Twenty-four mini-swines were randomized into 3 study groups: 8 in control group, 8 in
fosinopril-treated group (1 mg.kg(-1).d(-1)) and 8 in
sham-operated group. Animals in the former two groups were subjected to 3 hours of
coronary occlusion followed by 60 minutes of reperfusion. Data on haemodynamics and coronary blood flow volume (CBV) were collected, and the area of no-reflow was evaluated with both myocardial contrast echocardiography (MCE) in vivo and pathological means.
Necrosis area was measured with
triphenyltetrazolium chloride (TTC) staining.
RESULTS: (1) In the control group, systolic and diastolic blood pressure (SBP and DBP), left ventricular systolic pressure (LVSP), maximal rate of increase and decrease in left ventricular pressure (+/- dp/dt(max)) and cardiac output (CO) 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 occlusion of left anterior descending artery (both P < 0.01). Compared with those at the end of 3 hours of occlusion, +/- dp/dt(max) further significantly declined (P < 0.05) at 60 minutes of reperfusion. In the
fosinopril group, the changes of SBP and DBP, LVSP, +/- dp/dt(max), CO, LVEDP and PCWP were similar as those in the control group after 3 hours of acute
myocardial infarction. In contrast, LVSP, +/- dp/dt(max), CO, LVEDP and PCWP recovered significantly at 60 minutes of reperfusion. (2) In the control group, the coronary
ligation area was similar on both MCE in vivo and pathological evaluation, and the area of no-reflow was similarly as high as 78.5% and 82.3%, respectively, with final
necrosis area reaching 99% of
ligation area. In the
fosinopril group, there was no significant difference in
ligation area on both MCE and pathological evaluations between the
fosinopril and control groups, although the area of no-reflow on both methods was significantly decreased to 24.5% and 25.2%, respectively, (P < 0.01) with final
necrosis area of pathological evaluation being also significantly decreased to 88.9% of LA (P < 0.05). (3) In the control group, CBV was significantly declined to 45.8% and 50.6% from at baseline, immediately after release of occlusion (3 hours) and at 60 minutes of reperfusion (P < 0.01). In the
fosinopril group, CBV was also significantly declined immediately after release of occlusion (3 hours), and at 60 minutes of reperfusion (P < 0.05), but significantly increased to 69.1% and 72.1% from at baseline, that were significantly greater than those in the control group (both P < 0.01).
CONCLUSION: