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)

The carcinoid syndrome can arise when effluent blood from carcinoid tumor tissue gains access to the systemic, as opposed to the portal, venous system. Features include facial flushing, diarrhea, wheezing, right-sided cardiac lesions, and retroperitoneal fibrosis. Attacks of flushing, diarrhea, and wheezing can be provoked by bolus injections of adrenaline, noradrenaline, or pentagastrin. While serotonin usually predominates, carcinoid tumors can also secrete, in varying proportions, 5-hydroxytryptophan, kallikrein, kinins, substance P and other neuropeptides, prostaglandins, catecholamines, and histamine. Of these, serotonin, kinins, histamine, and substance P are possible mediators of flushes; serotonin and substance P of hyperperistalsis; and serotonin, kinins, or histamine of bronchial constriction. Despite the gross excess of circulating serotonin, nearly all is platelet bound and therefore inactive. Very little is free in plasma. Demonstration of a contribution of serotonin to carcinoid attacks requires assay of free plasma serotonin; measurements of whole blood or serum serotonin are of little value. Some, but not all, provoked flushes have been shown to be accompanied by a rise in free plasma serotonin or substance P; an increase in circulating kinins has been more consistently shown. The 5HT2 antagonist ketanserin has been found to inhibit both provoked and spontaneous attacks of flushing, diarrhea, and dyspnea in a proportion of patients with carcinoid syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovasc Drugs Ther 1990 Jan
PMID:Carcinoid syndrome and serotonin: therapeutic effects of ketanserin. 228 51

Pulmonary surfactant during lung transplantation was investigated in the control group of a canine single lung transplantation model by measuring dipalmitoyl-phosphatidylcholine, the main phosphocholine fraction of surfactant in bronchoalveolar lavage. In a second group of dogs, L-carnitine, an essential cofactor for transfer of long-chain fatty acids into the mitochondria, was applied. Organ function after pulmonary artery flushing with modified Euro-Collins solution and hypothermic storage for 4 hours was adequate in both groups, with significantly higher arterial oxygen pressure levels in the L-carnitine group after 12 (p less than 0.05) and 24 (p less than 0.025) hours, respectively. In the control group, a reduction of the dipalmitoyl-phosphotidylcholine portion on total phosphotidylcholines was observed 4 and 12 hours after transplantation of the left lung (p less than 0.005 and p less than 0.01, respectively, both specified by Student's t test for dependent data, not significant by Bonferroni correction). In the simultaneously stored right lungs, a constant fall of the dipalmitoyl-phosphotidylcholine portion was demonstrated. In the L-carnitine group, significantly higher dipalmitoyl-phosphotidylcholine levels were observed in the transplanted left lungs after 4 hours (p less than 0.01) and in the continuously stored right lungs after 24 hours (p less than 0.005), when compared with the control group. These results suggest that dipalmitoyl-phosphotidylcholine portion on total phosphotidylcholine decreases parallel to the extent of the ischemic damage. Furthermore, the application of L-carnitine improved pulmonary function after transplantation, possibly by reducing the impairing effect of ischemia on alveolar type II cell metabolism and thereby on pulmonary surfactant system.
J Thorac Cardiovasc Surg 1990 Jun
PMID:Pulmonary surfactant in bronchoalveolar lavage after canine lung transplantation: effect of L-carnitine application. 235 22

The complementary antihypertensive effects of the beta-blocker/calcium antagonist combination has to be weighed against their additive and potentially detrimental negative inotropic, chronotropic, and dromotropic effects inherent in both classes of drugs. We reviewed the main adversity, particularly electrophysiological and hemodynamic effects, of combined treatments with beta-blockers and the calcium antagonists verapamil, diltiazem, and nifedipine. In patients with coronary artery disease, a different picture emerged between the verapamil and nifedipine combination with a beta-blocker. Verapamil was more often associated with conduction problems (up to 9%) and dyspnea or heart failure (up to 8%). These problems had rarely been reported with nifedipine but ankle edema (up to 11%), flushing (up to 11%), and headaches (up to 7%) predominated. The cardiovascular unwanted effects led to withdrawal in 5-8% for the verapamil/beta-blocker or nifedipine/beta-blocker combination. Although there was little cardiac adversity with the nifedipine/beta-blocker combination, the intravenous administration of verapamil in patients on beta-blockers is contraindicated and the oral verapamil/beta-blocker combination should not be sought in patients with impaired left ventricular function and when conduction disturbances are likely to occur. In treating hypertensive patients without overt coronary artery disease, there is no argument against the use of the nifedipine/beta-blocker combination but there is a need for definitive studies of the verapamil/beta-blocker combination.
J Cardiovasc Pharmacol 1985
PMID:Review of the cardiovascular adversity of the calcium antagonist beta-blocker combination: implications for antihypertensive therapy. 241 10

Serotonin (5-HT) and substance P (SP) were assayed in peripheral blood in patients with known midgut carcinoids and hepatic metastases. All patients had supranormal basal levels of 5-HT and SP. The clinical and hormonal response was evaluated by two provocation tests, pentagastrin (PG) injection or calcium infusion. Pentagastrin caused flushing and gastrointestinal symptoms and elevated levels of circulating 5-HT, but not of SP. Pretreatment with a 5-HT2 receptor blocking agent (ketanserin) alleviated gastrointestinal symptoms but had no influence on either 5-HT release or PG-induced flushing. Calcium infusion induced carcinoid symptoms in only two of six patients, which were associated with elevated 5-HT levels (whereas elevated SP levels were seen in only one patient). We conclude that 5-HT is important for the development of gastrointestinal symptoms but not of flushing. Ketanserin may alleviate gastrointestinal symptoms but does not influence PG-induced release of 5-HT. Substance P and 5-HT do not seem to share a common release mechanism. It appears that PG testing is superior to calcium infusion as a provocative test in patients with the carcinoid syndrome.
J Cardiovasc Pharmacol 1985
PMID:The pentagastrin test in the diagnosis of the carcinoid syndrome. 241 67

Felodipine lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels. The selective action may be considered a safeguard against untoward effects on cardiac contractility and conduction. Felodipine does not cause orthostatic hypotension since it has no effect in clinical doses on venous smooth muscle. Felodipine has a natriuretic/diuretic effect, which counteracts the salt and water retention that is often seen during treatment with other potent vasodilators. In clinical studies, felodipine has proved more effective than several established antihypertensive drugs. The combination of felodipine and a beta-adrenergic blocker appears to be a good alternative to standard triple treatment, and felodipine is often effective in patients with previously "refractory" hypertension. The antihypertensive effect of felodipine is dose related. In patients with moderate hypertension, a dose regimen of 5 mg twice a day is usually sufficient, and doses greater than 10 mg twice a day are not often required. Felodipine is generally well tolerated. The most common adverse effects are those expected from a potent arteriolar dilator: ankle swelling, headache, dizziness, flushing, etc. Adverse effects are usually transient or diminish in intensity with continued treatment. The overall frequency of adverse effects with felodipine appears to be similar to that for the established antihypertensive drugs, although the adverse effects differ. Felodipine is a potent arteriolar dilator with therapeutic advantages, especially for patients with moderate to severe hypertension.
J Cardiovasc Pharmacol 1987
PMID:Felodipine in hypertension--a review. 244 9

A double-blind controlled, randomized, parallel, multicenter 12-week study was conducted to compare the antihypertensive efficacy of lisinopril with that of metoprolol in treatment of moderate to severe hypertension. Initially, 118 patients were recruited on lisinopril and 61 on metoprolol; and for the purpose of efficacy analysis at week 8, 115 patients on lisinopril and 60 on metoprolol were included. The doses of lisinopril or metoprolol were 40-80 mg/day and 100-200 mg/day, respectively. At week 4, the pretreatment diastolic blood pressure of 111 mm Hg was decreased to 97 mm Hg (p less than 0.01) with lisinopril: metoprolol decreased the diastolic blood pressure from 110 to 99 mm Hg (p less than 0.01). Similar decreases were noted at week 8; however, the drop in blood pressure with lisinopril was not significantly different from that with metoprolol. Systolic blood pressure also demonstrated a decrease of about 18 mm Hg with lisinopril and 12 mm Hg with metoprolol (p less than 0.01). This larger decrease in systolic blood pressure with lisinopril was statistically significant at week 4 (p less than 0.05). These decreases in systolic blood pressures were maintained at week 8, again with statistical significance (p less than 0.01). Of the 118 lisinopril-treated patients, four were discontinued from lisinopril therapy because of headache, dizziness, rash, flushing, or lymphadenopathy. Four patients out of 61 (9.8%) were discontinued from metoprolol therapy because of fatigue, somnolence, asthenia, weight gain, flatulence, tremor, or bronchospasm. In conclusion, lisinopril 40-80 mg once daily is as effective as metoprolol 100-200 mg once daily in reducing diastolic blood pressure in patients with moderate to severe hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1987
PMID:Evaluation of antihypertensive efficacy of lisinopril compared to metoprolol in moderate to severe hypertension. 244 53

The antihypertensive efficacy and safety of lisinopril, a long-acting angiotensin-converting enzyme inhibitor, were assessed in 40 elderly patients (aged 65 years or over) with mild to moderate systolic/diastolic or isolated systolic hypertension, in an open study of 12 weeks' duration. Lisinopril was given orally in single daily doses. The starting dose was 5 mg in patients with glomerular filtration rate (GFR) of 30-60 ml/min and 10 mg in patients with GFR greater than 60 ml/min. The dose of lisinopril could be titrated upwards to a maximum of 40 mg daily according to blood pressure response. A thiazide diuretic was then added if blood pressure was not controlled. Thirty-six patients completed the study. Mean sitting blood pressure was significantly reduced by lisinopril treatment. There was no significant alteration in the heart rate, and postural hypotension did not occur. The median dose of lisinopril given was 20 mg daily (range 5-40 mg daily), and only two patients had a diuretic added to the lisinopril. One patient was withdrawn from the study because of unstable angina, and another was discontinued from lisinopril treatment because of anorexia and facial flushing. One patient was withdrawn after 8 weeks because of interruption of lisinopril therapy for a transurethral resection of the prostate, and one patient was lost to follow-up. No clinically significant haematological or biochemical changes were observed. The mean glomerular filtration rate was unchanged during the study. Proteinuria did not occur de novo, nor did established proteinuria increase. Thus lisinopril was well-tolerated and effective therapy in a group of elderly hypertensive patients.
J Cardiovasc Pharmacol 1987
PMID:Lisinopril in elderly patients with hypertension. 244 57

