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Biomedical subjects

T Thien

Publications and source records attributed to T Thien.

At least 235 records · Page 13Linked to original sources
PubMed1988

Laser Doppler velocimetry of fingertips during heat provocation in normals and in patients with Raynaud's phenomenon.

Measurements of Laser Doppler flow were performed on the fingertip during heating in a group of normals and in a group of patients with different types of Raynaud's phenomenon. During heating a group of 24 normals was distinguished from a group of 29 primary Raynaud's patients. A group of 17 patients with secondary Raynaud's phenomenon due to scleroderma and 8 patients with arteriographically proven severe vascular occlusive disease of the fingers showed a significantly lower response in comparison to the two above-mentioned groups. Patients with or without slight or severe trophic skin lesions were identified. In patients with scleroderma the maximal vasodilation during heating was inversely related to the number of organs affected. In conclusion, measurements of the hyperaemia during heating may play a role in determining the degree of obstructive vascular involvement in Raynaud's phenomenon.

Adult↗
PubMed1988

Transcutaneous pO2 measurements in Raynaud's phenomenon. Value and limitations.

To determine whether measurements of transcutaneous pO2 (TcPO2) by Tacomette (Novametrix Medical Systems Inc., Connecticut, U.S.A.) could be a valuable method to evaluate nutritive skin perfusion, baseline TcPO2 was measured under standardized conditions in normals and in patients with several types of Raynaud's phenomenon (RP). The control group (n = 41; TcPO2 = 34.4 +/- 14.3 mm Hg) and the patients with primary RP (n = 81; TcPO2 = 25.0 +/- 9.7 mmm Hg) had a significantly higher baseline TcPO2 (p less than 0.05) in comparison to the secondary RP-patients with a connective tissue disease (n = 54; TcPO2 = 10.5 +/- 7.9 mm Hg). In RP patients the group with trophic skin lesions showed a significant lower TcPO2 (p less than 0.01). The reproducibility expressed as the standard error of a single observation was moderate (13-27%). After 20 minutes acclimatization it took 32 minutes before a stable baseline value was reached which makes the procedure a lengthy one. Its non-invasive nature is severely hampered by the skin injuries observed in 3 patients, while the abolition of vascular tone induced by the heating makes the interpretation of intervention studies difficult. In conclusion baseline TcPO2 measurements were found lower in patients with disturbances of nutritional skin blood flow. However, because of the overlap of values between groups the discriminative value of this method is limited. Comparative studies with other techniques that determine capillary perfusion like the 133Xenon wash out technique and dynamic capillary microscopy are necessary to validate this technique as a reliable alternative.

Adult↗
PubMed1988

The urinary excretion of prostaglandins and thromboxane B2 in healthy volunteers: a study in males and females, and on the influence of seminal fluid contamination.

Radioimmunoassay measurements of prostaglandins (PGs) E2, F2 alpha, 6-keto-PGF1 alpha and thromboxane (Tx) B2 in 24 h urine specimens from a male and a female healthy volunteer on several consecutive days revealed a dramatic increase of PGE2, PGF2 alpha, 6-keto-PGF1 alpha on days, upon which they had sexual intercourse; only TxB2 remained stable. Furthermore, the PGE2/PGF2 alpha ratio rose to values greater than 0.5 on days with sexual intercourse. This was found to be due to contamination of the urine samples by seminal fluid. Two 24 h urine samples from each of 26 healthy male and female volunteers (HV) revealed higher (p less than 0.01) mean PGE2 and PGF2 alpha values in males than in females. The results show that the interpretation of the urinary PG excretion as a measure of renal PG synthesis should be considered carefully, and that a PGE2/PGF2 alpha ratio greater than 0.5 indicates probable seminal contamination of urine.

Coitus↗
PubMed1987

Intravenous pinacidil in the acute treatment of hypertension.

Pinacidil (N''-cyano-N-4-pyridyls-N'-1,2,2-trimethyl-propyl guanidine, monohydrate), a recently developed direct-acting vasodilator, was given intravenously in a dosage of 0.1-0.2 mg/kg body weight to ten untreated hypertensive patients. Pinacidil caused a fall of blood pressure from 170/108 +/- 6/3 to 156/80 +/- 5/4 mm Hg (mean +/- SE). The proportional decrease of mean arterial pressure (MAP) was 13.7 +/- 1.6%. Together with the decrease of blood pressure an increase of heart rate by 29.7 +/- 6.2% occurred. The heart rate increased by 13.6 beats/min per 10 mm Hg decrease of MAP. Pinacidil also caused significant rise of plasma noradrenaline and plasma renin activity, whereas plasma adrenaline and aldosterone remained unchanged. The serum concentrations of pinacidil and its major metabolite pinacidil-N-oxide were within the expected limits. The authors conclude that intravenously administered pinacidil causes a rapid decrease of blood pressure, but at the cost of a considerable increase of heart rate, and thus does not offer advantages over other vasodilators.

