Decreased flow reserve in "stunned" myocardium after a 10-min coronary occlusion
- PMID: 1887925
- DOI: 10.1152/ajpheart.1991.261.3.H793
Decreased flow reserve in "stunned" myocardium after a 10-min coronary occlusion
Abstract
The effect of brief reversible ischemia on coronary vascular function remains controversial. Studies using a 15-min coronary occlusion have reported an impairment of vasodilator reserve, whereas studies using shorter occlusions have not. To elucidate the relation between postischemic vascular abnormalities and duration of ischemic insult, we evaluated coronary reserve after a 10-min coronary occlusion in the same model previously used for a 15-min occlusion. Open-chest dogs (n = 12) underwent a 10-min left anterior descending coronary artery occlusion followed by reflow. Four hours after reperfusion, coronary resistance was higher in the postischemic "stunned" myocardium than in the nonischemic myocardium, both at rest and during adenosine-induced maximal vasodilation; in addition, all indexes of reactive hyperemia after a 40-s coronary occlusion were significantly lower than at baseline. There was no appreciable correlation between systolic wall thickening in the stunned myocardium and 1) the resting myocardial perfusion, 2) the hyperemia attained during adenosine, and 3) the hyperemic response to a 40-s coronary occlusion. The loss of coronary reserve was less than that previously observed after a 15-min occlusion, suggesting that the magnitude of the postischemic vascular abnormalities increases with the duration of the ischemic insult. In control dogs (n = 8), there was no change in coronary reserve. We conclude that a brief ischemic insult lasting only 10 min is sufficient to cause a prolonged increase in resting vascular resistance and a prolonged impairment in vasodilator responsiveness, both of which persist for at least 4 h, indicating the presence of a postischemic microvascular dysfunction. The severity of these vascular derangements is not related to the severity of the contractile depression, suggesting that they may represent a relatively independent phenomenon. The differences among previous studies may be due, in part, to the fact that the abnormalities observed after a 10-min occlusion are relatively subtle.
Similar articles
-
Prolonged impairment of coronary vasodilation after reversible ischemia. Evidence for microvascular "stunning".Circ Res. 1990 Aug;67(2):332-43. doi: 10.1161/01.res.67.2.332. Circ Res. 1990. PMID: 2376075
-
Does preconditioning protect the coronary vasculature from subsequent ischemia/reperfusion injury?Circulation. 1993 Aug;88(2):659-72. doi: 10.1161/01.cir.88.2.659. Circulation. 1993. PMID: 8339428
-
Preservation of coronary flow reserve in stunned myocardium.Am J Physiol. 1989 May;256(5 Pt 2):H1303-10. doi: 10.1152/ajpheart.1989.256.5.H1303. Am J Physiol. 1989. PMID: 2719131
-
Effect of verapamil on postischemic "stunned" myocardium: importance of the timing of treatment.J Am Coll Cardiol. 1988 Mar;11(3):614-23. doi: 10.1016/0735-1097(88)91540-9. J Am Coll Cardiol. 1988. PMID: 3278036 Review.
-
The stunned myocardium: prolonged, postischemic ventricular dysfunction.Circulation. 1982 Dec;66(6):1146-9. doi: 10.1161/01.cir.66.6.1146. Circulation. 1982. PMID: 6754130 Review.
Cited by
-
Reperfusion Injury: Does It Exist and Does It Have Clinical Relevance?J Thromb Thrombolysis. 1997 Jan;4(1):25-34. doi: 10.1023/a:1017521727913. J Thromb Thrombolysis. 1997. PMID: 10639219
-
Common methodological problems and artifacts associated with studies of myocardial stunning in vivo.Basic Res Cardiol. 1995 Jul-Aug;90(4):257-62. doi: 10.1007/BF00797893. Basic Res Cardiol. 1995. PMID: 8534240 Review. No abstract available.
-
Myocardial stunning and hibernation revisited.Nat Rev Cardiol. 2021 Jul;18(7):522-536. doi: 10.1038/s41569-021-00506-7. Epub 2021 Feb 2. Nat Rev Cardiol. 2021. PMID: 33531698 Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources