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KMID : 0377619970620060489
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Korean Jungang Medical Journal
1997 Volume.62 No. 6 p.489 ~ p.496
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No penetrating Injuries of the Heart and Experimental Model of Blunt Trauma on the Chest in Rats
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Abstract
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The injuries of the heart are classified into the penetrating and the no penetrating myocardial injuries with or without underlying heart disorders and they are clinically emergent. Generally, no penetrating myocardial injuries are combined with the other relatively emergent injuries of the lung, brain, skeleton, or abdominal organs. In these cases, sometimes, clinicians overlook the myocardial injuries due to externally serious symptoms of other injuries, in spite of life-threatening myocardial injury.
To save the patients with no penetrating myocardial injuries, close observation, several laboratory tests, and intensive care with exact diagnosis are necessary. And in autopsy, clinical data must be reviewed, and the whole heart must be examined grossly and microscopically. However, in the cases combined with underlying heart disorder which could be the cause of sudden unexpected natural death, minute trauma which is not valuable in the healthy person and has no visible injuries in myocardium grossly or microscopically act as a triggering factor of sudden death. No penetrating injuries of the heart are cardiac concussion, cardiac contusion, complete or partial rupture of atrium, ventricle, papillary muscle, or corda tendinae, and delayed rupture of cardiac structures, myocardial infarct, cardiac tamponade, sudden or delayed onset of arrhythmia, and so on. All of these injuries are engaged in the sudden death, regardless to the underlying heart disease. In autopsy reports, to decide the direct cause of sudden death such as trauma induced injury, underlying heart disorder, or both, the relationship between them must be clarified.
Experimental rats injured by blunt chest trauma with optimum kinetic energy reveal abnormal ECG findings such as increased amplitude of impulse, bradycardia, or arrhythmia in early stage of trauma, and ST segment elevation after 24 hours. Microscopically the injured myocardium is replaced by mononuclear cells in posttraumatic 48 or 72 hours and path physiologically expected to be replaced by fibrosis after several days or weeks. From these results, experimental model may be useful to investigate about the path physiology, clinical course, and response to various treatment in posttraumatic myocardial injury.
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KEYWORD
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