Contractile and biochemical effects of coronary reperfusion after extended periods of coronary occlusion

Puri, Pritpal S.

doi:10.1016/0002-9149(75)90533-0

Cited by 107 publications

(9 citation statements)

References 24 publications

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“…These data differ from those reported by Mathur et al (1975), Costanrini et al (1975), Puri (1975), and Theroux et al (1976). All of these prior studies reported substantial return of function in severely ischemic tissue with reperfusion at either 2 or 3 hours after coronary artery occlusion.…”

Section: Figure 7 Time Course Of Systolic Shortening In the Moderatecontrasting

confidence: 75%

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

Lavallée¹,

Cox²,

Patrick³

et al. 1983

Circulation Research

192

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SUMMARY. The effects of coronary artery occlusion and reperfusion at 1 hour (1-hr group), 2 hours (2-hr group), and 3 hours (3-hr group) were compared with a permanently occluded group (P group) on measurements of overall left ventricular and regional endocardial function over a 4-week period. The studies were conducted in conscious dogs 1-2 weeks after recovery from instrumentation with solid state left ventricular pressure gauges, aortic, and left atrial catheters, hydraulic occluders, and Doppler flow transducers on the left anterior descending or left circumflex coronary arteries, and multiple pairs of ultrasonic transducers implanted in the endocardial third of the left ventricular free wall to measure endocardial segment shortening. During coronary artery occlusion, similar effects were observed in the four groups. At 1 hour after coronary artery occlusion, three classes of ischemia-induced dysfunction were observed; dyskinetic (systolic shortening completely lost and replaced by paradoxical bulging), severely hypokinetic (systolic shortening depressed by 65-95%), and moderately hypokinetic (systolic shortening depressed by 40-65%). Compared with the P group, significant (P < 0.05) return of systolic shortening and velocity of shortening gradually occurred over the 4-week period following reperfusion in all classes of segments in the 1-hour group. In the 2-hour group, systolic shortening returned in the moderately and severely hypokinetic segments, but was slight and not significant in the dyskinetic segments. In the 3-hour group, significant systolic shortening returned only in the moderately hypokinetic segments. The effects of isoproterenol, 0.04 /ig/kg per min, and exercise were compared on 'salvaged' dyskinetic segments prior to and at 1, 2, 3, and 4 weeks after coronary artery occlusion and reperfusion. The responses to isoproterenol were significantly depressed at 1 week after reperfusion and gradually recovered over the 4-week period. At 3-4 weeks after reperfusion, severe exercise also increased shortening and velocity of shortening in 'salvaged' segments. Thus, in the conscious dog, coronary artery reperfusion at 1 hour after coronary artery occlusion results in substantial return of endocardial function even in the most severely ischemic myocardium. The 'salvaged' myocardium responds adequately to myocardial stress with increases in the extent and velocity of systolic shortening, as long as 3-4 weeks after reperfusion are allowed for recovery. However, after 3 hours of coronary artery occlusion, little salvage of regional myocardial function can be induced by acute reperfusion in this model. (Circ Res 53: 235-247, 1983)

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Section: Figure 7 Time Course Of Systolic Shortening In the Moderatecontrasting

confidence: 75%

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

Lavallée¹,

Cox²,

Patrick³

et al. 1983

Circulation Research

192

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“…The study was limited to pa tients in whom treatment could be initiated within the first 4 h following the onset of pain, as laboratory studies have shown that myocardium may not be preserved if reper fusion is achieved later [11][12][13], Patients with a history of previous infarction have preexisting myocardial dysfunction and were excluded to avoid interference with in terpretation of catheterization data. Ante rior infarcts on average have a more pro found effect on left ventricular function than do inferior infarcts, and were therefore viewed separately.…”

Section: Discussionmentioning

confidence: 99%

Early Prediction of Left Ventricular Function in Streptokinase-Treated Acute Myocardial Infarction

Fine

Weiss²,

Welber³

et al. 1988

Cardiology

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We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.

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“…By electronmicroscopy tissue samples exhibited mild to moderate alterations of mitochondrial ultrastructure typically found in ischemically damaged myocardium (36).…”

Section: Histologic Examinationmentioning

confidence: 95%

“…84, No. I (1989) function are common findings in reversibly injured myocardium (20,21,36), many authors believe that a causal relationship between these postischemic alterations exists (32,33,39,51). However, there might be only a non-causal coincidence of the time courses in reduction of adeninenucleotides and of basal function (29,30,47,48).…”

Section: Introductionmentioning

confidence: 99%

High-energy phosphates, myocardial contractile function and material properties after short periods of oxygen deficiency

et al. 1989

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To investigate myocardial performance and diastolic properties after repeated periods of oxygen deficiency auxotonic and isovolumic measurements were performed after three periods (4 min) of asphyxia in Wistar rats (n = 19). Additionally, the response of the peak isovolumic left ventricular pressure to postextrasystolic potentiation was measured. The hemodynamic results were compared to the levels of high-energy phosphates. Already after 15 min of recovery from asphyxia auxotonic measures of systolic function were completely normal compared to the control group (n = 19). Isovolumic measurements after 20 min of postasphyctic recovery, however, demonstrated a considerable reduction of the peak left ventricular pressure (226.5 +/- 7.5 mm Hg vs. 262.6 +/- 3.4 mm Hg in controls, mean +/- SEM (p less than 0.01) indicating persistence of decreased postischemic contractile performance. The relative effect of postextrasystolic potentiation was similar in both groups, but could not compensate for the reduced performance of the postasphyctic hearts: the absolute postextrasystolic peak isovolumic pressure of the postasphyctic hearts was lower than the value of the regular isovolumic peak pressure in the controls. Diastolic properties (pressure/volume and stress/strain relationships) of the postasphyctic myocardium remained unchanged. The total sum of the adenine-nucleotides decreased from 7.2 +/- 0.2 to 5.6 +/- 0.3 mumol/gww (p less than 0.01). ATP was reduced from 4.8 +/- 0.2 to 3.9 +/- 0.3 mumol/gww (p less than 0.01). Phosphocreatine was elevated to 7.0 +/- 0.6 mumol/gww, x +/- SEM (p less than 0.01). Our results demonstrated normal postasphyctic basal hemodynamics and material properties. Thus, the energy supply was sufficient to maintain steady state conditions - in spite of decreased overall adenine-nucleotide levels. Isovolumic measurements and postextrasystolic potentation tests, however, indicated that the contractile performance of the postischemic myocardium was still reduced. This functional limitation cannot be explained by altered material properties and is probably not causally related to the decreased overall ATP content.

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Contractile and biochemical effects of coronary reperfusion after extended periods of coronary occlusion

Cited by 107 publications

References 24 publications

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs.

Early Prediction of Left Ventricular Function in Streptokinase-Treated Acute Myocardial Infarction

High-energy phosphates, myocardial contractile function and material properties after short periods of oxygen deficiency

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