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Objective: To compare the different expressions of cardiac inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta(IL-1beta), interleukin-6 (IL-6) in two types of cardiac hypertrophy rat models induced by volume overload and pressure overload., Methods: Volume overload-induced cardiac hypertrophy was established by abdominal arteriovenous fistula (ACF) and pressure overload-induced cardiac hypertrophy was developed by constriction of aorta (CA). Heart weight measurement and histological examination were performed 1 week or 2 weeks after the operation respectively. The cytokine expression was measured by enzyme linked immunosorbent assay., Results: All the operated groups developed cardiac hypertrophy. The left ventricular fractional shortening of each operated group had no significant difference with the sham-operated groups respectively. As far as the total amount of each cytokine in left ventricular myocardium was concerned, compared to the sham-operated groups, IL-6 and IL-1beta both increased significantly in CA groups [IL-6(23 722+/-8 671)pg vs (17 693+/-5 705)pg,P<0.05 ;IL-1beta(335+/-95)pg vs (159+/-99) pg,P<0.01].There was no difference of TNF-alpha between operated and sham-operated groups in ACF or CA groups ., Conclusion: The contents of IL-6 and IL-1beta in myocardium increased in pressure overload-induced cardiac hypertrophy.

To get insights into the principles of gene expression changes during cardiac hypertrophy, three rat cardiac hypertrophy models were prepared, i.e., suprarenal abdominal aortic stenosis (SRS), arterial-vein fistula (AVF) and continuous jugular vein infusion of norepinephrine (NEi). The cardiac function and structure were analyzed by echocardiograph as well as histological examination. Total RNA of left ventricles was extracted and gene expression profiles were analyzed by cDNA microarray. SRS and NEi induced concentric cardiac hypertrophy and AVF induced eccentric hypertrophy in rats, among which NEi caused obvious cardiac fibrosis. The changes of gene expression profiles were compared comprehensively across different pathologic cardiac hypertrophy models. While gene expression profiles of different cardiac hypertrophy models compared with pairs, parts of the genes involved were found overlapped, and mostly the gene expression changed in the same direction between two models, but some of them changed in the opposite directions. Expression levels of 19 genes were found changed across all cardiac hypertrophy models, and genes relatively regulated in a specific model was also found when comparison of all the three models was carried out. Novel clues for further study might derive from the results mentioned above, and some genes might be the marker genes of cardiac hypertrophy or the targets of therapy.