacetic transaminase (GOT) showed obvious reduction (P > 0.05) after lOh heat stress; All detected organs of heat stressed chickens such as liver, kidney, heart showed obvious degeneration, especially but some tissues began to recover at lOh. HSP90, HSP70 and HSP60 widely distributed in cytoplasm and nuclei in tissue cells. HSP90 strongly expressed in artery wall and in endothelial cells of all detected tissue organs. It was inferred that the expressional change of HSP90, HSP70 and HSP60 in the endothelial cells of artery wall of heat stressed chickens probably affects organ function by influencing vasoconstriction causing the decrease of blood flow in some organs.