Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet-activating factor (PAF), one of the harmful substances released after coronary reperfusion, has been reported to increase pulmonary vascular permeability and induce pulmonary edema. In this study, we sought to examine the possible role of PAF in the genesis of pulmonary edema after coronary reperfusion. Extravascular lung water (EVLW) was measured by the thermal-dye double indicator dilution method during coronary ligation and after reperfusion in situ in dogs. The proximal left anterior descending coronary artery was occluded for 15 min and reperfused in 5 dogs (group 1), while five other dogs (group 2) were treated with PAF-antagonist (TCV-309, 1 mg/kg) before coronary artery occlusion. EVLW and hemodynamic indices were measured at baseline, 15 min of coronary occlusion, and 15 and 30 min after coronary reperfusion. EVLW increased at 15 min of coronary occlusion in both groups, but there was no significant difference between the two groups (6.4 to 10.3 ml/kg and 5.4 to 7.1 ml/kg in groups 1 and 2, respectively). After coronary reperfusion, EVLW increased further in group 1 (6.4 to 16.5 ml/kg, p < 0.01), but no further increase was observed in group 2 at 30 min after coronary reperfusion. There were no significant differences in hemodynamic indices between the two groups throughout the test. Thus, PAF-antagonist attenuated the increase in EVLW after coronary reperfusion independent of hemodynamic indices, and hence, PAF may play an important role in the genesis of pulmonary edema caused by coronary reperfusion.
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PMID:Role of platelet-activating factor on extravascular lung water after coronary reperfusion in dogs. 963 51

Wellens' syndrome represents critical occlusion of the proximal left anterior descending coronary artery. Electrocardiographic changes similar to Wellens' wave are not exceptional to acute coronary occlusion and can also be seen in cardiac and non-cardiac conditions, such as left ventricular hypertrophy, persistent juvenile T wave, bundle branch blocks, cerebral haemorrhage, pulmonary oedema, pulmonary embolism, pheochromocytoma, Takotsubo syndrome, digitalis and cocaine-induced coronary vasospasm. Cocaine-induced pseudo-Wellens' syndrome should be considered as one of the differentials, since cocaine is used frequently by young adults and can cause left anterior descending coronary vasospasm mimicking Wellens' syndrome. Initiation of the beta-blocking agent in pseudo-Wellens' syndrome as a part of acute coronary syndrome management can be disastrous. We illustrated a case of cocaine-induced pseudo-Wellens' syndrome presented with typical chest pain associated with Wellenoid ECG.
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PMID:Cocaine-induced pseudo-Wellens' syndrome: a Wellens' phenocopy. 2924 35