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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was done to quantitate the evolution of myocardial ischemic cell death within the framework of (1) the anatomical boundaries of the ischemic bed at risk and (2) the magnitude and transmural distribution of collateral blood flow. Myocardial ischemia was produced by proximal circumflex (LCC) occlusions in open chest dogs. Infarcts reperfused at 40 minutes, 3 hours, or 6 hours were compared with permanent infarcts. All dogs were sacrificed at 4 days. Regional myocardial blood flow was measured with 9-micrometer tracer microspheres before, and 20 minutes after, LCC occlusion. The location and size of the ischemic LCC bed at risk was determined by a dye injection technique. Infarct size was quantitated from multiple histologic sections. Necrosis involved 28 per cent, 70 per cent, and 72 per cent of the ischemic bed at risk in infarcts reperfused at 40 minutes, 3 hours, and 6 hours versus 79 per cent following permanent LCC ligation. Viable and potentially salvageable subepicardial muscle persisted for at least 3 hours after the onset of ischemia. Most of the salvageable myocardium was in the subepicardial region. In all groups, the lateral margins of necrosis were sharp in the subendocardial zone and were determined by the anatomical boundaries of the ischemic LCC bed at risk. LCC bed size ranged from 29 to 48 per cent of the left ventricle and thus contributed to variation in infarct size. However, infarct size, as a percentage of bed size, was determined by the transmural extent of necrosis within that bed (r = -0.97). This transmural extent of necrosis was related to subepicardial collateral flow after 3 hours (r = 0.92) and 6 or 96 hours (r = -0.85) but not after 40 minutes (r = -0.26) of ischemia. Thus, irreversible injury of ischemic myocardium developed as a transmural wavefront, occurring first in the subendocardial myocardium but ultimately becoming nearly transmural. Eventual transmural necrosis, and therefore over-all infarct size was determined by, and can be predicted from flow measurements obtained shortly after coronary occlusion.
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PMID:The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. 44 73

Fourteen mongrel dogs were anesthetized and instrumented to measure arterial pressure (AP), left ventricular pressure (LVP), aortic blood flow, and heart rate (HR). Hydraulic occluders were placed around the left anterior descending (LAD, n = 9) and left circumflex (LCC, n = 14) coronary arteries. A bilateral carotid occlusion (BCO) was made before and during either anterior (LAD occlusion) or posterior (LCC occlusion) ischemia. Posterior ischemia significantly (P less than 0.01) reduced the BCO-induced increases in mean AP (by 44.3 +/- 7.3%), systolic LVP (by 65.5 +/- 6.9%), first derivative of LVP (dLVP/dt, by 95.7 +/- 44.3%), and aortic resistance (by 117.7 +/- 26.9%). In contrast, anterior ischemia failed to alter significantly the hemodynamic response to BCO. Bilateral vagotomy attenuated or eliminated many of the effects of posterior ischemia on the BCO response. In fact, the change in aortic resistance was no longer affected by the ischemia and increased to the same extent, as noted during the control BCO. However, mean AP (38.7 +/- 6.8%), systolic LVP (40.3 +/- 8.7%), and dLVP/dt (62.4 +/- 11.0%) remained significantly reduced when compared with the control (no coronary occlusion) response. These data suggest that 1) posterior ischemia elicits a greater reduction in the BCO response than anterior ischemia, and 2) vagal afferents as well as depression of contractile function may both contribute to the BCO response inhibition noted during posterior ischemia.
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PMID:Effect of myocardial ischemia on hemodynamic response to carotid occlusion. 292 33

The ischaemic bed size (myocardium at risk) and collateral flow are major determinants of experimental myocardial infarct size. These parameters were compared in dogs with coronary occlusions at four commonly used sites. Regional blood flow was measured 5 min after proximal coronary occlusion of the circumflex (LCC) or anterior descending (LAD) arteries, or after distal occlusion of the LAD, or its apical branch. Occlusions were done sequentially in random order separated by 30 min intervals. The anatomic regions normally supplied by each occluded artery (ischaemic beds) were identified by simultaneous postmortem coronary perfusion with different coloured dyes. Proximal occlusions of the LCC and LAD produced equivalent areas of ischaemia (37 and 36% of the left ventricle) and these ischaemic beds had similar amounts of collateral flow (0.12 and 0.16 cm3.min-1.g-1). In comparison, distal LAD and apical branch occlusions involved 23 and 11% of the LV and collateral flow averaged 0.23 and 0.36 cm3.min-1.g-1. Thus, proximal LAD or LCC occlusion produce comparable areas of severe ischaemia. Experimental models using distal occlusions are characterised by more variable but often less severe ischaemia.
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PMID:Effect of coronary occlusion site on ischaemic bed size and collateral blood flow in dogs. 732 85