| The purpose of this paper was to study the relationship between calcium signal transduction and ascites syndrome (AS) in broiler chickens.1. The cardiac muscle cell (CMC) and pulmonary arterial smooth muscle cell (PASMC) of broiler chickens were cultured by explant, enzyme-dispersed and differential attachment. Cultured cells were identified by immunohistochemistry. The a -actin antigen positive rate of cultured ceils was more than 95%, indicating that high concentration of CMC and PASMC has been obtained.2. The total calcium in right ventricle (RV) of broiler was measured by atomic absorption spectrophotometer. The result showed that the total calcium of RV with AS is significantly higher than that of broilers bred in low ambient temperature and normal temperature (71.2 ± 6.5, 58.0±4.4, 46.8± 3.15mg/kg, p<0.01).The quantity and distribution of Ca2+ in the heart and lung was observed by pyroantimonate precipitation. The result showed that Ca" was mainly located in cytoplasm, sarcoplasmic reticulum, mitochondrion of CMC and PASMC. The quantity of Ca2+ in the heart and lung of broiler with AS was more than that of normal broiler.The increase of total calcium of RV and the precipitation of Ca2+ in the CMC and PASMC of broiler with AS suggested that calcium signal transduction was important to the development of AS .3. The Ca2+ channels of broiler CMC and PASMC were investigated by using Fluo-3/AM as Ca2+ indicator with laser scanning confocal microscope (LSCM). kcl, noradrenalin (NE), procaine and AngII can increase the cytoplasm Ca2+ of the CMC and PASMC of broiler.This experiment showed that Ca2+ channels of Voltage-operated, Receptor-operated, IP3 receptor and Ryanodine receptor were exist in the CMC and PASMC of broiler.4. Hypoxia is the important cause of AS. The transmembrane movement of Ca2+ in the CMC and PASMC was observed by LSCM. The results showed that hypoxia could significantly increase intracellular Ca2+ of CMC and PASMC (CMC: normal oxgen:99.3±13.1, hypoxia:129.4±24.3,p<0.01. PASMC: normal oxygen: 95.0±14.6,hypoxia: 152.6± 21.9,p<0.01). The Ca2+ antagonist (nifedipine, Nif; verapamil, Ver) can significantly restrain the Ca2+ increase of CMC and PASMC treated by hypoxia (CMC: hypoxia + V:100.9±28.2, hypoxia + N:107.6±27.7; PASMC: hypoxia + V: 92.7±14.8, hypoxia+N: 118.2 ± 21.8, p<0.01).The results also suggest that the calcium signal transduction play an important role in the development of AS .5. CMC hypertrophy and PASMC proliferation were the important course of AS. The effect of calcium sitinal transduction on the oncogene c-fos and c-myc expression induced by hypoxia was observed by in situ hybridization, immunohistochemistry and image analysis. The results showed that hypoxia can significantly increase c-fos and c-myc expression (CMC: c-fos protein: normal oxygen 159.1 + 37.1.hypoxia 240.3+49.6; c-myc protein: normal oxygen 149.6+24.9, hypoxia 236.3+55.4; c-fos mRNA: normal.oxygen 149.6+22.4, hypoxia 205.4+57.6 P<0.01. PASMC: c-fos protein: normal oxygen 150.9+33.2, hypoxia 225.9+37.0; c-myc protein: normal oxygen 162.1 +28.5, hypoxia 228.8 +33.4; c-fos mRNA: normal oxygen 144.6+20.2,hypoxia 198.1+32.8 P<0.01) . But Ver, Nif and Cyclosporin A can restrain such an expression (CMC: c-fos protein: hypoxia+V 165.2 +52.2, hypoxia+C 190.8+33.6, hypoxia+N 166.5+49.8; c-myc protein: hypoxia+V 178.9 + 42.1, hypoxia+C 164.8+49.5, hypoxia+N 174.4+36.3; c-fos mRNA: hypoxia+V 151.3+20.1, hypoxia+C 166.5 + 22.1, hypoxia+N 154.5+25.2 P<0.01. PASMC: c-fos protein: hypoxia+V 162.3+33.6, hypoxia+C 151.6+ 37.3, hypoxia+N 157.4 + 28.9; c-myc protein: hypoxia+V 170.2 + 26.7, hypoxia+C 179.1+29.2, hypoxia+N 170.7+28.5; c-fos mRNA: hypoxia+V 161.6 + 24.1, hypoxia+C 159.0+32, hypoxia+N 173.7+35.8, P<0.01).CsA can significantly restrain c-fos and c-myc expression of CMC and PASMC indicating that the Ca~7CaM-CaN path is important to c-fos and c-myc expression that were necessary to CMC hypertrophy and PASMC proliferation.Ca2+ antagonist (Nif, Ver) can...
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