Article

[Beneficial effects of adenosine on myocardial no-reflow in a mini-swine model of acute myocardial infarction and reperfusion].

Department of Coronary Heart Disease, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100037, China.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2005; 33(5):453-8.
Source: PubMed

ABSTRACT To evaluate the beneficial effects of adenosine on myocardial no-reflow in a mini-swine model of acute myocardial infarction (AMI) and reperfusion.
Twenty-four animals were randomly assigned to 3 groups: 8 in controls, 8 in adenosine-treated and 8 in sham-operated. The groups were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion except the sham-operated group. Data on hemodynamics and coronary blood flow volume (CBV) were collected. The area of no-reflow was evaluated by both myocardial contrast echocardiography (MCE) in vivo and histopathological means and necrosis area was measured with triphenyltetrazolium chloride staining.
(1) In control group, systolic and diastolic blood pressure (SBP and DBP), left ventricular systolic pressure, maximal rate of increase and decline in left ventricular pressure (+/- dp/dtmax) and cardiac output significantly declined (P < 0.05-0.01), while left ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) significantly increased at the end of 3 hours of LAD occlusion (both P < 0.01), with +/- dp/dtmax further significantly declined (both P < 0.05) at 60 minutes of reperfusion. In adenosine treated group, the changes of SBP and DBP, left ventricular systolic pressure, +/- dp/dtmax, cardiac output, LVEDP and PCWP were the same as those in the control group after AMI and reperfusion, while left ventricular systolic pressure, +/- dp/dtmax, cardiac output, LVEDP and PCWP recovered significantly at 60 minutes of reperfusion compared with those at 6 hours AMI. (2) In control group, the coronary ligation areas (LA) were similar (P > 0.05) detected by MCE in vivo and histopathological evaluation, and the areas of no-reflow were both as high as 67.5% and 69.3%, respectively. The final necrosis area reached 99% of LA. Compared with those in the control group, there was no significant difference in LA on both MCE and histopathological evaluation in the adenosine-treated group, though the areas of no-reflow on both methods were significantly decreased to 21% and 22% (both P < 0.01) and final necrosis area was also significantly decreased to 75% of LA (P < 0.05). (3) In the control group, CBV were significantly declined to 45.8% and 50.6% of the baseline at immediately after release of 3 hours occlusion and at 60 minutes of reperfusion, respectively (both P < 0.01). In the adenosine-treated group, CBV were also significantly declined at immediately after release of 3 hours occlusion, and at 60 minutes of reperfusion (both P < 0.05), though significantly increased to 79.5% and 79.9% of the baseline which were both significantly higher than those in the control group.
Adenosine has an effective role in preventing myocardial no-reflow, improving left ventricular function and reducing infarct area during AMI and reperfusion in mini-swine.

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