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)

Fenfluramine is a substituted phenylethylamine structurally related to amphetamine. Within three hours following the ingestion of 1,600 mg of fenfluramine, a 17-year-old girl, who was initially agitated and had tachycardia, developed convulsions, cardiac arrhythmia, and cardiorespiratory arrest. In previously reported cases, flushing, sweating, mydriasis, tachycardia, and agitation commonly occur, as well as convulsions and abrupt cardiorespiratory arrest. The rapid onset and progression of symptoms, the short interval between ingestion and death, and the lack of responsiveness to resuscitative measures are common findings in fatal cases.
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PMID:Fenfluramine poisoning. 115 34

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c) AMP is known to act as a second messenger for inhibition of platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side-effects, primarily, nausea, emesis, flushing, diaphoresis, and restlessness. In hypertensive patients blood-pressure responses are complex and are influenced to some extent by renin secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and it also has an indirect effect by activating the sympathetic nervous system. Thus, it is useless as an antihypertensive agent even apart from its debilitating side-effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize large amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be greatly reduced. Some drugs (thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to reduce their antihypertensive effects. The effects of low- and high-dose aspirin on prostacyclin and thromboxane synthesis are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prostacyclin in hypertension]. 149 51

Diethyldithiocarbamate (DDTC), a heavy metal-chelating agent, has been shown to decrease cisplatin (CP) toxicity in preclinical studies. This phase I dose-escalation study was undertaken to investigate DDTC as a chemoprotector in patients with advanced cancer. Thirty-five courses of CP in doses ranging from 120 to 160 mg/m2 were given intravenous (IV) bolus to 19 patients. DDTC at 4 g/m2 was infused over 1 hour, starting 45 minutes after CP. There was minimal nephrotoxicity with a mean creatine clearance of 99 mL/min +/- 4 pretreatment and 86 mL/min +/- 4 on day 21. Two courses were associated with a WBC count less than 2,000/mm3 and one course with a platelet count of 15,000/mm3. Two patients had grade 2 neurotoxicity. Hearing loss occurred in 11 patients: five greater than or equal to 20 dB, five greater than or equal to 40 dB, and one greater than or equal to 60 dB. All patients who received cranial irradiation had ototoxicity compared with 43% of those without radiation (P less than .05). All patients experienced toxicity during the DDTC infusion, including hypertension, flushing, diaphoresis, agitation, and local burning. We conclude that DDTC can protect against CP nephrotoxicity at doses up to 160 mg/m2. Ototoxicity became the dose-limiting factor.
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PMID:Modification of cisplatin toxicity with diethyldithiocarbamate. 164

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c)AMP is known to act as a second messenger for platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP, for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side effects, primarily nausea, emesis, flushing, diphoresis and restlessness. In hypertensive patients blood pressure responses are complex and are influenced to some extent by secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and also has an indirect effect by activating the sympathetic nervous system. Thus it is useless as an antihypertensive agent even apart from its debilitating side effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize larger amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension, endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be defective. Some drugs (cicletanine, thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to abolish their antihypertensive effects. Whether stimulation of PGI2 synthesis affects the antihypertensive efficacy of these drugs is not yet known.
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PMID:Prostacyclin in hypertension. 225 88

Safety, tolerance, and pharmacology of 9-beta-methylcarbacyclin calcium (ciprostene calcium) was investigated in healthy male volunteers. This stable prostacyclin analogue was infused intravenously into groups of 12, 11, and three volunteers for three, six, and eight hours, respectively, in doses up to 480 ng/kg/min. Based on the tolerance data obtained, a single-blind, placebo-controlled study was conducted. Seven subjects were infused for 8 hr/d for three days with ciprostene at a maximum dose of 160 ng/kg/min and seven subjects received placebo. One subject from each group did not complete the infusion schedule, and they were not included in the final analysis. During infusion of ciprostene, consistent changes in blood pressure and heart rate did not occur. Most frequent adverse drug reactions consisted of headache, restlessness, nausea, perspiration, flushing, and jaw pain. As compared with placebo, ADP-induced platelet aggregation was inhibited during the infusion period (P = .048). Significant (P = .04) elevations of platelet cyclic AMP were observed in subjects during infusion of ciprostene. Pre- versus postinfusion routine laboratory evaluations, fibrinogen concentration, antiplasmin activity, and plasminogen and template bleeding times remained unchanged. Placebo- and drug-treated subjects had a daily postinfusion shortening of euglobulin clot lysis time (ECLT). The preinfusion minus postinfusion ECLT for ciprostene subjects on days 2 and 3 (133 and 118 min, respectively) compared with placebo (239 and 217 min) suggest a trend to increased fibrinolytic activity. Based on the outcome of this trial, it is estimated that ciprostene is about 15 times less potent than prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance and pharmacology of ciprostene, a stable epoprostenol (prostacyclin) analogue in humans. 300 77

