Contribution to the Problem of Morphological Evidence of Hypoxic Changes in the Myocardium

Kolín, A

doi:10.1159/000167354

Cited by 8 publications

(1 citation statement)

References 2 publications

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“…Lipid accumulation in the myocardium as a result of hypoxia has been reported clinically in patients with angina pectoris, diphtheria, and particularly during over doses of catecholamines [Anderson. 1957: Kolin. 1961.…”

Section: Discussionmentioning

confidence: 99%

Isoproterenol-Induced Myocardial Ischemic Injury in the Rabbit: Functional and Ultrastructural Alterations

Bhimji¹,

Godin

McNeill³

1986

Cells Tissues Organs

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The functional and ultrastructural changes observed during myocardial ischemic injury (Mil) in the rabbit are described. Mil was induced by repeated subcutaneous injections of increasing doses of isoproterenol (ISO; 0.5 mg/kg on day 1, to 15.5 mg/kg on day 15). Measurement of cardiovascular changes revealed a significant decrease in the mean arterial pressure and an increase in heart rate of the ISO-treated animals. ISO treatment also initiated a variety of atrial and ventricular arrhythmias, including ventricular fibrillation, as well as significant ST segment elevations and the appearance of Q waves. Electron-microscopic analysis of hearts from ISO-treated animals showed accumulation of lipid and depletion of glycogen. The myofibrils had poorly defined Z bands and appeared as a homogenous mass. The most marked effects of ISO treatment were on the mitochondria, which appeared swollen and fragmented. The mitochondrial cristae were also disrupted and fragmented. A few amorphous electron-dense bodies were observed in and around the mitochondria. The changes observed in this study are qualitatively similar to those observed in the rabbit following coronary artery ligation.

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Section: Discussionmentioning

confidence: 99%

Isoproterenol-Induced Myocardial Ischemic Injury in the Rabbit: Functional and Ultrastructural Alterations

Bhimji¹,

Godin

McNeill³

1986

Cells Tissues Organs

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The response of the early chick embryo heart to anoxia

Roberts

1966

Journal Cellular Physiology

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Isolated 3-and 5-day chick embryo hearts contain sufficient endogenous substrates to maintain their pulsatile activity for several hours under aerobic conditions, and even after five hours in substrate-free medium the rates are 40 to 50% of the original rates. Carbohydrate appears to be an important component of the endogenous substrates since 1 mM 2-deoxyglucose causes rapid failure of rate, and glycolysis appears to be a major energy pathway since the rate is depressed only about 50% by 2-hour's exposiire t o 10mM fluoroacetate. In nitrogen the hearts rapidly become asystolic in the absence of added substrate. Recovery of the rate occurs if oxygen is reintroduced within one hour, but longer periods of anoxia result in progressively less recovery, especially with the 3-day hearts which appear to be particularly susceptible to irreversible damage. With 5.55 mM glucose as substrate there is little decrease in the original aerobic heart rate during five hours, and the hearts can tolerate total anoxia for five hours with rates only slightly less than the aerobic rates. The hypothesis of a preferential pentose phosphate pathway of glucose catabolism in the very young chick embryo heart is discussed, but no direct evidence in support of its existence is revealed in this study.

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A Histochemical Study of Long Term Changes in Myocardial Lipid Distribution Induced by Isoproterenol

Bawa

Singal

Relan

et al. 1985

Developments in Cardiovascular Medicine

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Contribution to the Problem of Morphological Evidence of Hypoxic Changes in the Myocardium

Cited by 8 publications

References 2 publications

Isoproterenol-Induced Myocardial Ischemic Injury in the Rabbit: Functional and Ultrastructural Alterations

Isoproterenol-Induced Myocardial Ischemic Injury in the Rabbit: Functional and Ultrastructural Alterations

The response of the early chick embryo heart to anoxia

A Histochemical Study of Long Term Changes in Myocardial Lipid Distribution Induced by Isoproterenol

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