The involvement of AQP1 in heart oedema induced by global myocardial ischemia

• Published in: Cell biochemistry and function Vol. 31; no. 1; pp. 60 - 64
• Main Authors: Ding, Fang-Bao, Yan, Yu-Mei, Huang, Jian-Bin, Mei, Ju, Zhu, Jia-Quan, Liu, Hao
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.01.2013; Wiley Subscription Services, Inc
• Subjects: Animals; Aorta; AQP1; Aquaporin 1 - antagonists & inhibitors; Aquaporin 1 - biosynthesis; Aquaporin 1 - genetics; Aquaporin 1 - physiology; Body Water - metabolism; cardiopulmonary bypass; Constriction; Coronary Artery Bypass - adverse effects; Edema, Cardiac - etiology; Edema, Cardiac - physiopathology; Edema, Cardiac - prevention & control; Goats; HgCl2; Intraoperative Complications - etiology; Intraoperative Complications - physiopathology; Mercuric Chloride - pharmacology; Mercuric Chloride - therapeutic use; Myocardial Reperfusion Injury - complications; Myocardial Reperfusion Injury - physiopathology; Myocardial Stunning - etiology; Myocardial Stunning - physiopathology; oedema; RNA, Messenger - biosynthesis; RNA, Messenger - genetics; Time Factors
• ISSN: 0263-6484; 1099-0844
• DOI: 10.1002/cbf.2860

Aquaporin‐1 (AQP1) is a member of aquaporin family that was previously proven to be involved in myocardial dysfunction; however, the role of AQP1 in myocardial stunning is less clear. To determine the change of AQP1 expression level in the heart and its effect on oedema after global myocardial ischemia, 40 adult goats underwent cardiopulmonary bypass (CPB) with an aortic cross‐clamp time of 2 h and total bypass time of 6, 12, 24, 48 and 72 h followed by subsequent reperfusion. AQP1 function of eight goats was inhibited by HgCl2 during the 24 h on CPB. All groups were compared with eight sham bypass control goats. Myocardial water content was measured, and the APQ1 mRNA and protein levels were detected by RT‐PCR and immunoblotting, respectively. The results showed that the degree of myocardial oedema increased significantly at 6, 12, 24 and 48 h of reperfusion after CPB as compared with the control and recovered at 72 h of subsequent reperfusion. Expression levels of AQP1 mRNA and protein began to increase at 12 h and peaked at 24 h of CPB following reperfusion. Furthermore, myocardial oedema was reduced in the HgCl2 group compared with the time‐matched CPB and control groups. These data suggested that AQP1 expression increases in CPB and AQP1 plays an important role in myocardial oedema during CPB. Copyright © 2012 John Wiley & Sons, Ltd.