A case of intravenous labetalol in the treatment of a resistant hypertensive emergency is reported. Although there have been several reports of the use of oral labetalol in resistant hypertension, no intravenous administration in hypertensive emergency resistant to other drugs has been reported to date. A 36-year-old black female with BP of 270/160 mm Hg with complaints greater than one month's duration of dizziness, severe headaches, blurred vision, shortness of breath, vomiting, palpitations, flushing, agitation, diarrhea, weakness, and weight loss, was treated successfully with intravenous labetalol after she failed to respond to other established parenteral antihypertensive drugs. The patient received labetalol 20 mg iv bolus, and then 20 mg every ten minutes until a cumulative dose of 200 mg was attained. Labetalol produced a prompt but smooth reduction in BP without any reflex tachycardia or other adverse effects. Intravenous labetalol may be safe and effective for the management of rapid BP control in hypertensive emergencies resistant to other parenteral antihypertensive agents.
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PMID:Intravenous labetalol in the management of resistant hypertensive emergency. 360 97

The ancient Chinese formula of "San-Huang-Hsieh-Hsin-Tang" (S-T) was originally used for patients with "epigastric fullness, flushing, restlessness, constipation and a hard pulse" (Chang 115 B.C.). All these symptoms are frequently observed in patients with essential hypertension. We assessed the antihypertensive and hemodynamic effects of this formula, and found that S-T decreased blood pressure, total peripheral resistance, heart rate and cardiac contractile force. S-T had no apparent effects on cardiac output and blood volume.
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PMID:Hemodynamic effects of "san-huang-hsieh-hsin-tang" in patients with essential hypertension. 379 32

Available published material of adverse reactions to prostaglandins (PGs) at various dosages routes and levels is reviewed. Animal studies are of 2 kinds: studies of pharmacological effects and studies of toxicological reactions (i.e., acute dose levels). The pharmacology of PGs show the drugs have 3 areas of action: 1) smooth muscle effects, either contraction or relaxation (cardiovascular effects and reproductive tract; relaxation of vascular smooth muscles by some PGs and contraction by others); 2) nervous system effects; and 3) lipid and carbohydrate metabolism. In humans, PGE1 was administered intravenously and it was found that adverse effects were related to rate of administration rather than to total dose; side effects included flushing, headache, visual disturbances, and restlessness, factors which might suggest a correlation with central nervous system effects (as found in animal studies). PGE1 administered at acute doses orally, by inhalation, and intradermally show effects attributable to gastrointestinal disturbances, respiratory problems, and erythematous responses. In general, studies in humans of other PGs have found similar adverse reactions, all of which are explained by known mechanisms of action of PGs. Dose levels constituting acutity are dependent on route (i.e., oral doses are much higher than intravenous doses), with rapid intravenous infusion causing the most adverse reactions.
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PMID:Toxicology of the prostaglandins. 421 9

Intravenous clonidine self-administration was studied in rhesus monkeys under conditions of limited and unlimited access. Limited access consisted of daily 2-h experimental sessions with drug available on a fixed ratio 10 schedule. For unlimited access, drug was available 23 h/day with each response resulting in an injection. In all animals under both conditions, responding was maintained at levels that were above those maintained by saline injections at doses between 0.3 and 10 microgram/kg/inj, and the number of injections taken per session depended upon the dose. Under conditions of limited access, peak self-administration rates varied between animals but averaged approximately 30 inj/session. Total session intake was occasionally in excess of 1.0 mg/kg. Under conditions of unlimited access animals frequently self-administered more than 300 inj/day and intakes averaging 3.6 mg/kg/day occurred at the highest dose tested (10 microgram/kg/inj). When saline was substituted for clonidine after periods of clonidine access that ranged from 10-40 days, withdrawal signs included facial flushing, refusal of preferred food, restlessness, salivation, and emesis. These signs could be reversed with IV clonidine but could not be reliably precipitated with IV naloxone.
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PMID:Reinforcing properties of clonidine in rhesus monkeys. 681 15

1 Fifty infusions of epoprostenol (PGI2) were made, usually increasing the infusion rate until adverse effects were encountered. The volunteers were appraised that they might experience headache and facial flushing. 2 Facial flushing, headache, tachycardia and decrease in diastolic blood pressure were seen in almost all subjects. Erythema over the venous infusing site was also encountered in 13 infusions. Less common effects were sudden bradycardia, pallor and sweating--the vagal reflex--(seven times) and chest pain (twice). Other complaints included restlessness, abdominal discomfort, nausea and drowsiness. 3 The literature on side effects reported during PGI2 infusion is reviewed and recommendations are made concerning administration of PGI2.
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PMID:Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man. 704 12


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