Wu Sheng-Ying, Wang Xiong, Chen Yan, Pen Ji-Xia, Li Li, Qi Yong-Fen, Tang Chao-Shu
Department of Pathophysiology, Yunyang Medical College, Shiyan 442000, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Aug;23(3):338-42.
To observe the effect of angiotensin-converting enzyme inhibitors (ACEI) and aldosterone receptor blockers on cardiac function to explore the mechanism of cardiac function descending and myocardial injury in calcium-overload rats.
Calcium-overload in rat was induced by administration of Vitamin D3 plus nicotine. To Estimate the extent of calcium-overload by calcium content. Angiotension II and aldosterone levels in the myocardia were measured by radioimmunoassay. Cardiac function (+/- LVdp/dt, LVESP and LVEDP) were measured by Powerlab. The malondialdehyde (MDA) content, activities of lactate dehydrogenase (LDH) and creatine kinase (CPK) were measured by biochemistry.
Calcium content increased by 3.2-, 5.8 -fold in myocardial and artery, compared with controls. VDN-treated survivors showed lower + LVdp/dt(max) and -LVdp/dt(max) values, by 27% and 34%, respectively (both P < 0.01). Higher LVESP, and LVEDP by 42 % and 32% (P < 0.01); heart rate and mean arterial pressure were not significantly altered (P > 0.05). The lipid peroxidation products MDA and conjugated diene in myocardia were increased 22% (P < 0.01), 68% (P < 0.05) (P < 0.05), respectively. The plasma activity of CPK and LDH was greatly increased by 4.5-and 3.1-fold (P < 0.01), respectively. ACEI and spironolactone obviously relieved degree of calcium-overload and improved cardiac function and myocardial injury(P < 0.01). Calcium content in myocardia and artery was lower 44%, 39% and 57%, 34%. Lower MDA by 20%, 30%, lower conjugated diene by 44%, 35% than calcium-overload group. The plasma activity of CPK and LDH were obviously decreased 28%, 34% and 20%, 27%, compared with calcium-overload group.
Calcium-overload could lead to cardiac function descending and myocardial injury in calcium-overload rats by VDN. ACEI and spironolactone could reduce calcium-overload in myocardial and ameliorate cardiac function and decrease myocardial injury.
观察血管紧张素转换酶抑制剂（ACEI）和醛固酮受体阻滞剂对心脏功能的影响，探讨钙超载大鼠心脏功能下降及心肌损伤的机制。
给予维生素D3加尼古丁诱导大鼠钙超载。通过钙含量评估钙超载程度。采用放射免疫分析法测定心肌组织中血管紧张素II和醛固酮水平。使用Powerlab测定心脏功能（±LVdp/dt、LVESP和LVEDP）。通过生物化学方法测定丙二醛（MDA）含量、乳酸脱氢酶（LDH）和肌酸激酶（CPK）活性。
与对照组相比，心肌和动脉中的钙含量分别增加了3.2倍和5.8倍。VDN处理的存活大鼠的+LVdp/dt（max）和-LVdp/dt（max）值分别降低了27%和34%（均P<0.01）。LVESP和LVEDP分别升高了42%和32%（P<0.01）；心率和平均动脉压无明显变化（P>0.05）。心肌中的脂质过氧化产物MDA和共轭二烯分别增加了22%（P<0.01）、68%（P<0.05）（P<0.05）。血浆中CPK和LDH的活性分别大幅升高了4.5倍和3.1倍（P<0.01）。ACEI和螺内酯明显减轻了钙超载程度，改善了心脏功能和心肌损伤（P<0.01）。心肌和动脉中的钙含量分别比钙超载组降低了44%、39%和57%、34%。MDA比钙超载组降低了20%、30%，共轭二烯降低了44%、35%。与钙超载组相比，血浆中CPK和LDH的活性明显降低了28%、34%和20%、27%。
VDN诱导的钙超载可导致钙超载大鼠心脏功能下降和心肌损伤。ACEI和螺内酯可减轻心肌钙超载，改善心脏功能，减少心肌损伤。
