Objective To study the influence of perdipine on the proliferation and proline-rich tyrosine kinase 2 (PYK_ 2 ) expression in cultured adult rat cardiac fibroblast stimulated by angiotensin Ⅱ, and to explore the mechanism of perdipine on cardiac fibrosis. Methods Adult rat cardiac fibroblasts (CFs) were treated with angiotensin Ⅱ(AngⅡ) to establish fibrosis model. The effects of perdipine on proliferation of CFs were analysed by MTT colorimetric assay, and fibronectin was tested by immunohistochemistry method. PYK_ 2 mRNA and protein level were examined by RT-PCR and Western blot analysis respectively. Results Perdipine inhibited CFs proliferation and fibronectin synthesis stimulated by angiotensin Ⅱ in a dose dependent, and the levels of PYK_2 mRNA and protein were decreased significantly. Conclusion Perdipine can inhibit cardiac fibrosis stimulated by angiotensin Ⅱ by suppressing CFs proliferation and fibronectin synthesis. PYK_2 is involved in the effect of perdipine.

Objective To study the relationship between ? 1-aderenergic receptor (? 1-AR) and cardiac function in hypoxic newborn guinea-pig myocardia undergoing ischemic reperfusion, and the effects of St. Thomas Hospital cardioplegic solution Ⅱ (STS) and cold blood cardioplegia (CBC) on the ? 1-AR and cardiac function. Methods Normobaric hypoxic guenia-pig model and isolated perfused working heart preparation were established. Cardiac functions were recorded by a multichannel biologic signal analyzer. Myocardial ? 1-AR density (B max ) and affinity (K d) were investigated by radial ligand binding. Results Significant decrease of B max was found in hypoxic newborn guinea-pig myocardia suffering from hypothermic (20 ℃)-ishemic reperfusion (P0.05). Conclusion The impairment of cardiac function in hypoxic newborn guinea-pig undergoing myocardial ischemic reperfusion might be associated with the decline of B max , but not with K d. Different effects of STS and CBC on cardiac function may result from their different influences on B max .