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)

It has been suggested that patients who present with episodes of unexplained anaphylaxis (UEA) or unexplained flushing (UEF) have systemic mastocytosis (SM), a proposal believed to be supported by the presence of excess mast cell (MC) numbers in the skin of these individuals. To examine this hypothesis, we determined the number and distribution of MCs in the skin of nine normal subjects, nine patients with UEA/UEF, six patients with urticaria pigmentosa (UP), and 14 patients with SM. Skin biopsy specimens of normal subjects contained 38.4 +/- 4 (mean +/- SEM) MCs per square millimeter. Biopsy specimens of patients with UEA/UEF contained 71.8 +/- 13 MCs per square millimeter. Although the numbers were significantly different from numbers in skin of normal subjects (p less than 0.05), similar modest increases in MC numbers are observed in a number of skin conditions. In marked contrast, lesional biopsy specimens of patients with UP contained 596.5 +/- 278 MCs per square millimeter (p less than 0.05, n = 6, compared to MC numbers in the skin of normal subjects), and patients with SM had 720.6 +/- 176 MCs per square millimeter in lesional skin (p less than 0.01, n = 12, compared to normal skin). Patients with UP or SM also had increased MC numbers in nonlesional skin compared to normal skin (168.0 MCs per square millimeter, p less than 0.05, n = 5, and 184.4 MCs per square millimeter, p less than 0.01, n = 10, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A survey of the number and distribution of mast cells in the skin of patients with mast cell disorders. 317 Sep 91

Plasma levels of histamine and Nt-methylhistamine were measured simultaneously by high performance liquid chromatography during the intravenous infusion of histamine acid phosphate in six normal volunteers. Progressive, dose-related increases in plasma histamine were noted, reaching a maximum value of 3.1 +/- 0.14 ng ml-1 corresponding to a maximum infusion rate of 180 ng kg-1 min-1 (means +/- SEM). Increases in plasma histamine were accompanied by a significant dose-related fall in mean diastolic blood pressure (baseline 74.0 +/- 4.4 mm Hg falling to 60.0 +/- 3.3 mm Hg at maximum infusion rate, p less than 0.001) and an increase in pulse rate (baseline 76.3 +/- 2.8 beats min-1 rising to 89.24 beats min-1 at maximum infusion rate, p less than 0.05). All subjects exhibited facial flushing, the threshold plasma histamine level for this effect being 1.3 +/- 0.15 ng ml-1 corresponding to an infusion rate of 60 ng kg-1 min-1. Elevation of plasma Nt-methylhistamine was seen in only one subject, who exhibited a level of 0.5 ng ml-1 at the highest infusion rate. These results suggest that measurements of plasma Nt-methylhistamine are unlikely to provide a useful index of histamine release into the circulation.
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PMID:Histamine and Nt-methylhistamine in the circulation during intravenous infusion of histamine in normal volunteers. 321 6

To assess the dosing equivalency and the early and late antianginal efficacy of a gastrointestinal therapeutic system for once-daily, continuous-release nifedipine (N-GITS), 10 patients with stable angina pectoris, who were previously receiving chronic treatment with nifedipine, completed a 12-week trial comparing N-GITS with standard nifedipine. All patients (nine men and one woman; mean age 54 +/- 2 [SEM] years) who were receiving standard nifedipine (mean dose 40 +/- 5 mg/24 hr) for more than 2 weeks (mean 8 +/- 2 months, range 2 to 36 months) were switched to an equivalent once-daily dose (39 +/- 5 mg/24 hr) of N-GITS. Standard nifedipine and N-GITS were compared by symptom-limited exercise treadmill tests with a baseline test (A) performed 3 hours after a standard dose of nifedipine. Exercise tests were also performed after 2 weeks of treatment with N-GITS 3 hours (B) and 24 hours (C) after the drug was given, and after 12 weeks of treatment with N-GITS, 24 hours after dosing (D). Results of exercise tests showed no significant difference in mean exercise time--(A) 422 +/- 25 vs (B) 426 +/- 36 vs (C) 438 +/- 35 vs (D) 487 +/- 37 seconds. Likewise, there was no significant mean difference in peak double product, resting heart rate, peak exercise heart rate, or resting or maximal systolic blood pressure for any of the exercise test points. Furthermore, five patients (50%) reported side effects with standard nifedipine (all vasodilator-flushing, dizziness, or both), which resolved after treatment with N-GITS (p +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative dosing and efficacy of continuous-release nifedipine versus standard nifedipine for angina pectoris: clinical response, exercise performance, and plasma nifedipine levels. 335 8

