Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated myocardial interstitial norepinephrine kinetics in both the ischemic and nonischemic regions during reperfusion after 40 min of coronary occlusion in anesthetized cats. By use of a cardiac dialysis technique, dialysate norepinephrine contents from both regions were monitored as an index of myocardial interstitial norepinephrine levels. For vehicle perfusate (n = 8), the accumulated dialysate norepinephrine level in the postischemic region decreased from 3,010 +/- 923 pg/ml at 30-40 min of occlusion to 957 +/- 178 pg/ml at 0-10 min of reperfusion and returned to near control level at 30-40 min of reperfusion. After 40 min of reperfusion, there were no significant differences in tyramine (100 micrograms/ml, norepinephrine-releasing sympathomimetic amine)-induced norepinephrine release between both regions. For perfusate containing 100 microM desipramine (neural uptake inhibitor, n = 6), at 0-10 min of reperfusion, the dialysate norepinephrine in the postischemic region did not significantly decrease. The dialysate norepinephrine then returned to near preocclusion level at 30-40 min of reperfusion. These data suggest that reperfusion rapidly returns accumulated myocardial norepinephrine to the preischemic level and neuronal norepinephrine uptake greatly contributes to this return in the early phase of reperfusion. Forty minutes of coronary occlusion cause neither norepinephrine exhaustion nor irreversible impairment of norepinephrine uptake function in nerve terminals.
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PMID:Regional myocardial interstitial norepinephrine kinetics during coronary occlusion and reperfusion. 876 58

This review article integrates empirical findings from various scientific disciplines into a proposed psychoneuroimmunological (PNI) model of the acute coronary syndrome (ACS). Our starting point is an existing, mild, atherosclerotic plaque and a dysfunctional endothelium. The ACS is triggered by three stages. (1) Plaque instability: Pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha) and chemoattractants (MCP-1, IL-8) induce leukocyte chemoattraction to the endothelium, and together with other triggers such as the CD40L-CD40 co-stimulation system activate plaque monocytes (macrophages). The macrophages then produce matrix metalloproteinases that disintegrate extra-cellular plaque matrix, causing coronary plaque instability. Acute stress, hostility, depression and vital exhaustion (VE) have been associated with elevated pro-inflammatory cytokines and leukocyte levels and their recruitment. (2) Extra-plaque factors promoting rupture: Neuro-endocrinological factors (norepinephrine) and cytokines induce vasoconstriction and elevated blood pressure (BP), both provoking a vulnerable plaque to rupture. Hostility/anger and acute stress can lead to vasoconstriction and elevated BP via catecholamines. (3) Superimposed thrombosis at a ruptured site: Increases in coagulation factors and reductions in anticoagulation factors (e.g. protein C) induced by inflammatory factors enhance platelet aggregation, a key stage in thrombosis. Hostility, depression and VE have been positively correlated with platelet aggregation. Thrombosis can lead to severe coronary occlusion, clinically manifested as an ACS. Thus, PNI processes might, at least in part, contribute to the pathogenesis of the ACS. This chain of events may endure due to lack of neuroendocrine-to-immune negative feedback stemming from cortisol resistance. This model has implications for the use of psychological interventions in ACS patients.
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PMID:Molecular and cellular interface between behavior and acute coronary syndromes. 1223 62