Quantitative assessment of the extent of myocardial infarction in the conscious dog by means of analysis of serial changes in serum creatine phosphokinase activity

Shell, William E.; Kjekshus, John; Sobel, Burton E.

doi:10.1172/jci106762

Cited by 516 publications

(132 citation statements)

References 24 publications

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“…At least in part it represents loss into the plasma since a correlation exists between loss of myocardial CPK activity and the appearance of CPK in the plasma.26 Also, it has been shown that CPK leaks from the injured area through the lymphatics.27 The observed correspondence between depression of tissue CPK activity and histologic necrosis is consistent with earlier studies.20 26,28 Our conclusions concerning the beneficial effects of an F102 of 0.40 are further strengthened by the observation that epicardial ST-segment elevation following coronary occlusion reflects reduction of cellular PO2,29…”

Section: Discussionsupporting

confidence: 65%

Reduction of infarct size by oxygen inhalation following acute coronary occlusion.

Maroko¹,

Radvany²,

Braunwald³

et al. 1975

Circulation

171

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SUMMARYThis study was carried out in order to determine the effects of the inspiration of 02-enriched air on the size of myocardial infarction. In 15 anesthetized dogs, epicardial electrograms were recorded from 10 to 14 sites on the anterior surface of the left ventricle before and after intermittent occlusion of the left anterior descending coronary artery or one of its major branches. In MethodsThe effect of hyperoxia on myocardial damage following coronary artery occlusion was studied using two protocols.Protocol A: Thirty-six dogs, weighing between 18 and 25 kg, were anesthetized with sodium thiamylal (25 mg/kg) with respiration maintained by a Harvard respirator. The heart was exposed through the fifth left intercostal space and was suspended in a pericardial cradle. The left anterior descending coronary artery (LAD), or its apical branch, was dissected free from the adjacent tissue and occluded intermittently when desired, using a Schwartz intracranial arterial clamp. As previously described,'1 epicardial electrograms were obtained from ten to 14 sites on the anterior surface of the left ventricle, distributed in areas supplied by the occluded artery as well as in areas remote to it and presumably adequately perfused. Two occlusions of 20 min each were carried out with an interval of 60 min for reflow. In 15 dogs two successive occlusions using a fraction of inspired oxygen (F102) of 0.20 (20% 02 concentration) were carried out. In another 15 dogs the first occlusion was with an FIO2 of 0.20 and the second with an FI02 of 0.40 (40% 02 concentration). In six additional dogs, the effects of an F102 of 0.40 during one occlusion were compared to those

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Section: Discussionsupporting

confidence: 65%

Reduction of infarct size by oxygen inhalation following acute coronary occlusion.

Maroko¹,

Radvany²,

Braunwald³

et al. 1975

Circulation

171

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“…In addition to these changes, an increase in sympathetic activity seems to be an important regulatory alteration. Increased activity of the sympathetic nervous system has been implicated in the morbidity induced by myocardial infarction (23,24), and this augmented sympathetic activity facilitates the development of cardiac arrhythmias and the increased extension of the ischemic injury (25) and contributes to some extracardiac regulatory alterations such as sodium balance, with sodium retention expanding extracellular fluid volume (14). This compensatory mechanism may be seen as a compensatory phenomenon acting to preserve the hemodynamic balance despite the decreased cardiac output induced by ventricular dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Chronic experimental myocardial infarction produces antinatriuresis by a renal nerve-dependent mechanism

