n Cardiovascular Journal of South Africa - C-reactive protein in acute and delayed preconditioning of the rat heart : cardiovascular topic
|Article Title||C-reactive protein in acute and delayed preconditioning of the rat heart : cardiovascular topic|
|© Publisher:||Clinics Cardive Publishing|
|Journal||Cardiovascular Journal of South Africa|
|Author||A. Valtchanova-Matchouganska, M. Gondwe and A. Nadar|
|Publication Date||Mar 2005|
|Pages||118 - 123|
The involvement of C-reactive protein (CRP) in early (acute) and delayed ischaemic (IPC) and pharmacological (chemical) (CPC) preconditioning in an <I>in vivo</I> model of rat myocardial infarction is presented. Acute IPC was produced by three 5-min occlusion (ischaemia) periods interspersed with 5 min reperfusion, followed by 30-min occlusion of the left coronary artery and 2 h reperfusion injury. Acute CPC was produced by a <SPAN lang=AF style="FONT-FAMILY: Symbol; mso-ascii-font-family: 'Times New Roman'; mso-hansi-font-family: 'Times New Roman'; mso-char-type: symbol; mso-symbol-font-family: Symbol"><SPAN style="mso-char-type: symbol; mso-symbol-font: Symbol">k</SPAN></SPAN>-opioid receptor agonist U50488H (5 mg/kg) applied i.v. 15 min before 30-min ischaemia /2-h reperfusion. Delayed preconditioning was produced by 30-min ischaemia /2-h reperfusion, induced 24 h after either ischaemic or pharmacological preconditioning. The myocardial ischaemia / reperfusion injury was evaluated on the basis of total and cardiac creatine kinase isoenzyme activity, functional recovery of the heart (ECG), infarct size (% IS/RA) and mortality at the end of the experiments. <br>The results obtained showed that: <ul> <li>The <SPAN lang=AF style="FONT-FAMILY: Symbol; mso-ascii-font-family: 'Times New Roman'; mso-hansi-font-family: 'Times New Roman'; mso-char-type: symbol; mso-symbol-font-family: Symbol"><SPAN style="mso-char-type: symbol; mso-symbol-font: Symbol">k</SPAN></SPAN>-opioid receptor agonist U50488H mimics both the acute and delayed IPC in the above experimental protocol. </li> <li>Both acute IPC and CPC produce effects by opening of the K<sub>ATP</sub> channels (the effects were blocked by nonspecific ATP-sensitive K channel blocker glybenclamide), and via activation of protein kinase C (a selective protein kinase C inhibitor chelerythrine blocked the effects). </li> <li>C-reactive protein was significantly elevated by 54% in non-preconditioned acute ischaemia / reperfusion injury. The elevation was more pronounced (82% increase) 24 h after non-preconditioned ischaemia/ reperfusion injury. It reflected very well the increase in cardiac isoenzymes, infarct size and mortality of the rats, and can be used as a marker of the severity of myocardial injury in this model. </li> <li>The increase of CRP was prevented by both IPC and CPC in early, and especially in late preconditioning. This shows the involvement of CRP, not only as a marker, but as a causative factor in cardiac ischaemic / reperfusion injury.</li></ul> <I>Conclusion:</I> In addition to the established involvement of adenosine, bradykinin, opioid and other receptors, a suppression of myocardial CRP / complement production might be involved in the biological mechanism of preconditioning. This could be a promising perspective in clinical interventions against ischaemia / reperfusion injuries of the heart.
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