Ultrastructural changes of ischemic injury due to coronary artery occlusion in the porcine heart

Myocardial cells undergo extensive ultrastructural changes during ischemia, easily observed after 30 minutes of coronary artery occlusion. Although various membranous organelles remain intact during acute ischemia, biochemical evidence indicates several metabolic alterations in affected cells. Since cell membranes and membranes of intracellular organelles play an important role in the pathogenesis of myocardial cell injury, changes in their interiors could be informative. However, such changes are not easily detectable in conventional thin sections. This study examined ultrastructural alterations in the membranous organelles of ischemic myocardium using the freeze-fracture technique to improve detection of such changes.After 5 and 24 hours of coronary artery occlusion the hearts from dogs and rats were perfused with buffered glutaraldehyde. Small pieces of the left ventricle were dipped in Freon 22 and immediately frozen in liquid nitrogen before fracturing in a Balzer's freeze-etch apparatus at -100 or -120°C.

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Bradykinin as an endogenous myocardial protective substance with particular reference to ischemic preconditioning–a brief review of the evidence

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y95-114 ◽

1995 ◽

Vol 73 (7) ◽

pp. 837-842 ◽

Cited By ~ 49

Author(s):

James R. Parratt ◽

Agnes Vegh ◽

Julius Gy. Papp

Keyword(s):

Coronary Artery ◽

Myocardial Ischemia ◽

Ischemic Preconditioning ◽

Myocardial Injury ◽

Ischemic Injury ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Ventricular Pacing ◽

Acute Myocardial Injury ◽

Rapid Ventricular Pacing

The present brief review summarizes the evidence for the possibility that endogenously released bradykinin plays a major role in protecting the heart against the consequences of acute myocardial injury. This evidence includes the facts that kinins are generated under myocardial ischemia; that when they are administered, they are cardioprotective (e.g., antiarrhythmic); that drugs that enhance the release of bradykinin from the ischemic heart reduce the ischemic injury and, conversely, drugs that block bradykinin receptors attenuate the reduction in ischemic injury resulting from the release of, or administration of, bradykinin. The possible mechanism of bradykinin in the cardioprotection afforded by ischemic preconditioning is summarized. Ischemic preconditioning can be defined as the marked reduction in the severity of ischemic changes that result from coronary artery occlusion when that occlusion is preceded by brief periods of myocardial ischemia, either regional or global, induced, for example, by complete or partial coronary artery occlusion or by rapid ventricular pacing. The possible mechanisms of cardioprotection elicited by bradykinin (and ischemic preconditioning) are summarized. The most likely is the generation of cyclic GMP within the ischemic myocardium following bradykinin-stimulated nitric oxide generation and release from endothelial cells.Key words: endogenous myocardial protective substances, bradykinin, ischemic preconditioning, cardiac arrhythmias, myocardial ischemia.

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Intramural PCO2: a reliable index of the severity of myocardial ischemic injury

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1979.237.2.h253 ◽

1979 ◽

Vol 237 (2) ◽

pp. H253-H259 ◽

Cited By ~ 1

Author(s):

S. F. Khuri ◽

R. A. Kloner ◽

L. D. Hillis ◽

D. E. Tow ◽

E. M. Barsamian ◽

...

Keyword(s):

Coronary Artery ◽

Histological Examination ◽

Mass Spectrometer ◽

Ischemic Injury ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Regional Myocardial Blood Flow ◽

Severity Of Injury ◽

Anesthetized Dogs ◽

Myocardial Ischemic Injury

The present study was performed to evaluate the usefulness of changes in intramural oxygen (PmO2) and carbon dioxide (PmCO2) tensions shortly after coronary artery occlusion as indices of the severity of myocardial ischemic injury. In 14 open-chest, anesthetized dogs, a 60-min coronary artery occlusion was performed, during which PmO2 and PMCO2 were measured continuously with a mass spectrometer. Regional myocardial blood flow (RMBF) adjacent to the mass spectrometer probes was measured by the xenon-127 washout technique both before and 30 min after coronary artery occlusion. At the end of 60 min of occlusion, the dogs were killed, and biopsies for histological examination of 1-micron-thick sections were obtained from the tissue surrounding each mass spectometer probe. The decline in PmO2 during the 60-min occlusion bore no relationship either to the severity of ischemic injury as assessed by histological examination, or to the reduction of RMBF. In contrast, the magnitude of rise in PmCO2 during the 60 min of occlusion corresponded closely to both the severity of injury assessed histologically and the reduction of RMBF.

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