The Protective Effect of Intravenous Adenosine on Myocardial Reperfusion Injury in Feline Heart Model.
10.4070/kcj.1994.24.4.633
- Author:
Dong Gu SHIN
;
Young Jo KIM
;
Bong Sub SHIM
;
Jun Ha LEE
;
Chong Min PARK
;
Mi Jin KIM
- Publication Type:Original Article
- Keywords:
Intravenous adenosine;
Reperfusion injury
- MeSH:
Adenosine*;
Administration, Intravenous;
Animals;
Blood Pressure;
Capillaries;
Cats;
Coronary Occlusion;
Coronary Vessels;
Heart Rate;
Heart*;
Incidence;
Myocardial Reperfusion Injury*;
Myocardial Reperfusion*;
Necrosis;
Neutrophils;
Peroxidase;
Reperfusion;
Reperfusion Injury;
Ventricular Function;
Ventricular Function, Left
- From:Korean Circulation Journal
1994;24(4):633-644
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Among the various mechanisms of Myocardial reperfusion injuries, neutrophil is thought to be one of them. Endogenous coronary vasodilator adenosine is known to have myocardial protective effect through variable pharmacologic action, influencing the function of several cell types involved in the pathogenesis of myocardial reperfusion injury. This study was designed to determine the beneficial effect of adenosine on the left ventricular function during reperfusion and whether this effect is due to the adenosine on the role of neutrophil. METHODS: 27 open-chest cats were randomly divided into 3 groups. 6 cats received ischemic injury without reperfusion(group 1). 21 cats were subjected to 60 minutes of proximal left anterior descending coronary artery occlusion followed by a 60-minute reperfusion. 11 of 21 cats received intravenous adenosine(0.15mg/Kg/min) infusion starting 5 minutes before reperfusion throughout the entire period(group 3). 10 cats received equal volume of saline instead of adenosine(group 2). RESULTS: 1) During the experimental period, significant decrease of heart rate, blood pressure, RPI, negative dP/dT and increase of LVEDP were noted in group 2 and 3 with no difference between the two groups. The reduction of positve dP/dT was more significant in group 2 at 30 and 60 minute of reperfusion than the preocclusion value(1404+/-111, 1631+/-161 vs 1832+/-169mmHg/sec at baseline, p<0.05). In contrast, positive dP/dT in group 3 at 30 and 60 minute of reperfusion were similar to baseline values(1890+/-92, 2052+/-112 vs 2025+/-227mmHg/sec at baseline, p=NS). These were significantly higher(p<0.05) than untreated group 2. 2) Infarct size was significantly reduced in adenosine-treated group 3, when expressed as a percentage of the area at risk(28.4+/-3.3% vs 44.5+/-3.2% of group 2, p<0.05). The significant increase in myeloperoxidase activity observed after reperfusion was not detected in adenosine treated group 3.(0.18+/-0.05 vs 0.46+/-0.09 unit/100mg wet tissue weight, p<0.05). A significant correlation was present between infarct size (% of left ventricle) and myeloperoxidase activity(r=0.72, p<0.01). 3) Light microscopic examination demonstrated the decreased acute interstitial and intra vascular inflammatory infiltration and capillary plugging together with decreased tendency of incidence of contraction band necrosis in adenosine treated group 3. CONCLUSION: These findings suggest that intravenous administration of adenosine during the early reperfusion period significantly reduces infarct size, improving the early recovery of global ventricular function. The probable cause is the effect of adenosine on neutrophil as one of the various protective mechanisms of adenosine in feline heart model subjected to coronary occlusion and reperfusion, 60 minutes each.