Criteria indicating injury of endothelial cells (craters, protrusion, denudation) in saphenous veins for aorto-coronary bypass grafting have been examined and quantitated by use of light-(LM), scanning electron (SEM) and transmission electron microscopy (TEM). The specimens were fixed either by immersion or under pressure. It was shown that the conventional way of handling saphenous vein grafts prior to implantation results in serious damage of the endothelial lining. The factors responsible are presumed to be hypoxia, manual flushing and distension with isotonic saline for blood removal, control of leakage, and counteracting spasm of the graft. Even samples collected by a "no touch" technique and exposed to a short hypoxic interval sometimes revealed slight injury.
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PMID:A quantitative study of endothelial cell injury in aorto-coronary vein grafts. 348 41

The acute effects of a single, 20 mg oral dose of nitrendipine were studied in 10 women at between 32 and 42 weeks gestation with stable pregnancy-induced hypertension (PIH). Blood pressure (BP), maternal heart rate and fetal heart rate (FHR) were assessed for 8 h after nitrendipine intake together with the plasma levels of nitrendipine, noradrenaline, adrenaline, plasma renin activity (PRA) and vasopressin. The mean initial systolic/diastolic BP was 158 (SEM 3.7)/108 (SEM 2.7) mmHg. Within 1 h stable, reduced mean BP-levels of 141-145/90-95 mmHg were reached and maintained for 4 h after medication. This antihypertensive effect was closely related to the maternal plasma concentration of nitrendipine, which reached a maximum of 9.1 (SEM 2.6) ng/ml 3 h after tablet intake. After 4 h, systolic and diastolic BPs slowly increased in parallel to a successive decrease in plasma concentrations of nitrendipine. Maternal heart rate increased by less than 10%, while FHR remained unchanged. No hypotensive incidents occurred. The initial mean plasma concentrations of noradrenaline, adrenaline, vasopressin and PRA did not change during the treatment. No major maternal and no fetal side-effects were observed. Three of 10 patients experienced mild, transient facial flushing.
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PMID:Acute effects of nitrendipine in pregnancy-induced hypertension. 356 18

Human pancreatic GRF (hpGRF-40; 1 microgram/kg, iv) selectively stimulates GH release in normal men (9). We now report the effects of graded doses of hpGRF-40 on GH release in 12 normal men. Mean peak increments in serum GH after vehicle and the various doses of hpGRF-40 were 1.13, 11.40, 14.60, 17.01, 14.45, and 15.60 ng/ml after vehicle and 0.1, 0.33, 1.0, 3.3, and 10 micrograms/kg hpGRF-40 (iv bolus), respectively. Peak values were observed 30-60 min after hpGRF-40 treatment. There was considerable variability of responsiveness among individual subjects, and no dose-response relationship between the doses and maximal GH values was found. However, the higher doses of 3.3 and 10.0 micrograms/kg resulted in a more prolonged and biphasic pattern of GH release. A side effect of facial flushing of less than 5-min duration occurred in 4 or 6 subjects who received 3.3 micrograms/kg and in all 5 who received 10 micrograms/kg of hpGRF-40. No changes in serum glucose, LH, TSH, PRL, plasma cortisol, or 8 enteropancreatic hormones occurred after hpGRF-40 treatment. There were small increases in serum somatomedin C levels 24 h after the administration of various doses of hpGRF-40 in 11 of 13 studies. Plasma immunoreactive GRF levels measured 5 min after injection were 0.09, 2.0, 4.9, 23.9, and 66.6 ng/ml after 0.1, 0.33, 1.0, 3.3, and 10 micrograms/kg hpGRF-40, respectively. Serum GH responses after insulin-induced hypoglycemia were compared to GH responses after hpGRF-40. Comparable peak GH stimulation occurred with both provocative tests. Mean +/- SEM peak GH was 20.2 +/- 1.0 ng/ml after insulin and 20.9 +/- 3.2 after hpGRF-40 treatment. hpGRF-40 selectively stimulates GH release in normal men over a dose range of 0.1-10 micrograms/kg and is an effective probe to investigate the dynamics of GH release.
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PMID:Human pancreatic tumor growth hormone-releasing factor: dose-response relationships in normal man. 642 60

