Related Experiment Videos
An antiarrhythmic effect of adenosine during myocardial ischaemia and reperfusion
1Department of Physiology and Pharmacology, University of Strathclyde, U.K.
Insights
Adenosine and dipyridamole reduced cardiac extrasystoles after coronary artery occlusion in dogs. Adenosine may be an endogenous antiarrhythmic agent, protecting against ventricular fibrillation.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Cardiac Electrophysiology
Background:
- Coronary artery occlusion can trigger cardiac arrhythmias.
- Adenosine's role in cardiac protection is under investigation.
- Purine derivatives accumulate during myocardial ischemia.
Purpose of the Study:
- To investigate the antiarrhythmic effects of adenosine and dipyridamole on cardiac extrasystoles following coronary artery occlusion.
- To determine if adenosine acts as an endogenous antiarrhythmic agent.
- To assess the impact of adenosine and dipyridamole on ventricular fibrillation incidence.
Main Methods:
- Anesthetized greyhound dogs underwent coronary artery occlusion.
- Adenosine and dipyridamole were administered via left ventricular or intravenous routes.
- Cardiac extrasystoles and ventricular fibrillation incidence were monitored.
- Purine derivative levels in coronary venous blood were measured.
Main Results:
- Left ventricular adenosine (10 µg/kg/min) and intravenous dipyridamole (0.25 mg/kg) significantly reduced extrasystoles post-occlusion.
- Intracoronary adenosine (1 µg/kg/min) into the ischemic area increased extrasystoles.
- Left ventricular adenosine reduced ventricular fibrillation from 88% to 43%.
- Adenosine caused hypotension but did not alter blood gases.
- Ischemic myocardium showed increased purine derivatives; dipyridamole elevated baseline purines.
Conclusions:
- Adenosine, particularly when infused into the left ventricle, demonstrates significant antiarrhythmic properties.
- Dipyridamole potentiates adenosine's effects and may also possess antiarrhythmic activity.
- Results support adenosine's role as a locally produced, endogenous antiarrhythmic agent during myocardial ischemia.
Abstract:
Adenosine (10 micrograms kg-1 min-1, infused into the lumen of the left ventricle) and dipyridamole (0.25 mg kg-1 intravenously, a dose that potentiated markedly the fall in arterial pressure in response to bolus doses of adenosine) each reduced the number of extrasystoles which occurred during the first 30 minutes following coronary artery occlusion in anaesthetised greyhound dogs (from 786 +/- 115 in control dogs to 156 +/- 44 in those treated with adenosine and to 388 +/- 167 with dipyridamole). Intracoronary adenosine (1 microgram kg-1 min-1, infused into the ischaemic area) however appeared to increase the number of extrasystoles to 1230 +/- 214. Left ventricular infusion of adenosine reduced the incidence of ventricular fibrillation (from 88 to 43%) when the ischaemic myocardium was perfused at the end of a 40 min occlusion period. In the dose used in this study (10 micrograms kg-1 min-1) adenosine caused a sustained fall in blood pressure but did not alter blood gases. In control dogs the levels of purine derivatives in blood draining the myocardium rendered ischaemic by coronary artery occlusion (local coronary venous samples) increased gradually during the ischaemic period (from 9 +/- 3 microM pre-occlusion to 25 +/- 7 microM post-occlusion). Dipyridamole increased the resting plasma concentration of purines prior to occlusion by approximately 90%; these remained raised for the occlusion period. These results support the suggestion that adenosine may act as a locally produced endogenous antiarrhythmic agent.