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)

Prostacyclin (PGI2) was given intravenously in doses of 1 to 5 ng/kg/min to eight consecutive patients with end stage peripheral arteriosclerosis and ischaemic ulcers. Seven patients had intense ischaemic pains. Complete or partial healing of ulcers were seen in six cases (complete in three). In those whose ulcers healed (complete or partially) relief of ulcer pain was remarkable. Acute studies of the effect of prostacyclin on skin temperature of ischaemic areas showed no correlation with clinical effects. Seven patients had more or less pronounced subjective side effects, most often flushing, nausea, headache and uneasiness. As we previously have seen equally good healing and pain relieving effects by the administration of prostaglandin E1 without these side effects the latter compound is so far preferred in the treatment of severe peripheral artery disease. Controlled studies of the effect are needed.
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PMID:The effect of intravenous prostacyclin on resting pains and healing of ischaemic ulcers in peripheral artery disease. 702 66

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

We reviewed reactions previously reported in patients treated with isoniazid, who ate certain fish and cheeses. We observed similar reactions in two patients after they ingested cheese and wine. Isoniazid is an inhibitor of both monoamine and diamine oxidases, which contribute to the metabolism of histamine that may be present in some fish and cheeses. Monoamine oxidase also acts in the metabolism of tyramine, present in some cheeses and wines. Reactions reported after eating fish or cheese, in patients treated with isoniazid, are similar in that both are characterized by headache, palpitations, skin flushing, nausea, vomiting, and pruritus. Reactions after fish have not been associated with increased blood pressure, whereas those following cheese ingestion frequently result in modest increases in blood pressure. Patients treated with isoniazid should be alerted to the possibility of reactions after eating certain foods.
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PMID:Interactions of isoniazid with foods. 710 82

Thirty-four patients were submitted to the conventional cervical myelography by administration of metrizamide (Amipaque) through three routes (lumbar 23, suboccipital 6, C1-C2 lateral 5). After the injection of metrizamide (4-11 ml, 170-250 mgI/ml), all procedures of the cervical myelography were done as soon as possible within 9 minutes. The adverse reactions of Amipaque were observed in 29 cases (85%) out of 34 cases initially 1 hour after cervical myelography and disappeared completely in an average of 16 hours. The total number of the side effects was 140 incidences such as meningeal irritation (headache 18, nausea 17, vomiting 17), cerebellar signs (dizziness 11, dysarthria 8, tremor 5, bradylalia 2, dysmetria 2, tipsy feeling 2, dysdiadochokinesis 1), autonomic signs (flushing 7, pale face 4, fever 4, sweating 2, hiccup 2, fatigability 2, micturition disturbance 1), sensory signs (exacerbation of numbness 6, perioral numbness 3, back pain 1, chest pain 1), motor signs (focal muscle spasm 5, exacerbation of paresis 4, areflexia 1), psychiatric signs (dysphasia 3, disturbance of consciousness 2, euphoria 1, persecutory delusion 1) and muddiness 7. We observed that waxing and waning of side effects correlated tightly with transient cortical penetration of dye in CT and cortical dysfunction mainly slowing of the background activity and slow wave burst in EEG. According to high frequency of side effects in our study, we suggest that a greater incidence of side effects may result when high concentration of Amipaque comes in contact with the cerebral cortex by using an inadequate fluoroscopic table which has only fixed one plane image and rough positioning control. Slow absorption into blood stream may affect appearance and maintenance of side effects. In order to decrease side effects after Amipaque cervical myelography, we propose that we should introduce a mobile rotating chair coupled with high power image and chose C1-C2 lateral route using 1500-1700mgI of Amipaque.
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PMID:[Side effects of metrizamide (Amipaque) cervical myelography (author's transl)]. 711 May 15

Much can be learned about the brain's function in pain processing through electrical stimulation. The spinothalamic tract which is conceived to be the chief pathway for nociceptive pain and whose interruption induces dissociated sensory loss can be recognized from the anterolateral columns of the spinal cord to the posterior thalamus by the induction of feelings of chiefly contralateral, somatotopographically organized, warm, cool, or cold sensations, less often burning and rarely pain. The spinoreticulothalamic tract, whose function in normal pain processing is controversial and whose interruption produces no clinically detectable sensory loss, is normally silent to stimulation. However, in patients with deafferentation pain, it appears to become sensitive to electrical stimulation, both in the anterolateral columns and in midbrain and medial thalamus, giving rise to chiefly contralateral, non-somatotopographically organized, burning or painful sensations which often reproduce fairly accurately the patient's pain. This phenomenon, which does not appear to occur in patients with nociceptive pain, may reflect denervation neuronal hypersensitivity which is a possible pathophysiological mechanism explaining deafferentation pain. The dorsal column/lemniscal system can be recognized by electrical stimulation from the spinal cord to the somatosensory cortex by the induction of paraesthesiae. Its chronic stimulation at the level of the dorsal column, the ventrocaudal nucleus or the internal capsule appears capable of suppressing deafferentation pain. The arc of neuronal tissue extending from the septal area through hypothalamus and periventricular grey to the periaqueductal grey, which acts as a receptor area for opiates and endorphins, thereby exerting an inhibitory effect on access to the spinothalamic tract, can also be exploited through chronic stimulation for the control of pain. Stimulation of the periventricular area gives rise to feelings of warmth, comfort and relaxation, of the hypothalamus, horror and autonomic effects while that of the periaqueductal grey induces discomfort, distress, anxiety and weeping, and of the septal area flushing, paraesthesiae, nausea, nystagmus and a feeling of warmth. Thus four brain systems involved in pain signalling can be recognized by electrical stimulation, one which conveys nociceptive pain to consciousness, another that suppresses it, one that may undergo denervation neuronal hypersensitivity and bring deafferentation pain into consciousness, possibly by establishing novel connectivity and one that is presumably capable of suppressing that hyperactivity.
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PMID:Identification of pain processing systems by electrical stimulation of the brain. 718 96

