Acute Heat Stress Damage And Its Pathogensis In Heat-stressed Broilers

The main topic of this paper is to study pathological tissue injury and its reason of broiler in acute heat stress . 100 AA broilers were divided into 5 groups at random and 20 broilers per group. After 30 days adaptive feeding under the normal temperature, 80 conditioned broilers were suddenly stressed by increasing environment temperature from 22±1℃ to 40 ± 1 ℃ . Clinical blood parameter, histopathology and immunohistochemistry of timely killed heat stressed chickens were demonstrated at 2 h, 3 h, 5 h and 10 h respectively. The activity of creatine kinase (CK) which implies myocardium damage increased significently from 2 h to 5h (P<0.01) and decreased at 10 h. The activity of lutamic-oxaloacetic transaminase (GOT) showed obvious reduction (P>0.05) after 10 h heat stress; T- lymphocyte tranformation in blood decreased gradully from 2h to 5h(P<0.01) and renewed at 10 h (p>0.05) ; in vivo and in vitro Specific T- lymphocyte tranformation of heat-sressed broiler spleen markly increaseed at 10h (P<0.05) as well as content of IL-2.;antibody titre of Newcastle disease were reducted significantly during acute heat stress; All detected organs of heat stressed chickens such as liver, kidney, heart showed obvious degeneration, especially but some tissure began to recover at 10 h. HSP90 widely distributed in cytoplasm and nuclei in tissure cells. HSP90 strongly expressed in artery wall and in endotheium of all detected tissue organs. It is suspected to imply that the expressional change of HSP90 in heat stress probably affects organ function by influencing vasoconstriction, which can decrease blood flow in some organs.