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J Geriatr Cardiol. 2013 Mar;10(1):52-8. doi: 10.3969/j.issn.1671-5411.2013.01.009.

Effects of tirofiban on the reperfusion-related no-reflow in rats with acute myocardial infarction.

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1
Department of Cardiology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, Liaoning Province, China.

Abstract

OBJECTIVE:

To investigate the effects of tirofiban on the no-reflow phenomenon of acute myocardial infarction (AMI) rats received reperfusion, as well as the underlying mechanisms.

METHODS:

Fifty-six male Sprague-Dawley rats were randomly divided into four groups: Sham operation group (Sham), AMI/reperfusion group (AMI/R), Tirofiban group (Tiro) and Tiro+N-nitro-L-arginine group (L-NNA; an endothelial nitric oxide synthase inhibitor). To generate the animal model mimicking the no-reflow phenomenon, the rats first received occlusion of the left anterior descending coronary artery for 60 min and then followed by reperfusion for 120 min. Area of no-reflow, area at risk and area of necrosis were measured by thioflavine S, Evans blue and triphenyl tetrazolium chloride staining, respectively. Haemodynamic function was measured at the end. In the meantime, nitric oxide synthase (NOS) activity was determined by a NOS assay kit. The expression of myocardial endothelial nitric oxide synthase (eNOS) was determined by an enzyme-linked immunosorbent assay (ELISA). The expression of phosphorylated eNOS at Ser(1177) (p-eNOS Ser(1177)) and vascular endothelial-cadherin (VE-cadherin) were determined by western blot.

RESULTS:

Compared with AMI/R group, tirofiban significantly reduced the no-reflow area and infarct size (all P < 0.05). Tirofiban elevated eNOS activity, lessen inducible nitric oxide synthase (iNOS) activity and increased the expression of Ser(1177) phosphorylated eNOS and VE-cadherin in the ischemic myocardium (all P < 0.05). No statistical differences were found in the expression of eNOS among the four groups. Also, tirofiban improved cardiac function with significantly higher levels of left ventricular end systolic pressure, maximum change rate of left ventricular pressure rise and fall, heart rate, and lower level of left ventricular end diastolic pressure than those of the AMI/R group (all P < 0.05). Whereas, these effects of tirofiban were partially abolished by L-NNA.

CONCLUSIONS:

Tirofiban could reduce the size of no-reflow and infarct. A possible mechanism underlying this effect is that tirofiban could protect the structural and functional integrity of microvascular endothelium which is partially regulated by eNOS activity.

KEYWORDS:

Acute myocardial infarction; Nitric oxide synthase; Tirofian; Vascular endothelial-cadherin

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