The calcium antagonist nifedipine (Adalat) was administered to 60 patients with essential hypertension and investigations were performed on acute and chronic hypotensive effects. The following results were obtained: 1. Acute hypotensive effects: Nifedipine (20 mg) was either orally or sublingually administered. Following oral administration, significant hypotensive effect was attained 20 min after administration and the maximum hypotensive response was obtained 2-4 h after administration. In cases of sublingual administration, significant hypotensive effect was notable 5 min after administration and blood pressure reached the lowest level 2-3 h after administration. The hypotensive effects lasted for a relatively longer period and significantly lower blood pressure than the control level was observed even 3 h after administration. 2. Chronic hypotensive effects: Nifedipine (30-60 mg/d) was orally administered consecutively. Significant hypotensive effect was attained in and after the 4th week of administration. The yearly changes in the long-term administration cases over 3 years demonstrated significant hypotensive effects. The cases who did not respond to single administration of thiazides or beta-blockers exhibited significant hypotensive response by the combined use of nifedipine. 3. Change in heart rate: In the acute study, heart rate increased after nifedipine administration and lasted for several hours. In the long-term administration cases, the changes in heart rate were not significant. 4. Side effects attributable to nifedipine such as headache in 2 cases, facial flushing, palpitation, warm sensation and nausea in 1 case each were observed early after the administration but there were no cases in whom administration was discontinued due to these side effects.
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PMID:Antihypertensive effects of the calcium antagonistic agent nifedipine. 720 Jul 85

The efficacy and safety of 0.3 mg buprenorphine on single and repeated intramuscular administration (every 4 to 8 hours as needed) were compared to those of 10 mg intramuscular morphine. Fifty adult patients experiencing moderate to severe postoperative pain were evaluated up to three days following surgery. Results showed that 0.3 mg buprenorphine was as effective as 10 mg morphine, whether given as a single dose or on a repeat-dose schedule. The patterns of analgesia were similar and without indication of increasing dosage requirements with time. Minor side effects encountered were brief and minimal, including such conditions as drowsiness, dizziness, diaphoresis, flushing, and nausea.
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PMID:The study of analgesics following single and repeated doses. 722 17

We administered intravenous ergonovine maleate to 14 patients with chest pain resembling angina pectoris and to four healthy volunteers. Five of the patients experienced their typical chest pain after ergonovine, and manometric signs of esophageal spasm also developed. The remaining nine patients and the four volunteers did not experience chest pain, but all subjects except one had some symptomatic response to ergonovine, including chest warmth or heaviness, headache, mild choking sensation, facial numbness, flushing, or nausea. Two of the nine patients and one of the four volunteers developed manometric signs of esophageal spasm after ergonovine but experienced no chest pain. Intravenous ergonovine may be useful to identify esophageal spasm in selected patients with chest pain who have normal coronary arteries or in whom coronary artery disease is insufficient to explain symptoms. However, we believe that the potential risks of ergonovine do not justify its routine use as a provocative agent for esophageal spasm.
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PMID:Use of ergonovine to identify esophageal spasm in patients with chest pain. 723 19

Haemolytic transfusion reactions can be defined as the occurrence after transfusion of measurably increased destruction of red cells, of donor or recipient, by alloantibodies. They may be acute (occurring within 24 hours of transfusion) or delayed (when signs of red cell destruction do not occur until 4 to 10 days after transfusion). The severest signs and symptoms of acute reactions follow intravascular red cell lysis and progress to anaemia, fever, haemoglobinuria and jaundice. The subjective responses of pain, restlessness, nausea, skin flushing, dyspnoea and shock are mediated by cleavage products of complement (C3a, C5a) activated by red cell antigen-antibody reaction. The bleeding and renal failure complications that follow are multi-factoral in aetiology but also stem from the activation of intravascular clotting and from the vasomotor disturbances following histamine and kinin release.
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PMID:Clinical presentation of haemolytic transfusion reactions. 739 74

In a group of 95 patients having cardiac operations with extracorporeal circulation, intravenous (IV) amiodarone, administered in doses of 2.5 to 5 mg/kg, was used in the treatment of various perioperative arrhythmias. Conversion to sinus rhythm was achieved in 55 (61%) of 90 patients with supraventricular arrhythmias, the other patients showing a satisfactory slowing of their heart rate. Total suppression and control was obtained in 18 patients with persistent ventricular extrasystoles associated with various supraventricular arrhythmias. Amiodarone was administered in five patients with life-threatening ventricular arrhythmias resistant to other antiarrhythmic agents: Suppression was obtained in one of two patients with recurrent ventricular tachycardias and control was achieved in three patients with repetitive ventricular tachycardia and ventricular fibrillation, allowing the effective use of intra-aortic balloon counterpulsation (IABP) needed for hemodynamic support. Seven patients experienced minor side effects such as nausea or flushing. No complete atrioventricular (AV) block was noted. Significant hypotension occurred at the end of the IV injection in 17 (18%) patients. In all but five patients, hypotenion was transient, without clinical complications. In the five others, adrenergic drugs in four cases and IABP in one case were necessary. Those five patients had marked cardiomegaly with poor myocardial contractility. IV bolus injection of amiodarone seems prohibited in such patients; constant infusion would be preferable.
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PMID:Intravenous amiodarone in the treatment of various arrhythmias following cardiac operations. 745 41


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