The Effect of Coronary Occlusion on Myocardial Contraction

Tennant, Robert; Wiggers, Carl J.

doi:10.1152/ajplegacy.1935.112.2.351

Cited by 1,050 publications

(207 citation statements)

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“…Relative to the first of these features, it has been demonstrated that within seconds after ligation of a major coronary artery, the affected myocardium will cease contracting normally and will actually bulge during systole. 19 In the second series, therefore, the alteration in distribution of blood flow evoked by higher intraventricular pressures may be attributable either to its effects upon the non-contracting myocardium, or to its influence upon collateral rather than cognate channels.…”

Section: Discussionmentioning

confidence: 99%

Intraventricular Pressure and the Distribution of Coronary Blood Flow

Cutarelli

Levy

Zieske

et al. 1963

Circulation Research

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The subepicardial: subsendocardial ratio of Rb 86 contents was measured and used as an index of the distribution of coronary blood flow to the more superficial and deeper layers of the canine myocardium. In the normally beating heart, the level of intraventricular pressure did not exert any detectable influence upon this ratio of Rb 86 contents. In the fibrillating heart, or in an ischemic (and presumably non-beating) region of the beating heart, on the other hand, this ratio increased as intraventricular pressure was progressively raised. It is concluded, therefore, that the intraventricular pressure exerts a significant influence upon the distribution of blood flow to the deeper and more superficial layers of myocardium only in regions which are not beating normally.

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Section: Discussionmentioning

confidence: 99%

Intraventricular Pressure and the Distribution of Coronary Blood Flow

Cutarelli

Levy

Zieske

et al. 1963

Circulation Research

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“…Correlating the echocardiographic and morphologic data for each myocardial slice, we identified three categories: (1) To test the null hypothesis that there is no di-fference in systolic wall thickening or motion between tissue that was infarcted, adjacent to infarction, and distant normal, separate two-way analyses of variance were performed using a general linear model for the dependent variables of thickening and motion. The independent factors were tissue morphology and dog.…”

Section: Analysis Of Datamentioning

confidence: 99%

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Lieberman¹,

Weiss²,

Jugdutt³

et al. 1981

Circulation

527

136

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SUMMARY To study endocardial wall motion and thickness as indexes of infarction, we used two-dimensional echocardiography to examine regional percentages of systolic wall thickening (%Th) and endocardial motion (%EM) in infarcted canine hearts. Thirteen dogs were studied 48 hours after occlusion of the circumflex or left anterior descending coronary artery. Two-dimensional echocardiographic cross sections obtained every 16 msec at 1-cm intervals from apex to base in an open-chest, anesthetized preparation were analyzed with a computer-aided contouring system for quantification of segmental %EM and %Th at 16 equally spaced points per slice. Slices corresponding to each two-dimensional echocardiographic cross section were examined pathologically for evidence of infarction.Comparing histologically infarcted with distant normal zones in each slice, %Th and %EM both yielded clear separation with little overlap (-12.5% infarcted vs 37.4% normal for thickness; -11.3 vs 25.7% for motion, p << 0.001 for both). Endocardial motion was less precise than thickening, however, in distinguishing infarct from either distant normal zones or zones directly adjacent to infarct.Although wall thickening was useful in separating out true subendocardial infarct, change in systolic thickening was not accurate in detecting the transmural extent of infarction. In 827 individual two-dimensional echocardiographic segments with varying degrees of transmural involvement, segments with 1-20% extent of transmural infarction showed reduced thickening compared with noninfarcted segments (39.9 vs 15.2%, p < 0.001), whereas myocardial segments with 21-100% transmural infarction showed systolic thinning (-8.9 to -13.3%). There was no significant augmentation in the severity of systolic thinning as the extent of transmural infarction increased from 21% to 100%.We conclude that: (1) Wall motion abnormalities are less precise than thickening in discriminating between infarcted and noninfarcted zones and could lead to overestimation of infarct size. (2) There is an abrupt deterioration in systolic thickening in segments containing more than 20% transmural extent of infarction. (3) There is no significant augmentation in the degree of systolic thinning as the transmural extent of infarct increases from 21% to 100%. This "threshold" phenomenon may therefore preclude accurate estimation of infarct size by two-dimensional echocardiography. (4

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“…Furthermore Gd is commonly used to interrupt stretch-mediated changes in intracellular ion flux in the heart through a presumed blockade of specific stretch-activated ion channels (22)(23)(24). Since mechanical stretch causes pathophysiologic changes in the myocardium (1,22,25,26), and regional myocardial ischemia results in abnormal stretch (2,27,28), the effects of Gd observed herein may also be related to modulation of ion fluxes that are caused by ischemia-induced stretch. Effects on K ATP and perhaps other ion channels may be of particular importance when Gd is administered one minute before reperfusion, as cell signaling to induce gene expression (as postulated above) would be a less likely factor in such a short time frame.…”

Section: Discussionmentioning

confidence: 90%

Gadolinium limits myocardial infarction in the rat: Dose–response, temporal relations and mechanisms

Nicolosi

Strande

Hsu

et al. 2008

Journal of Molecular and Cellular Cardiology

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The lanthanide cation, gadolinium (Gd) attenuates post-ischemic myocardial stunning. This study tests the hypothesis that Gd also preconditions the myocardium against infarction following ischemia-reperfusion (IR), and explores potential mechanisms underlying Gd-induced cardioprotection. Regional myocardial infarction was induced in rats by occluding the left anterior descending artery for 30 minutes and reperfusing for 120 minutes. Rats (n = 6/group) were administered intravenous Gd (1 to 100 μmol/kg) 15 minutes prior to ischemia. Hearts were excised after reperfusion to determine infarct size (IS) and area at risk (AAR). The ratio IS/AAR (%) was reduced by Gd in a "U"-shaped, dose-dependent manner. The minimum dose that reduced IS/AAR was 5 μmol/kg (52 ± 5% vs. 64 ± 4%), while the dose that reduced IS/AAR maximally was 20 μmol/ kg (44 ± 4%). Gd also reduced IS/AAR when given 1 minute before reperfusion (47 ± 3%) but not when given 10 seconds after reperfusion (60 ± 3%). Cardioprotection was maintained if I-R was delayed 24-72 hours after Gd administration. Cardioprotection by Gd was abolished by inhibition of JAK-2 with AG-490, of p42/44 MAPK with PD98059 or of K ATP channels with glibenclamide.

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The Effect of Coronary Occlusion on Myocardial Contraction

Cited by 1,050 publications

References 0 publications

Intraventricular Pressure and the Distribution of Coronary Blood Flow

Intraventricular Pressure and the Distribution of Coronary Blood Flow

Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog.

Gadolinium limits myocardial infarction in the rat: Dose–response, temporal relations and mechanisms

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