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Biomedical subjects

T Thien

Publications and source records attributed to T Thien.

At least 55 records · Page 3Linked to original sources
PubMed1998

The role of 11 beta-hydroxysteroid dehydrogenase in the pathogenesis of hypertension.

The two 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) isozymes catalyze the interconversion of cortisol and cortisone. Type 1 11 beta-HSD (11 beta-HSD1) has bidirectional activity, while type 2 11 beta-HSD (11 beta-HSD2) mainly converts cortisol into cortisone. Of these two hormones only cortisol has affinity to mineralocorticoid receptors (MRs) and thus induces mineralocorticoid effects. A normal activity of 11 beta-HSD2 is crucial for prevention of mineralocorticoid activity of cortisol. Absent or decreased 11 beta-HSD2 activity results in cortisol-mediated hypermineralocorticoid hypertension. In several hypertensive syndromes a decreased 11 beta-HSD2 activity has been described as the pathogenetic mechanism of the increased blood pressure. In the apparent mineral corticoid excess (AME) syndrome type 1, absence of 11 beta-HSD2 activity is caused by mutations in the gene coding for 11 beta-HSD2. In licorice-induced hypertension glycyrrhetinic acid, the active substituent of licorice, inhibits 11 beta-HSD2 resulting in an acquired hypermineralocorticoid state. 11 beta-HSD2 activity is not decreased in glucocorticoid hypertension (Cushing's syndrome). In essential hypertension some evidence for decreased systemic and skin activity of 11 beta-HSD1 and/or 11 beta-HSD2 has been found, while renal activity of both isozymes appears to be normal. 11 beta-HSD2 activity is also present in cardiovascular myocytes of humans and dogs, and inhibition of 11 beta-HSD potentiates the vascular response to catecholamines. Although MRs in the central nervous system have been incriminated in the pathogenesis of mineralocorticoid hypertension, a pathophysiological role for 11 beta-HSD2 has not yet been described. Finally, in the placenta 11 beta-HSD2 reduces fetal exposure to maternal glucocorticoids and a decreased activity of this isozyme may result in low birth weight and increased risk of high blood pressure at adult age.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1998

Insulin stimulates epinephrine release under euglycemic conditions in humans.

In healthy subjects, acute physiological hyperinsulinemia induces activation of the sympathetic nervous system, but in the absence of hypoglycemia, plasma epinephrine levels have not been found to increase during insulin administration. However, the venous level of epinephrine reflects the net result of release, clearance, and uptake and therefore is not a good measure of adrenomedullary epinephrine secretion. The influence of 90 minutes of euglycemic physiological hyperinsulinemia (60 mU x m(-2) x min(-1); plasma insulin concentration, approximately 700 pmol x L[-1]) on epinephrine kinetics using the 3H-epinephrine tracer method was studied in 12 healthy normotensive, non-obese subjects. After bolus injection, [3H]-epinephrine was continuously infused with arterial and venous blood sampling at regular intervals, enabling calculation of total body (systemic) and forearm epinephrine release and clearance. Studies were performed in the basal state and during sympathetic stimulation by lower-body negative pressure (LBNP) of -15 mm Hg for 15 minutes. Control experiments ("sham" clamps, but with LBNP) were performed in four of the 12 individuals. Euglycemic hyperinsulinemia (all arterial glucose samples > or = 4.2 mmol x L[-1]) induced an increase of the arterial epinephrine concentration (P = .03), and tended to increase total body epinephrine release (P = .08). Total body epinephrine clearance did not change during hyperinsulinemia. The insulin-induced increase in forearm blood flow ([FBF] by plethysmography, from 3.0 +/- 0.4 to 3.8 +/- 0.6 mL x dL(-1) x min(-1), P = .01) was strongly correlated with the increase in arterial epinephrine (r = .78, P < .01). Plasma epinephrine concentrations did not change during control experiments (sham clamp). Sympathetic stimulation alone as induced by LBNP did not stimulate epinephrine release. However, the combination of insulin and LBNP significantly increased epinephrine release (from 0.37 +/- 0.06 to 0.56 +/- 0.12 nmol x m(-2) x min(-1), P = .03). We conclude that acute physiological hyperinsulinemia under euglycemic conditions induces epinephrine release. This effect is enhanced when hyperinsulinemia is combined with sympathetic stimulation by LBNP. Due to increased forearm removal, venous epinephrine concentrations hardly change. Epinephrine release was strongly correlated with the hemodynamic effects of insulin.

Adult↗
PubMed1998

Duplex ultrasound in the hemodynamic evaluation of the late sequelae of deep venous thrombosis.