Souza

Mill

Cabral

2004

Braz J Med Biol Res

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The present study focused on the role of sympathetic renal nerve activity, in mediating congestive heart failure-induced sodium retention following experimental chronic myocardial infarction. Groups of male Wistar rats (240-260 g) were studied: sham-operated coronary ligation (CON3W, N = 11), coronary ligation and sham-operated renal denervation (INF3W, N = 19), 3 weeks of coronary ligation and sympathetic renal nerve denervation (INF3WDX, N = 6), shamoperated coronary ligation (N = 7), and 16 weeks of coronary ligation (INF16W, N = 7). An acute experimental protocol was used in which the volume overload (VO; 5% of body weight) was applied for 30 min after the equilibration period of continuous iv infusion of saline. Compared to control levels, VO produced an increase (P < 0.01, ANOVA) in urine flow rate (UFR; 570%) and urinary sodium excretion (USE; 1117%) in CON3W. VO induced a smaller increase (P < 0.01) in USE (684%) in INF3W. A similar response was also observed in INF16W. In INF3WDX, VO produced an immediate and large increase (P < 0.01) in UFR (547%) and USE (1211%). Similarly, in INF3W VO increased (P < 0.01) UFR (394%) and USE (894%). Compared with INF3W, VO induced a higher (P < 0.01) USE in INF3WDX, whose values were similar to those for CON3W. These results suggest that renal sympathetic activity may be involved in sodium retention induced by congestive heart failure. This premise is supported by the observation that in bilaterally renal denervated INF3WDX rats myocardial infarction was unable to reduce volume expansion-induced natriuresis. However, the mechanism involved in urinary volume regulation seems to be insensitive to the factors that alter natriuresis.

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“…Myocardial CK depletion measured directly from the myocardium, as an index of infarct size, is independent of CK released into the plasma and has been shown to correlate closely with morphology in a variety of animals including the rat (Maclean et al, 1976), dog (Shell et al, 1971), baboon (Yasmineh et al, 1977), and the rabbit (Kjekshus and Sobel, 1970). This correlation is unaffected by a variety of interventions including propranolol (Maroko et al,197 1 ), hyaluronidase (Maroko et al, 1972), nifedipine (Henry et al, 1978), nitroglycerin (Epstein et al.…”

Section: Discussionmentioning

confidence: 99%

The effect of intravenous nitroglycerin on coronary blood flow and infarct size during myocardial infarction in conscious dogs

Fukuyama

Roberts

1980

Clinical Cardiology

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Summary: Nitroglycerin (TNG), based on electrocardiographic evidence, has been shown to reduce myocardial ischemia, but its effect on morphometrically and enzymatically estimated infarct size has not been defined. Accordingly, coronary occlusion was produced in 50 conscious dogs without LV failure. Twenty-five received TNG (200-300 pg/min i.v. for 8 h) and the results compared with those in 25 untreated dogs. Coronary blood flow was measured with I4'Ce, 85Sr, and 95Nb (9 pm) after occlusion before TNG, 30 min after TNG, and again at 8 h. Mean blood pressure decreased from 103 to 84 mmHg with TNG vs. 99 to 94 mmHg in controls (p<0.02). Average heart rates were similar [ 135f26 vs. 120f33 beats/min (SD)]. TNG Did not increase total transmural coronary flow in any region but increased subendocardial flow in the central ischemic areas by 45% (0.09 ml/min/g vs. 0.13 ml/min/g). Animals were sacrificed after 24 h. Infarct size estimated morphometrically (25f 1.5 vs. 2 6 f 1.5 of LV weight) and from myocardial CK depletion ( 2 3 f 2 vs. 2 3 f 2 ) was similar for the two groups. Thus, despite increased subendocardial flow, prolonged i.v. TNG did not decrease infarct size even though a difference of 15% would have been detected with this sample size. TNG May relieve coronary spasm but does not appear to be beneficial with sustained coronary occlusion.

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Quantitative assessment of the extent of myocardial infarction in the conscious dog by means of analysis of serial changes in serum creatine phosphokinase activity

Abstract: A B S T R A

Cited by 516 publications

References 24 publications

Reduction of infarct size by oxygen inhalation following acute coronary occlusion.

Reduction of infarct size by oxygen inhalation following acute coronary occlusion.

Chronic experimental myocardial infarction produces antinatriuresis by a renal nerve-dependent mechanism

The effect of intravenous nitroglycerin on coronary blood flow and infarct size during myocardial infarction in conscious dogs

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