Adolescent↗
PubMed1987

Nifedipine in primary Raynaud's phenomenon and in scleroderma: oral versus sublingual hemodynamic effects.

In 16 patients with Raynaud's phenomenon a placebo-controlled single-dose study was performed on the hemodynamic effects of 10 mg nifedipine, sublingually administered, followed by an open eight-week study on the therapeutic efficacy of chronic oral nifedipine, 10 mg qid. After the acute sublingual nifedipine administration, a pronounced objective improvement of finger skin (P = .013) and forearm muscle blood flow (P = .04) during a standard finger-cooling test was found. During the chronic oral study the improvement in objective efficacy parameters disappeared, except for laser Doppler estimated shunt flow (P = .07). The acute hemodynamic effects did not predict the long-term results in individual patients. Patients with systemic sclerosis reacted as well as patients with primary Raynaud's phenomenon. This study shows that orally administered nifedipine does not convey long-term objective benefit to patients with Raynaud's phenomenon. The apparent increase in vasodilation during acute administration suggests that sublingual nifedipine prophylactically or during a vasospastic attack may be more useful.

Administration, Oral↗
PubMed1987

The influence of ibuprofen, diclofenac and sulindac on the blood pressure lowering effect of hydrochlorothiazide.

In an open triple crossover study in 8 patients with essential hypertension, the possibility has been investigated of whether the blood pressure lowering effect of hydrochlorothiazide 50 mg once daily was attenuated by co-administration for 4 weeks of ibuprofen 400 mg t.i.d., diclofenac 25 mg t.i.d. or sulindac 200 mg b.i.d. Only a slight, statistically nonsignificant change was found, with the exception of a significant increase in systolic blood pressure after 4 weeks treatment with ibuprofen. There was considerable variation in the blood pressure response during treatment with all three NSAIDs, with slight rises in blood pressure in 13 out of 24 periods. Body weight increased significantly on treatment both with ibuprofen and diclofenac, whereas the increase on sulindac was less and was transient. No significant change was found in various biochemical parameters, including plasma electrolytes, plasma renin activity (PRA), aldosterone, albumin and creatinine, in haematocrit or in the 24-h urinary excretion of sodium and potassium. The sole exception was a decrease in PRA during ibuprofen treatment. From these observations it is concluded that ibuprofen and diclofenac differ from sulindac in their interaction with the diuretic action of hydrochlorothiazide. It appears that all three NSAIDs can safely be combined with hydrochlorothiazide in hypertensive patients, but blood pressure should be monitored carefully when an NSAID are added.

Adult↗
PubMed1987

Evidence for an antagonism between caffeine and adenosine in the human cardiovascular system.

A randomized, double-blind and placebo-controlled study was performed in 10 normotensive male subjects to analyze a possible antagonism between caffeine and adenosine with respect to their effects on the cardiovascular system in humans. Caffeine alone, 250 mg intravenously (i.v.), increased blood pressure by 9/12 mm Hg, and resulted in a fall of heart rate (HR) of 3 beats/min. Plasma epinephrine (E) rose by 114% after caffeine. Adenosine alone, in an increasing dose of 0.04-0.16 mg/kg/min, induced an increase in systolic blood pressure (SBP) (17 mm Hg), and HR (33 beats/min), a moderate fall in diastolic blood pressure (DBP) (-4 mm Hg), and no change of mean arterial pressure (MAP). At the highest adenosine infusion rate, forearm blood flow, skin temperature (ST), and transcutaneous oxygen tension were lowered, whereas plasma (nor)epinephrine was increased 227.2 and 215.9%, respectively. Adenosine infusion after caffeine induced comparable effects, but the fractional adenosine-induced changes of SBP, HR, plasma catecholamines, plasma renin activity (PRA), and aldosterone all were significantly reduced by previous administration of caffeine. Our results indicate an antagonism between caffeine and adenosine in humans, which may support the suggestion that some circulatory effects of caffeine are caused by an interaction with endogenous adenosine.

Adenosine↗
PubMed1987

Respiratory stimulant effects of adenosine in man after caffeine and enprofylline.

In a double-blind and randomized study the respiratory stimulant effect of continuous intravenous adenosine infusion was studied after previous administration of caffeine, placebo and enprofylline in 10 healthy young volunteers. After placebo, adenosine induced an increase of minute ventilation (from 6.3 to 12.5 l min-1), tidal volume (from 0.60 to 0.96 l), and breathing rate (from 11.0 to 14.8 min-1). Venous pCO2 fell and pH rose after adenosine. Caffeine significantly reduced the adenosine-induced changes of minute ventilation, tidal volume, venous pCO2 and pH, whereas no changes occurred after enprofylline. Our results suggest that adenosine stimulates respiration in man by binding with specific P1-purinoceptors, which can be blocked by caffeine, but not by enprofylline.

