Key result
Coronary occlusion increases plasma VIP in the coronary sinus and portal vein, decreasing after reperfusion.
Why the study?
The role of vasoactive intestinal peptide release during coronary occlusion and its effects on myocardial and gastrointestinal vasodilation remain unclear.
Does coronary artery occlusion and reperfusion alter plasma vasoactive intestinal peptide concentrations in an experimental dog model?
Comparison
LCx occlusion for 60 min with reperfusion vs continuous occlusion for 6 h vs sham-operated controls
Design
Preclinical experimental study
Follow-up
6 hours
Authors
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Should not alter clinical CAD management; leaves open VIP as ischemia biomarker for translational studies.
Does coronary artery occlusion and reperfusion alter plasma vasoactive intestinal peptide concentrations in an experimental dog model?
Coronary artery occlusion causes a sustained increase in plasma VIP concentrations in the coronary sinus and portal vein, which decreases upon reperfusion.
Gyöngyösi et al. (1997) studied Experimental acute myocardial infarction (n=17). Coronary artery occlusion with or without reperfusion vs. Sham-operated controls was evaluated on Plasma concentration of vasoactive intestinal peptide (VIP). Coronary artery occlusion caused a long-term increase in plasma VIP concentrations in the portal vein and coronary sinus, which decreased after reperfusion.
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