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)

Five per cent heat treated stable plasma protein solution (SPPS) has been rapidly infused into 25 patients, as fluid replacement during large volume plasmapheresis. Reactions were produced in 20 patients. Subjective symptoms of flushing, nasal stuffiness, fullness and throbbing in the head, colicky abdominal pain, metallic taste or apprehension were observed in 16 patients, and 11 patients became hypotensive with an average systolic pressure of 70 mm Hg. These observations support earlier reports of hypotension due to rapid SPPS infusion, and document the occurrence of subjective symptoms which may be the harbingers of a hypotensive reaction. In view of the known presence of a bradykinin-like substance in some heat treated plasma protein solutions, hypotension during SPPS infusion should be interpreted with caution in the light of these findings.
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PMID:Reactions to rapid infusion of stable plasma protein solution during large volume plasma exchange. 93 17

To understand better the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema, we studied the effects of ACE-inhibitor treatment on wheal-and-flare responses to histamine, codeine, and bradykinin in 10 normal subjects. No change in the size of wheal-and-flare reactions to histamine occurred, but the size of wheal reactions to codeine and bradykinin increased in all study subjects after ingesting the ACE inhibitor, captopril. Five of 10 study subjects developed flushing reactions after ACE-inhibitor treatment. We conclude that inhibition of bradykinin metabolism by ACE inhibitors is the probable cause of ACE inhibitor-related angioedema and that substance P is not the predominant mediator in this process.
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PMID:Studies of the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema: the effect of an ACE inhibitor on cutaneous responses to bradykinin, codeine, and histamine. 218 92

Japanese healthy male subjects were divided into two groups, i.e., a normal aldehyde dehydrogenase (ALDH) group with a low Km isozyme of ALDH for acetaldehyde, and a deficient group without it. After intake of 0.4 g/kg alcohol, the deficient group showed high levels of blood acetaldehyde, facial flushing including an increased pulse rate and a fall in diastolic blood pressure, while the normal group did not manifest these changes. In the deficient group, the total kininogen concentration gradually decreased after alcohol intake due to a reduction in low molecular weight kininogen, and plasma prekallikrein remained unchanged. The normal group showed no significant changes in any of these values after alcohol intake. In an in vitro study with pooled plasma, the low concentrations of urinary kallikrein caused a decrease in the low molecular weight kininogen only. These results suggest that kinins released by acetaldehyde-induced activation of glandular kallikreins are associated with the changes in cardiovascular symptoms in deficient group which display flushing after alcohol intake.
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PMID:Possible involvement of kinins in cardiovascular changes after alcohol intake. 232 Jun 52

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

1. To test the hypothesis that angiotensin converting enzyme (ACE) inhibitors potentiate the tissue effects of bradykinin, the thickness of weals produced by intradermal injections of bradykinin was measured in 17 hypertensive subjects whose antihypertensive regimen included an ACE inhibitor, and in 12 whose treatment did not. 2. Weal thickness increased linearly with the logarithm of the bradykinin dose in both groups (P less than 0.0001). 3. The patients receiving ACE inhibitors showed a mean response of 1.18 +/- 0.08 mm (mean +/- s.e. mean), compared with a mean response of 0.75 +/- 0.08 mm for patients not receiving an ACE inhibitor (P = 0.002). Mean weal response (1.08 +/- 0.9 mm) was not significantly different in patients taking captopril (n = 11) compared with that (1.29 +/- 0.12 mm) in patients taking enalapril (n = 9). 4. Facial flushing during the experiment occurred in six patients taking ACE inhibitors but none who were not. 5. Dermal responses to bradykinin are enhanced in patients taking ACE inhibitors as routine antihypertensive therapy. This study supports the hypothesis that bradykinin may be responsible for some of the adverse effects of these drugs.
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PMID:The effects of intradermal bradykinin are potentiated by angiotensin converting enzyme inhibitors in hypertensive patients. 254 53

Carcinoid syndrome produces flushing, bronchoconstriction and gastrointestinal hypermotility secondary to serotonin, histamine, bradykinin and prostaglandin release. A variety of drugs, foods and anaesthetic agents may provoke this syndrome. Under anaesthesia, the flushing produced may be associated with acute hypotension and cardiovascular collapse; this phenomenon is called a carcinoid crisis. Recently, somatostatin analogue has been used successfully to treat intraoperative carcinoid crisis. In this report, we present a 66-year-old lady with carcinoid syndrome who was pre-treated with 50 micrograms somatostatin analogue IV and IM prior to surgical manipulation. The anaesthetic course was relatively uneventful and the patient did well postoperatively.
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PMID:Pre-treatment with somatostatin in the anaesthetic management of a patient with carcinoid syndrome. 290 85

