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J Thorac Cardiovasc Surg 2009;137:991-996
© 2009 The American Association for Thoracic Surgery

Cardiopulmonary Support

Cyclophosphamide protects against myocardial ischemia/reperfusion injury in rats: One of the therapeutic targets is high sensitivity C-reactive protein

Qi-qi Wang, MD, Yuan-gang Qiu, MD*, Yu-juan Zhu, MD, Jian-hua Zhu, MD, Li-hong Wang, MD, PhD, Xiao-sheng Hu, MD, PhD, Shen-jiang Hu, MD, PhD, Liang-rong Zheng, MD, PhD, Qian-min Tao, MD, Fu-rong Zhang, MD, Yun Zhang, MD

Department of Cardiology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Institute of Cardiology, Zhejiang University, Hangzhou, People's Republic of China

Received for publication January 4, 2008; revisions received February 29, 2008; accepted for publication April 13, 2008.

* Address for reprints: Yuan-gang Qiu, MD, Department of Cardiology, the First Affiliated Hospital, College of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou, 310003, P.R.China. (Email: qiuyuangang1{at}yahoo.com.cn).

Objective: Cyclophosphamide has a role of decreasing high-sensitivity C-reactive protein in the treatment of autoimmune disorders. The effect of cyclophosphasmide on high-sensitivity C-reactive protein was investigated in myocardial ischemia/reperfusion rat.

Methods: Open-chest rats were submitted to 30 minutes of ischemia and followed for 3, 12, or 24 hours of reperfusion. All 72 rats survived and were divided into sham, ischemia/reperfusion (I/R) and cyclophosphamide groups, and each group included 3 time-point subgroups (3, 12, and 24 hours; n = 8 for each subgroup). Cyclophosphamide (0.75 g/m2) or saline was intraperitoneally administrated in the cyclophosphamide or I/R group. A polyethylene tube was inserted into the left ventricular cavity to detect left ventricular systolic pressure, left ventricular end-diastolic pressure, and maximum rate of rise or fall of left ventricular pressure. In the end, blood was collected for detection of high-sensitivity C-reactive protein, and hearts were harvested for histopathologic assessment and infarct size determination.

Results: Compared with the I/R group, rats treated with cyclophosphamide showed a significant recovery in myocardial function with improved left ventricular systolic pressure (88.27 ± 3.78 vs 68.62 ± 3.78 mm Hg at 3 hours, 92.04 ± 3.77 vs 63.74 ± 4.87 mm Hg at 12 hours, and 90.41 ± 3.98 vs 64.21 ± 4.88 mm Hg at 24 hours; P < .05, respectively). Left ventricular end-diastolic pressure and maximum rate of rise or fall of left ventricular pressure also had similar trends. Infarct size was reduced (26.1% ± 0.4% vs 40.4% ± 0.4% at 3 hours, 21.6% ± 0.4% vs 49.9% ± 0.4% at 12 hours, and 21.6% ± 0.4% vs 40.0% ± 0.4% at 24 hours; P < .01, respectively). Histopathologic damage score was attenuated (1.83 ± 0.14 vs 2.17 ± 0.14 at 3 hours, 2.33 ± 0.14 vs 3.17 ± 0.14 at 12 hours, and 2.83 ± 0.14 vs 3.83 ± 0.14 at 24 hours; P < .01, respectively). Plasma high-sensitivity C-reactive protein concentration was significantly reduced (29.28 ± 0.51 vs 32.26 ± 0.51 ng/mL at 3 hours, 29.06 ± 0.50 vs 31.8 ± 0.51 ng/mL at 12 hours, and 28.61 ± 0.51 vs 31.86 ± 0.51 ng/mL at 24 h; P < .01, respectively).

Conclusion: Cyclophosphamide protects myocardial ischemia/reperfusion injury in the rat with a decrease in plasma concentration of high-sensitivity C-reactive protein.

Abbreviations and Acronyms CRP = C-reactive protein; ±dp/dtmax = maximum rate of rise or fall of left ventricular pressure; hs-CRP = high-sensitivity C-reactive protein; I/R = ischemia/reperfusion; LVEDP = left ventricular end-diastolic pressure; LVSP = left ventricular systolic pressure






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