Human pancreatic tumor GH-releasing factor-40 (hpGRF-40) selectively stimulates GH secretion in normal men and in some adults with GH deficiency. To study its effects in women, we administered hpGRF-40 (3.33 micrograms/kg) or an equivalent volume of vehicle as an iv bolus at 0900 h to 10 normal women during the early follicular, late follicular, and midluteal phases of the menstrual cycle. Serum concentrations of GH, PRL, LH, and FSH were measured at intervals between 0800-1100 h. Serum somatomedin-C concentrations were measured before and 24 h after the administration of vehicle of hpGRF-40. Within 1-3 min after the injection of hpGRF-40 all women described warmth localized to the head and neck and exhibited facial flushing. No changes in pulse rate or blood pressure were noted. When expressed as change from baseline and compared to control values, peak levels of serum GH (nanograms per ml; mean +/- SEM) were higher after hpGRF-40 treatment during the early follicular (5.4 +/- 3.2 vs. 34.9 +/- 8.3; control vs. test day; P = 0.011), late follicular (5.6 +/- 1.5 vs. 25.2 +/- 6.8; P = 0.014), and luteal (0.8 +/- 1.0 vs. 32.7 +/- 12.8; P = 0.033) phases of the menstrual cycle. Similarly, integrated serum GH levels (nanograms per ml/h) were higher after hpGRF-40 administration during the early follicular (0.72 vs. 16.1; P = 0.011), late follicular (0.83 vs. 9.9; P = 0.037), and luteal (-1.54 vs. 17.0; P = 0.036) phases of the cycle. When the increases in serum GH after hpGRF-40 treatment were compared among the phases of the menstrual cycle, however, no differences were found. Serum somatomedin-C values 24 h after hpGRF-40 treatment were higher than those 24 h after vehicle at all stages of the menstrual cycle. hpGRF-40 did not stimulate the release of PRL, LH, or FSH. We conclude that hpGRF-40 stimulates the release of GH, but that in response to the dose used, hpGRF-40-stimulated GH release does not vary during the menstrual cycle.
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PMID:Effects of human pancreatic growth hormone-releasing factor-40 on serum growth hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, and somatomedin-C concentrations in normal women throughout the menstrual cycle. 643 83

Circulating basal levels of prostanoids were measured in non-insulin dependent diabetics (NIDDs) who showed chlorpropamide alcohol flushing (CPAF), with and without diabetic complications, and in non-diabetic controls. Prostanoids were also measured during CPAF in those diabetics in whom CPAF is or is not blocked by indomethacin and also in CPAF-negative patients. There was no significant difference in circulating prostanoids between diabetics with and without severe vascular disease. The level of prostaglandin F, however, was significantly higher in the diabetic than in the non-diabetic subjects (mean +/- SEM PGFM 521 +/- 23 v. 414 +/- 18 pmol/l respectively P less than 0.01). In the group in whom CPAF could be blocked by indomethacin there was a significant rise in thromboxane during CPAF when compared with basal values (mean +/- SEM 905 +/- 48 v. 688 +/- 46 pmol/l respectively P less than 0.01) which was abolished by prior administration of indomethacin. There was no significant rise in prostacyclin or PGF. The group in which CPAF could not be blocked by indomethacin and the CPAF negative group showed no rise in any of the prostanoids measured. These findings support the concept of at least two different groups of CPAF positive NIDDs, one in which prostanoids are involved in CPAF and one in which they are not. It is the group in which prostanoids are involved in CPAF who seem to be highly protected against vascular disease.
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PMID:Circulating prostanoid levels, both basal and during the chlorpropamide alcohol flush, in non-insulin dependent diabetes. 689 21