The exact etiology of carcinoid flushing remains unknown, but the symptoms are probably mediated through release of one or several humoral substances. Flushing seen in fore-gut carcinoids (gastric carcinoids) has been ascribed to excessive histamine release, whereas flushing seen in mid-gut carcinoids (ileal carcinoids) tentatively has been ascribed to excessive release of serotonin, bradykinin, substance P, substance K or eledoisin. In this study plasma histamine was measured in 8 patients with mid-gut carcinoids and carcinoid syndrome using an enzymatic isotopic method in order to evaluate histamine as the vasoactive agent in patients with ileal carcinoid tumours and carcinoid syndrome. All patients had raised plasma histamine values. In patients with mid-gut carcinoids histamine may be one of the substances mediating flushing.
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PMID:Histamine in carcinoid syndrome. 318 38

Bradykinin concentrations in peripheral venous blood were measured in seven patients with carcinoid syndrome. The diagnosis was based on typical symptoms and raised urinary excretion of 5-hydroxy-3-indole acetic acid; the carcinoid tumour was verified histologically. Two patients were flushing constantly and the other patients had flushing attacks two to 10 times daily. Several blood samples were taken at weekly intervals from six of seven patients. During 30 sampling procedures the patients were flushing during sampling in 12 instances. Bradykinin was measured by a sensitive solid phase radioimmunoassay technique. Blood bradykinin concentration was normal in all patients. Bradykinin is unlikely to be the vasoactive mediator of flushing.
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PMID:Bradykinin in carcinoid syndrome. 342 66

Flushing in rosacea has been investigated by means of (a) pharmacological inhibition of some possible chemical mediators and (b) titration of bradykinin as a possible effector directly in the blood. Clonidine-inhibited flushing was seen in all patients (mean 45%), other drugs had poorer results. Bradykinin increased in all patients at the climax of flushing (mean 60%). These findings support the hypothesis that epinephrine promotes a bradykinin release responsible for vasodilation.
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PMID:Flushing in rosacea: a possible mechanism. 621 30

RMP-7, a nine amino acid peptide bradykinin agonist, increases the delivery of hydrophilic compounds across the blood-tumour barrier. In this dose ranging study, 14 patients with progressing malignant glioma (9 glioblastoma multiforme, 4 anaplastic astrocytoma, 1 anaplastic oligodendroglioma; age range 31-68 years, baseline Karnofsky range 60-90%, 5 having had prior chemotherapy) were treated with intravenous RMP-7 and carboplatin to assess the safety, tolerability, and side-effect profile of increasing doses of this combination. Carboplatin dosing was by target area under the curve (AUC) according to the Calvert protocol. Patients were allocated to one of five treatment regimes: cohort A (n = 2) received 50 ng/kg RMP-7 and target AUC 5 mg/ml/min carboplatin; cohort B (n = 3) 100 ng/kg RMP-7 + AUC 5; cohort C (n = 2) 100 ng/kg RMP-7 + AUC 7; cohort D (n = 2) 200 ng/kg RMP-7 + AUC 7; cohort E (n = 5) 300 ng/kg RMP-7 + AUC 7. Treatment was given once every 4 weeks with magnetic resonance imaging scans every 2 months. Patients received 37 cycles in total (median 2, range 1-7). The drug combination, as a cancer treatment, was tolerated in all groups. Effects possibly related to RMP-7 included flushing, nausea, headache and mild increase in heart rate, all transient. 3 patients in cohort E experienced grade 3/4 neutropenia and thrombocytopenia. These toxicities are consistent with known effects of carboplatin at this dose range. In cohort E (n = 5) 1 patient improved and another remained stable for > or = 6 months. In summary, the dose was escalated to the maximum dose of RMP-7 given to volunteers without additional related side-effects. The side-effects of the combination were consistent with giving the two drugs alone and would merit further study for efficacy.
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PMID:A phase I study of intravenous RMP-7 with carboplatin in patients with progression of malignant glioma. 989 73


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