Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion

Sharma, Gyan Prakash; Varley, Kenneth G.; Kim, Sung W.; Barwinsky, J; Cohen, Morley; Dhalla, Naranjan S.

doi:10.1016/0002-9149(75)90532-9

Cited by 86 publications

(7 citation statements)

References 19 publications

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“…High-energy phosphate content of the reperfused myocardium showed a pattern similar to that of contractile recovery.29 Myocardial cell swelling and edema during ischemia36' 37 and after reperfusion are also potential causes of delayed recovery of myocardial contractility. Sharma et al 27 reported that reperfusion after 60 and 90 min of ischemia produced swelling of the sarcoplasmic reticulum and mitochondrial damage. In our study, during the early phase of CIRCULATION Downloaded from http://ahajournals.org by on April 4, 2019 reperfusion EDWTh in the ischemic area was increased significantly in association with reactive hyperemia while wall thickness in the control area was unchanged (tables 2 and 3, figures 3 and 5), but mean coronary flow velocity and EDWTh in the ischemic area had returned to control levels at 24 hr after reperfusion, giving no definite evidence of edema.…”

Section: Resultsmentioning

confidence: 99%

Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.

Matsuzaki¹,

Gallagher²,

Kemper³

et al. 1983

Circulation

254

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Prolonged nontransmural ischemia was produced and the early and late effects of reperfusion were studied in 10 conscious dogs instrumented over the long term. Five hours of partial circumflex coronary artery-stenosis was produced with a hydraulic occluder, followed by gradual release over 20 min, with measurements of left ventricular pressure, regional myocardial function (systolic wall thickening by sonomicrometry), coronary blood flow velocity (pulsed Doppler), and myocardial blood flow (microspheres). During coronary stenosis the occluder was adjusted frequently to maintain a reduction of systolic wall thickening to 50% to 75% of control (average 62.6% of control). Myocardial blood flow in the ischemic area at 4 hr of partial coronary stenosis was reduced in the inner layers of the myocardium (subendocardium, from 0. 170-182, 1983. WITH the advent of surgical and nonsurgical revascularization of ischemic myocardium in man, coronary artery reperfusion has become an important therapeutic intervention. Many investigators" have reported the effects of reperfusion on ischemic myocardium after various periods of total coronary occlusion, but the value of this intervention remains controversial. The question of whether or not prolonged but revers- 170ible myocardial ischemic dysfunction can occur without coronary occlusion has also remained unexamined. In addition, despite recent clinical experience with coronary artery reperfusion by clot lysis or surgical means after acute myocardial infarction,9-there is little information on recovery of contractile function in zones that are partially perfused and exhibit nontransmural myocardial ischemia. In this study we investigated the effects of reperfusion on myocardial function and blood flow distribution over a 7 day period after 5 hr of partial coronary stenosis in conscious dogs instrumented over the long term. MethodsTen adult mongrel dogs weighing 22.1 to 39.6 kg (mean 28.4) were premedicated with acepromazine maleate (0.5 mg/ CIRCULATION

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Section: Resultsmentioning

confidence: 99%

Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.

Matsuzaki¹,

Gallagher²,

Kemper³

et al. 1983

Circulation

254

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“…ATP, required for optimal binding of cardiac glycosides to (Na+ + K+) -ATPase (6), has been shown to be rapidly depleted during acute ischemia (2). In addition, reperfusion instituted after 1 h of coronary occlusion has been shown in an experimental model to result in a greater decrease in myocardial ATP and ATP/ADP ratio than was observed with occlusion alone (25). Third, acute myocardial ischemia might cause reduced cardiac glycoside-binding activity of (Na+ + K+) -ATPase due to structural and/or functional damage to the transport enzyme complex that would be demonstrable even in the presence of optimal binding conditions.…”

Section: Discussionmentioning

confidence: 99%

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

Conroy¹,

Smith²

1976

J. Clin. Invest.

100

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“…Al though the ultrastructural changes following cardiac ischemia are reversed within 1 h of reperfusion [3,4], myocardial metabolic and contractile functions remain depressed for several hours to a few days [2,5,6], This state of prolonged myocardial dysfunction, without irreversible cellular injury, has been termed the stunned myocardium [5], Although a wide variety of mechanisms have been proposed to explain this abnormality, the mechanisms re sponsible for this prolonged dysfunction have not been established.…”

Section: Introductionmentioning

confidence: 99%

Facilitated Recovery of Cardiac Performance by Triiodothyronine following a Transient Ischemic Insult

Yokoyama

Novitzky²,

Deal³

et al. 1992

Cardiology

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Reperfusion following a transient ischemic insult has been shown to result in a delayed recovery of myocardial function. A reduction in plasma triiodothyronine (T₃) has been reported in these acute cardiovascular challenges. To test whether the replacement of T₃ can facilitate the recovery of myocardial function following a transient regional ischemia, we investigated cardiac performance for 3 h after a 15-min, left anterior descending coronary artery occlusion in a canine model. Three groups of dogs were studied: I – control (n = 10); II -receiving T₃ (0.25 µg/kg i.v. and 0.25 µg/kg/h for 3 h, n = 9), and III – receiving T₃ (0.25 µg/kg i.v. and 0.5 µg/kg/h for 3 h, n = 9). Three hours following reperfusion, the T3 level in blood was significantly decreased in group I. Concomitantly, local segmental shortening was reduced from preocclusion control levels in group I (15.2 to 5.1%, p < 0.05), but recovered in both treated groups. The endsystolic elastance (Ees) and the external work (EW) efficiency (EW/PVA) in group I were depressed from preocclusion control (Ees = 95.5 ± 0.8%; EW/PVA = 90.2 ± 1.8%, both p < 0.05), the effective arterial elastance (Ea) and ventriculoarterial coupling (Ea/Ees) in group I were still elevated from preocclusion control (Ea = 122.5 ± 5.1%; Ea/Ees =128.3 ± 5.3%, both p < 0.05). But these measures of global cardiac performance in the treated groups recovered following reperfusion, and the extent of recovery was dose dependent. These data suggest that T₃ facilitates recovery of the stunned myocardium by improvement in local and global contractile function, in ventriculoarterial coupling, and in the energy efficiency.

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Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion

Cited by 86 publications

References 19 publications

Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.

Sustained regional dysfunction produced by prolonged coronary stenosis: gradual recovery after reperfusion.

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

Facilitated Recovery of Cardiac Performance by Triiodothyronine following a Transient Ischemic Insult

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