A total of 23 mares were inseminated once within 0-6 h after clinical detection of ovulation, 14 with fresh and 9 with deep-frozen semen containing 0.1 x 10(9) to 4.7 x 10(9) motile spermatozoa. Within these two groups, the mares were slaughtered 2, 4 or 6 h after insemination and their genital tracts removed. The utero-tubal junction, isthmus and ampulla ipsilateral to the ovary in which ovulation occurred were flushed separately for sperm recovery. In 1 or 2 mares of each group, the uterine horn and corpus uteri, the cervix and vagina were also flushed. Tissue samples were collected from the contralateral oviduct and the other genital regions and prepared for scanning electron microscopy to show spermatozoa distribution in situ. Flushings were also prepared for scanning electron microscopy. There were no significant differences in the extent of sperm migration and in the number of spermatozoa in the different regions of the oviduct 2, 4 or 6 h after insemination of fresh or frozen semen. There was, however, a striking difference in sperm number within the time intervals examined; the numbers were greatest at 4 h after insemination. SEM of spermatozoa in the various regions of the oviducts failed to indicate any alterations to the sperm-head membranes that could be associated with sperm capacitation. The majority of spermatozoa found in the uterotubal junction, isthmus and ampulla showed morphological integrity.
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PMID:An investigation of sperm migration into the oviducts of the mare. 696

Enhanced nitric oxide (NO) generation by stimulated NO synthase (NOS) activity may, through its oxidative metabolism contribute to tissue injury in experimental colitis. In this study the possible amelioration of experimental colitis by NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS activity, was evaluated. Colitis was induced in rats by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB) dissolved in 0.25 ml 50% ethanol or by flushing the colon of capsaicin pretreated rats with 2 ml of 5% acetic acid. In several experiments, L-NAME 0.1 mg/ml was added to the drinking water at the time of colitis induction with TNB or seven days before acetic acid treatment. Rats were killed at various time intervals after induction of colitis. A 10 cm distal colonic segment was isolated, weighed, lesion area measured, and explants organ cultured for 24 hours for determination of NO generation by the Greiss reaction. The rest of the mucosa was scraped for determination of myeloperoxidase and NOS activities and leukotriene generation. In TNB treated rats mean arterial pressure was also determined up to 72 hours after damage induction, with or without cotreatment with nitroprusside. L-NAME significantly decreased the extent of tissue injury in TNB treated rats. Seven days after TNB treatment lesion area was reduced by 55%, colonic weight by 37%, and myeloperoxidase and NOS activity by 59% and 42%, respectively. Acetic acid induced colitis in capsaicin pretreated rats was also significantly decreased by L-NAME. Twenty four hours after acetic acid treatment lesion area was reduced by 61%, colonic weight by 21% and NOS activity by 39%. Mean (SEM) arterial blood pressure in TNB+L-NAME treated rats was 37.6 (8.1) mm Hg higher than in TNB treated rats, an effect that was only partially abolished by nitroprusside. These results show that inhibition of NO synthesis by an L-arginine analogue significantly ameliorates the extent of tissue injury in two models of experimental colitis, an effect that is not due only to its vasoconstrictor properties. Modulation of NO generation may be a novel therapeutic approach in inflammatory bowel disease.
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PMID:Experimental colitis is ameliorated by inhibition of nitric oxide synthase activity. 867 8


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