Adenosine↗
PubMed1987

Antihypertensive treatment and postprandial blood pressure reduction in the elderly.

Recently it has been demonstrated that blood pressure in the elderly decreases after a meal. To evaluate the influence of antihypertensive treatment on postprandial blood pressure reduction in the elderly, the effects of a breakfast (405 kcal) on blood pressure and heart rate were studied in 15 healthy normotensive elderly subjects (mean age 79.5 +/- 6.0 years), in 10 healthy hypertensive elderly subjects (mean age 80.2 +/- 5.7 years) and in 22 hypertensive elderly subjects (mean age 71.4 +/- 5.0 years) treated with antihypertensive medication (diuretics, beta-blockers, vasodilators). In the three groups there was a fall of mean arterial blood pressure of 9.3 +/- 1.9%, 13.8 +/- 1.9% and 7.9 +/- 1.3%, respectively, at 40 min after the start of the breakfast. In all three groups heart rate increased significantly. It is concluded that antihypertensive treatment with the regimens used in this study does not induce an additional fall of blood pressure postprandially. However, the influence of eating should be avoided in the assessment of antihypertensive drug effects in the elderly.

Adrenergic beta-Antagonists↗
PubMed1987

Complications of (-)125I-iodocyanopindolol binding to human mononuclear cells.

(-)125I-Iodocyanopindolol (125ICYP) binding to intact and ultrasonically treated human mononuclear cells (MNC) was studied. Specific binding of 125ICYP defined as the difference in binding in the presence and absence of 2 microM (+/-)-propranolol displayed in intact cells a dissociation constant (Kd) of 11.8 +/- 2.7 pM and a beta-adrenoceptor number (Rt) of 2371 +/- 154 sites/cell. This specific binding, however, still had a complex character. In broken cells a homogeneous class of binding sites with a Kd-value of 6.7 +/- 1.0 pM and a Rt-value of 883 +/- 89 sites/cell was found. When in intact cells nonspecific binding was determined with CGP-12177, a hydrophilic beta-adrenoceptor antagonist, a homogeneous class of binding sites was found with a Kd of 7.0 +/- 0.3 pM and a Rt of 1645 +/- 95 sites/cell. Inhibition curves with (+)-, (-)-, (+/-)-propranolol, timolol and CGP-12177, obtained with ultrasonically treated cells were monophasic. In intact cells propranolol and timolol not only displaced 125ICYP from its specific sites, but in an almost monophasic way also from nonspecific binding sites. CGP-12177, however, showed a clear plateau. It is concluded that in broken MNC a loss of binding sites may occur, whereas in intact cells additional binding interferes with the correct determination of specific 125ICYP binding. The latter can be reduced to a minimum by using hydrophylic ligands such as CGP-12177 to measure nonspecific binding.

Binding, Competitive↗
PubMed1987

A pheochromocytoma of the urinary bladder.

This case report describes a patient with a pheochromocytoma of the urinary bladder. The patient demonstrated an excessive increase of blood pressure and plasma catecholamines immediately after micturition. Ultrasound and CT-scanning confirmed the localisation of the tumour in the urinary bladder.

Adult↗
PubMed1987

Vascular distribution of plasma catecholamines--pulmonary extraction, arterio-venous differences and effect of age.

In 19 normotensive patients undergoing cardiac catheterization, plasma samples were simultaneously collected from five different sites for measuring adrenaline and noradrenaline concentrations. Mean levels (+/- SEM) in pulmonary artery and aorta were 1.70 +/- 0.13 and 1.76 +/- 0.12 nmol/l for noradrenaline and 0.35 +/- 0.05 and 0.36 +/- 0.05 nmol/l for adrenaline, respectively. Thus, no pulmonary uptake of either catecholamine was demonstrated; this was independent of ventilatory lung function. Significant peripheral extraction was only found for adrenaline, and not for noradrenaline, so we found no evidence for the necessity of arterial blood sampling for noradrenaline determinations in this static study. Finally, a significant positive correlation of venous (r = 0.56; p less than 0.01), but not arterial noradrenaline concentration with age was found, as was a negative correlation of both arterial (r = -0.55; p less than 0.01) and venous (r = -0.62; p less than 0.005) adrenaline concentrations with age. The release of adrenaline by the adrenal glands proved to be significantly decreasing with increasing age (r = -0.53; p less than 0.02).

Adult↗