Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction

Hanich, Robert F.; Levine, Joseph; Prood, Charles; Weiss, James L.; Callans, David J.; Spear, Joseph F.; Moore, E. Neil

doi:10.1016/0002-8703(93)90052-b

Cited by 13 publications

(3 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…During coronary occlusion the pulse pressure significantly decreased in all experimental groups, and the pulse pressures remained significantly less than baseline values at the end of reperfusion. This depression could be a reflection of myocardial stunning due to the ischemic interventions (17) and/or due to loss of viable myocardium.…”

Section: Resultsmentioning

confidence: 99%

β₁-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

Spear¹,

Prabu²,

Galati³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

Protein kinase A (PKA) activation has been implicated in early-phase ischemic preconditioning. We recently found that during ischemia PKA activation causes inactivation of cytochrome- c oxidase (CcO) and contributes to myocardial damage due to ischemia-reperfusion. It may be that β-adrenergic stimulation during ischemia via endogenous catecholamine release activates PKA. Thus β-adrenergic stimulation may mediate both myocardial protection and damage during ischemia. The present studies were designed to determine the role of the β1-adrenergic receptor (β1-AR) in myocardial ischemic damage and ischemic preconditioning. Langendorff-perfused rabbit hearts underwent 30-min ischemia by anterior coronary artery ligation followed by 2-h reperfusion. Occlusion-reperfusion damage was evaluated by delineating the nonperfused volume of myocardium at risk and volume of myocardial necrosis after 2-h reperfusion. In some hearts ischemic preconditioning was accomplished by two 5-min episodes of global low-flow ischemia separated by 10 min before coronary occlusion-reperfusion. Orthogonal electrocardiograms were recorded, and coronary flow was monitored by a drip count. Three hearts from each experimental group were used to determine mitochondrial CcO and aconitase activities. Two-hour reperfusion after occlusion caused an additional decrease in CcO activity vs. that after 30-min occlusion alone. Blocking the β1-AR during occlusion-reperfusion reversed CcO activity depression and preserved myocardium at risk for necrosis. Similarly, mitochondrial aconitase activity exhibited a parallel response after occlusion-reperfusion as well as for the other interventions. Furthermore, classic ischemic preconditioning had no effect on CcO depression. However, blocking the β1-AR during preconditioning eliminated the cardioprotection. If the β1-AR was blocked after preconditioning, the myocardium was preserved. Interestingly, in both of the latter cases the depression in CcO activity was reversed. Thus the β1-AR plays a dual role in myocardial ischemic damage. Our findings may lead to therapeutic strategies for preserving myocardium at risk for infarction, especially in coronary reperfusion intervention.

show abstract

Section: Resultsmentioning

confidence: 99%

β₁-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

Spear¹,

Prabu²,

Galati³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In an open-chest dog model of myocardial stunning (15-min ischemia and reperfusion), spontaneous reentrant arrhythmias usually occurred within only a few minutes [35]. Stevens et al [36] reported that VF often occurred at reperfusion in an in vivo swine model of myocardial stunning.…”

Section: Discussionmentioning

confidence: 99%

Milrinone Administered Before Ischemia or Just After Reperfusion, Attenuates Myocardial Stunning in Anesthetized Swine

Use

Makita

Ureshino

et al. 2006

Cardiovasc Drugs Ther

View full text Add to dashboard Cite

show abstract

“…Reperfusion injury in the intact heart is characterized by a transient contractile dysfunction in the absence of myocardial necrosis and electrophysiological abnormalities [15,16] that outlasts the actual ischemic period for hours to days [1,18]. A variety of mechanisms have been suggested to account for the depressed function of the so-called stunned myocardium [3].…”

Section: Introductionmentioning

confidence: 99%

Ca 2+ sensitivity of stunned myocardium after skinning using retrograde infusion of detergent

Geyer¹,

Strauss²,

Rüegg³

et al. 1999

Pfl�gers Archiv European Journal of Physiology

View full text Add to dashboard Cite

Myofilament Ca2+ desensitization contributes to the contractile dysfunction of ischemic/reperfused ("stunned") myocardium. We examined the presence of reduced Ca2+ sensitivity of isometric force in chemically skinned fibers obtained from stunned myocardium using different modes of applying the detergent Triton X-100. Langendorff-perfused rat hearts underwent 20 min ischemia/20 min reperfusion, which caused a 35 +/- 3% decrease in left ventricular developed pressure, compared to continuously perfused control hearts. Stunned and control hearts were randomly allocated to two different permeabilization protocols: In group A, trabeculae were dissected and immersed in skinning solution containing 1% Triton X-100 for 20 min. Group B hearts remained fixed to the aortic cannula and skinning solution was infused retrogradely for 6 min prior to dissection of trabeculae. Extraction of cytosolic marker proteins was more complete in group-B than in group-A preparations. Group-A preparations from stunned hearts exhibited significant Ca2+ desensitization (pCa50 = 5.07 and 5.15 in stunned and control myocardium, respectively). In group B no such difference was observed, all preparations showing higher Ca2+ sensitivity and maximum force than group-A preparations (pCa50 = 5.32 in stunned versus 5.33 in control hearts). Prolonging group-A skinning to 150 min also abolished the difference in Ca2+ sensitivity between stunned and control myocardium. In conclusion, compared to a conventional protocol, skinning by perfusion results in more complete permeabilization and better preservation of myocardial contractile function. Ischemia/reperfusion at this moderate degree of contractile dysfunction induces Ca2+ desensitization at least partially by factors that can be extracted by thorough skinning.

show abstract

Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction

Cited by 13 publications

References 24 publications

β₁-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

β₁-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

Milrinone Administered Before Ischemia or Just After Reperfusion, Attenuates Myocardial Stunning in Anesthetized Swine

Ca 2+ sensitivity of stunned myocardium after skinning using retrograde infusion of detergent

Contact Info

Product

Resources

About

Electrophysiologic recovery in postischemic, stunned myocardium despite persistent systolic dysfunction

Cited by 13 publications

References 24 publications

β1-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

β1-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

Milrinone Administered Before Ischemia or Just After Reperfusion, Attenuates Myocardial Stunning in Anesthetized Swine

Ca 2+ sensitivity of stunned myocardium after skinning using retrograde infusion of detergent

Contact Info

Product

Resources

About

β₁-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning

β₁-Adrenoreceptor activation contributes to ischemia-reperfusion damage as well as playing a role in ischemic preconditioning