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Regional myocardial interstitial norepinephrine kinetics during coronary occlusion and reperfusion
T Shindo1, T Akiyama, T Yamazaki
1Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Osaka, Japan.
Insights
Reperfusion quickly restores myocardial norepinephrine levels after coronary occlusion. Neuronal norepinephrine uptake is crucial for this early recovery, indicating no lasting nerve damage.
Area of Science:
- Cardiovascular Physiology
- Neuropharmacology
Background:
- Myocardial interstitial norepinephrine kinetics during reperfusion are not fully understood.
- Investigating norepinephrine levels in ischemic and nonischemic regions is crucial for understanding cardiac recovery.
Purpose of the Study:
- To investigate myocardial interstitial norepinephrine kinetics during reperfusion following coronary occlusion.
- To determine the role of neuronal norepinephrine uptake in norepinephrine level restoration.
Main Methods:
- Cardiac dialysis technique in anesthetized cats to monitor interstitial norepinephrine levels.
- Measurement of dialysate norepinephrine content in ischemic and nonischemic regions during occlusion and reperfusion.
- Assessment of tyramine-induced norepinephrine release and the effect of desipramine (neural uptake inhibitor).
Main Results:
- Reperfusion rapidly decreased accumulated norepinephrine in the postischemic region to near control levels.
- Neuronal norepinephrine uptake inhibition with desipramine delayed the decrease in postischemic norepinephrine levels.
- No significant differences in tyramine-induced norepinephrine release were observed between regions after reperfusion, suggesting no irreversible impairment.
Conclusions:
- Reperfusion effectively restores myocardial norepinephrine levels post-coronary occlusion.
- Neuronal norepinephrine uptake plays a significant role in the early phase of norepinephrine level restoration.
- Forty minutes of coronary occlusion does not lead to norepinephrine depletion or impaired neuronal uptake function.
Abstract:
We investigated myocardial interstitial norepinephrine kinetics in both the ischemic and nonischemic regions during reperfusion after 40 min of coronary occlusion in anesthetized cats. By use of a cardiac dialysis technique, dialysate norepinephrine contents from both regions were monitored as an index of myocardial interstitial norepinephrine levels. For vehicle perfusate (n = 8), the accumulated dialysate norepinephrine level in the postischemic region decreased from 3,010 +/- 923 pg/ml at 30-40 min of occlusion to 957 +/- 178 pg/ml at 0-10 min of reperfusion and returned to near control level at 30-40 min of reperfusion. After 40 min of reperfusion, there were no significant differences in tyramine (100 micrograms/ml, norepinephrine-releasing sympathomimetic amine)-induced norepinephrine release between both regions. For perfusate containing 100 microM desipramine (neural uptake inhibitor, n = 6), at 0-10 min of reperfusion, the dialysate norepinephrine in the postischemic region did not significantly decrease. The dialysate norepinephrine then returned to near preocclusion level at 30-40 min of reperfusion. These data suggest that reperfusion rapidly returns accumulated myocardial norepinephrine to the preischemic level and neuronal norepinephrine uptake greatly contributes to this return in the early phase of reperfusion. Forty minutes of coronary occlusion cause neither norepinephrine exhaustion nor irreversible impairment of norepinephrine uptake function in nerve terminals.