The serotonergic antagonist ketanserin (K) was compared to nifedipine (N) in a five-center international study on hypertensive patients over the age of 50 years. After a 4-week placebo run-in period, patients were randomly assigned to receive for 3 months either ketanserin (40 mg b.i.d. after 2 weeks of 20 mg b.i.d.) or nifedipine (20 mg N retard b.i.d.). After 1 month, monotherapy patients whose blood pressure was not sufficiently reduced received a diuretic in combination therapy. At the end of the active treatment period, patients who had remained on monotherapy received placebo until hypertension returned or for a maximum of 2 months. One hundred and seventeen patients were entered in the study, 58 on K and 59 on N. More patients switched to combination with a diuretic in the K group (14 patients) than in the N group (6 patients). The overall reduction in blood pressure was similar for K and N. Total response rate was high (96%) for the two drugs. Blood pressure was reduced both at peak and trough drug levels. No orthostatic reactions were observed, and no rebound hypertension occurred at discontinuation of therapy. Ketanserin monotherapy slightly decreased heart rate (-1 beats/min). whereas N produced a significant increase (+6 beats/min). Body weight significantly increased with K (+1.1 kg) and was unchanged with N. More patients complained of adverse reactions during N monotherapy (47%) than during K monotherapy (34%). Flushing and leg edema were more frequent with N.
J Cardiovasc Pharmacol 1987
PMID:Ketanserin versus nifedipine in the treatment of essential hypertension in patients over 50 years old: an international multicenter study. 244 56

From a hemodynamic point of view, the calcium antagonists represent an interesting way of treating hypertension, because they reduce total peripheral resistance without compromising cardiac output. Blood flow is also maintained during muscular exercise. Verapamil and diltiazem induce slight reduction in heart rate, but this is compensated by increase in stroke volume. Verapamil and diltiazem also prolong atrioventricular conduction time, in contrast to the dihydropyridines. Most clinical data are available for verapamil, diltiazem, and nifedipine. In patients with mild-to-moderate hypertension, these compounds seem as effective as diuretics and beta-blockers. They do not induce disturbances in glucose metabolism, serum uric acid, or serum potassium, and unwanted disturbances in blood lipids have not been described. The dihydropyridines may safely be combined with beta-blockers, but the combination of either verapamil or diltiazem with a beta-blocker should be avoided (because of the high risk of bradycardia). The calcium antagonists seem particularly useful in patients with the combination of hypertension and angina pectoris or peripheral vascular diseases or chronic obstructive lung diseases or diabetes. They are also effective in hypertensive crises. They may also be tried as a first line drug in patients with mild and moderate essential hypertension, particularly when diuretics or beta-blockers are contraindicated. Temporary side effects due to vasodilatation (headache, flushing, and palpitations) are seen frequently, particularly on the dihydropyridines. Edema is the most frequent serious side effect of the dihydropyridines, and constipation is most common with verapamil. At this point, few long-term data are available and it is not known whether the calcium antagonists will give better or worse results, with respect to morbidity and mortality, than the beta-blockers, diuretics, or other more recent antihypertensive agents.
J Cardiovasc Pharmacol 1987
PMID:Clinical use of calcium antagonists in hypertension: update 1986. 245 35

The pharmacokinetics and antihypertensive effects of the nifedipine tablet and capsule have been examined in six male patients with diastolic pressure greater than 95 mm Hg despite metoprolol therapy. On two separate mornings, a 20 mg nifedipine tablet or 2 X 10 mg nifedipine capsules were administered with metoprolol 100 mg following a 12-h fast. Both capsule and tablet significantly reduced blood pressure (BP), with the maximum fall occurring at 45 min for the capsule and 4 h for the tablet. Two patients developed postural hypotension after the capsule and a third experienced flushing and palpitations. The maximum nifedipine plasma concentration after the capsule was 257 ng/ml compared with 50 ng/ml for the tablet, and the time of maximum concentration was significantly earlier for the capsule. Although the nifedipine capsule results in a fivefold higher maximum plasma concentration and is associated with a more rapid reduction in blood pressure than the tablet, its use may be limited by postural hypotension and other untoward symptoms.
J Cardiovasc Pharmacol 1987
PMID:Comparative pharmacokinetics and antihypertensive effects of the nifedipine tablet and capsule. 245 48


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