Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."
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PMID:Myocardial ischemia induced by prostacyclin and iloprost. 240 9

A case in which aminophylline solution was administered to a patient with congestive heart failure is reported and the problems caused by administration were solved by subsequent experiments. Dopamine solution was added from the side route using a mechanical pump, and mixed with aminophylline solution in the main route. Furosemide was administered after clamping and flushing the main route according to the supplier's information that indicated the compatibility of dopamine and aminophylline. However, the aminophylline solution turned black in color 3 h after furosemide administration. Several examinations were carried out to clarify the cause of the incompatibility in this case. The results showed that solutions with all possible combinations, including aminophylline and dopamine, turned black at 24 h after mixing, and the UV absorption at 430 nm increased from 0 to 0.28. UV absorption of the mixed solution increased in a dopamine dose-dependent manner in the range of 1.5-12 mg. When aminophylline was added to physiological saline or hypotonic electrolyte solution, the pH of each solution increased. These results suggested that degradation of dopamine to a melanin-like polymer under alkaline conditions caused the change in color of the solution. It is presumed that dopamine was inappropriately injected into aminophylline solution as the route was clamped tightly to shut out furosemide contamination. Aminophylline and dopamine are often co-administered to patients in critical condition. Thus, even if compatibility of aminophylline with dopamine is indicated by the supplier, they should be administered through separate routes.
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PMID:[Examination of the cause of changing solution color by mixing aminophylline and dopamine, the compatibility of which was indicated by the supplier]. 2449 31