Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia
Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. F...
Ausführliche Beschreibung
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Englisch |
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1986 |
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12 |
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Springer Online Journal Archives 1860-2002 |
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in: Basic research in cardiology - 1937, 81(1986) vom: März, Seite 219-230 |
Übergeordnetes Werk: |
volume:81 ; year:1986 ; month:03 ; pages:219-230 ; extent:12 |
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NLEJ208625240 |
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520 | |a Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. | ||
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(DE-627)NLEJ208625240 DE-627 ger DE-627 rakwb eng Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia 1986 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. Springer Online Journal Archives 1860-2002 Sédek, G. oth Michalowski, J. oth in Basic research in cardiology 1937 81(1986) vom: März, Seite 219-230 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:81 year:1986 month:03 pages:219-230 extent:12 http://dx.doi.org/10.1007/BF01907404 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 81 1986 3 219-230 12 |
spelling |
(DE-627)NLEJ208625240 DE-627 ger DE-627 rakwb eng Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia 1986 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. Springer Online Journal Archives 1860-2002 Sédek, G. oth Michalowski, J. oth in Basic research in cardiology 1937 81(1986) vom: März, Seite 219-230 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:81 year:1986 month:03 pages:219-230 extent:12 http://dx.doi.org/10.1007/BF01907404 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 81 1986 3 219-230 12 |
allfields_unstemmed |
(DE-627)NLEJ208625240 DE-627 ger DE-627 rakwb eng Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia 1986 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. Springer Online Journal Archives 1860-2002 Sédek, G. oth Michalowski, J. oth in Basic research in cardiology 1937 81(1986) vom: März, Seite 219-230 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:81 year:1986 month:03 pages:219-230 extent:12 http://dx.doi.org/10.1007/BF01907404 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 81 1986 3 219-230 12 |
allfieldsGer |
(DE-627)NLEJ208625240 DE-627 ger DE-627 rakwb eng Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia 1986 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. Springer Online Journal Archives 1860-2002 Sédek, G. oth Michalowski, J. oth in Basic research in cardiology 1937 81(1986) vom: März, Seite 219-230 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:81 year:1986 month:03 pages:219-230 extent:12 http://dx.doi.org/10.1007/BF01907404 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 81 1986 3 219-230 12 |
allfieldsSound |
(DE-627)NLEJ208625240 DE-627 ger DE-627 rakwb eng Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia 1986 12 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. Springer Online Journal Archives 1860-2002 Sédek, G. oth Michalowski, J. oth in Basic research in cardiology 1937 81(1986) vom: März, Seite 219-230 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:81 year:1986 month:03 pages:219-230 extent:12 http://dx.doi.org/10.1007/BF01907404 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 81 1986 3 219-230 12 |
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evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia |
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Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia |
abstract |
Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. |
abstractGer |
Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. |
abstract_unstemmed |
Summary Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3–5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance. |
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