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)

To examine the role of kallikrein in the etiology of flushing in the carcinoid syndrome, chromogenic substrates specific for kallikrein were used to measure two isoenzymes of this substance. The plasma and glandular kallikrein levels were determined in 20 carcinoid patients and in 17 controls. Kallikrein levels were not significantly different between these two groups. Twelve carcinoid patients and six controls were given alcohol and the kallikrein activity was measured before and at 2, 5, and 10 minutes after alcohol ingestion; kallikrein activity did not change significantly. Kallikrein was absent from the primary tumors of seven patients with carcinoids. These studies, therefore, indicate that kallikrein with subsequent induction of bradykinin formation is not solely responsible for the flushing in the carcinoid syndrome.
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PMID:Flushing in the carcinoid syndrome and plasma kallikrein. 242 58

Acetaldehyde (AcH), the first metabolite of ethanol (EtOH), is a chemically reactive and pharmacologically active compound. The author has been engaged in the study of AcH in cooperation with many researchers for three decades. We have found many biological actions of AcH which cause cardiovascular symptoms after drinking and also inhibited EtOH absorption via the canine and rat intestinal tract. This report covers the following five points. 1. The subjects were classified into a non-flushing group and a flushing group, according to the degree of facial flushing after drinking 200 ml of Sake (Japanese rice wire) at a rate of 100 ml per 5 min. Blood EtOH profile was much the same in both groups, yet peak blood AcH concentration in the flushing group was significantly higher than that in the non-flushing group. All subjects in the flushing group showed marked flushing and an increase in pulse rate after drinking, but these symptoms were not apparent in the non-flushing group. These results suggested that cardiovascular symptoms were caused by AcH itself. 2. Urinary excretions of both norepinephrine and epinephrine increased in the flushing cases after drinking Sake in comparison with those who drank the same volume of water. However, these catecholamines did not change in the non-flushing group. These results suggested that it is catecholamines released from the sympathetic nerve end or the adrenal medulla by AcH which caused an increase in pulse rate. 3. Bradykinin is released from high molecular kininogen by activated kallikrein and acts to dilate distal blood vessels and raise permeability in tissues. On the other hand, kallidin is released from low molecular kininogen by activated glandular kallikrein and its action is weaker than that of bradykinin. Blood low molecular kininogen levels in the flushing group decreased gradually after drinking and were mutually related to the blood AcH concentrations. But levels in the non-flushing group showed no difference before and after drinking. The decrease in low molecular kininogen levels indicates that kallidin released from glandular kallikrein exists in the glandular tissues such as the kidneys, sweat glands, saliva glands, etc. We hypothesize that kallikrein activated by AcH in the sweat glands produces kallidin which cause vessels around the glands to dilate, and flushing of the face and the whole body occurs due to escalation of the sphere of dilatation of blood vessels. 4. A isolated 30 cm length of the canine jejunum segment with intact vascular supply was performed. After pretreatment with cyanamide (CY), a potent inhibitor of aldehyde dehydrogenase, or pyrazole (PY), a potent inhibitor of alcohol dehydrogenase, a 17% EtOH solution (0.4 g/kg) was administered into the jejunum segment, and 150 min after the administration of EtOH, the fluid from the segment was collected to determine its volume and EtOH concentration. The CY-pretreatment group, in which an extremely high AcH concentration developed, in comparison with the control and PY-pretreatment groups, showed a gradual increase of portal blood EtOH, a 25% reduction in the amount of absorbed EtOH, and an 85% smaller absorption rate constant value (Ka value). These facts indicate that the presence of a high AcH concentration in the blood results in a reduction of EtOH absorption and retardation of EtOH reaching the systemic circulation. The rapid reduction of portal blood flow and lower EtOH level in the portal vein observed in the CY group, in comparison with the other groups, also indicate that the reduction of EtOH permeability through the absorption site to the blood is an important retarding factor induced by AcH. 5. After segmenting a 20 cm length of rat intestine, cannulae for EtOH perfusion were inserted into each end of the intestine segment. Perfusion of EtOH solution (4%) was performed for 30 min at steady rate, beginning 60 min after pretreatment with CY and/or PY. The blood EtOH and AcH concentrations in the f
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PMID:[Biological actions of acetaldehyde]. 1072 60