PURPOSE: The use of duplex ultrasound scanning to evaluate the hemodynamic outcome of deep venous thrombosis 7 to 13 years after the original diagnosis. METHODS: Duplex ultrasound was used to re-examine 1212 segments of vein from 72 patients (49 men, 23 women) with deep venous thrombosis previously diagnosed by means of phlebography to detect reflux and obstruction and evaluate flow; 611 segments were initially thrombosed and 601 segments were open. To define reflux, reversed flow in 31 healthy persons was measured. RESULTS: In a review of all veins of the 72 patients, 8 patients (11%) had completely normal duplex results in all veins, 33 (46%) had reflux, 6 (8%) had at least one noncompressible vein segment, and 25 (35%) had a combination of both. In the proximal vein segments without initial thrombosis a higher percentage was normal (73%) than in segments with initial thrombosis (46%). There was a significantly higher frequency of reflux (46%, p = 0.05) and noncompressibility (12%, p < 0.01) in initially thrombosed proximal vein segments than in vein segments without initial thrombosis (reflux 25%, noncompressibility 3%). Distal to the knee 125 (17%) of 720 vein segments were not traceable. Significantly more initially thrombosed vein segments were not traceable (p < 0.01). In distal vein segments there was no significant difference in reflux (7% versus 5%) and noncompressibility (10% versus 5%) between vein segments with and without initial thrombosis. Flow was present in 99% of the 611 previously thrombosed proximal and distal segments. CONCLUSIONS: Most patients with deep venous thrombosis still had venous abnormalities 7 to 13 years after the initial diagnosis. The most common abnormality was reflux. Significantly more abnormalities were found in initially thrombosed segments. The abnormalities were found in the proximal vein segments and in the distal vein segments, although less frequently in the latter.

Adult↗
PubMed1998

Influence of the arm position on intra-arterial blood pressure measurement.

The reference level for the measurement of blood pressure (BP) is the level of the right atrium. In practice this is regularly disregarded, as the patient's arm is usually placed lower than the right atrial level. The aim of the study was to determine the influence of first, different arm positions and second, different transducer positions on the intra-arterially (i.a.) recorded BP. In 16 healthy men (age 28.1 +/- 8.0 (s.d.) years), i.a. BP was recorded at the left arm in supine position, using a 5-7 cm long cannula. The baseline position was with the tip of the cannula placed precisely at the level of the right atrium. Subsequently, the following changes were made: 5, 10, 15 and 20 cm above and 5, 10, 15, and 20 cm below the baseline position. A 2-min rest period was allowed in each position before the BP was measured. The whole procedure was done either with the transducer connected to the arm at the place of the cannula (n = 7), or with the transducer placed next to the subject and continuously kept at the right atrial level during the BP measurement (n = 9). Simultaneously, baseline BP was measured indirectly, with a standard mercury sphygmomanometer, in the opposite arm maintained with the cubital fossa at the right atrial level during the whole procedure. This resulted in the first group of seven volunteers for both the i.a. systolic (SBP) and diastolic BP (DBP) values to significantly decrease (P < 0.001) when the arm together with the transducer were elevated above the level of the right atrium, and returned to the initial value when the arm and the transducer were placed back at the right atrial level. Intra-arterial SBP and DBP significantly (P < 0.001) increased as the arm, together with the transducer, were lowered below the right atrial level and returned to the initial value when the arm and the transducer were placed back at the right atrial level. In both directions, each 5 cm change in the arm level was accompanied by a 3-4 mm Hg change in the i.a. BP value. The baseline BP, measured sphygmomanometrically at the contralateral arm, remained constant during the whole duration of the procedure. The changes in the i.a. BP were minimal in the second group of nine subjects in which only the arm but not the transducer was placed at different levels. We conclude that small deviations in arm position above or below the 'gold standard', ie, the fossa cubiti at the right atrial level, will result in largely erroneous BP values. The correct positioning of the arm during BP measurement is therefore mandatory for the diagnosis and follow-up of hypertensive subjects.

Adult↗
PubMed1998

Dynamic vessel wall properties and their reproducibility in subjects with increased cardiovascular risk.

OBJECTIVE: To determine reproducibility figures of dynamic arterial wall properties such as cross-sectional compliance (CC) and distensibility (DC) in subjects with increased cardiovascular risk, in comparison with healthy adults. METHODS: A total of 34 persons were divided into three groups with varying cardiovascular risk factors. Diameters (D) and diameter changes (deltaD) during the heart cycle of both common carotid (CCA) and right common femoral (CFA) arteries were measured by a vessel wall movement detector system. Blood pressures (BP) were recorded non-invasively by a semi-automated oscillometric device. CC (=piD(deltaD/2deltaP) in unit mm2/kPa) and DC (=2deltaD/D)/deltaP in unit 10(-3)/kPa) were calculated from the above-mentioned parameters. Measurements were performed twice during one visit and twice again with a time interval of at least 3 days to determine intra-observer intra- and intersession variability. RESULTS: Reproducibility figures of CC and DC of the CCA varied between 8 and 12%, and between 13 and 22% for the CFA. Intra-observer intra- and intersession variability were similar in the three groups. CONCLUSIONS: In our studies the reproducibility of dynamic vascular wall properties determined by ultrasound was good. Despite differences in the absolute values for CC and DC in groups with increased cardiovascular risk, mean reproducibility figures remained at a similar level (8-12%) as in healthy volunteers.

Adult↗
PubMed1998

Deep venous thrombosis: a prospective 3-month follow-up using duplex scanning and strain-gauge plethysmography.

1. The purpose of the study was to evaluate the degree of thrombus regression, development of valvular insufficiency, impaired calf muscle pump function and clinical symptoms after a period of acute deep venous thrombosis. 2. Seventy patients with acute deep venous thrombosis, diagnosed by duplex scanning or venography, received treatment with heparin and oral coumarin derivatives according to a standard protocol. All patients wore graduated compression stockings during the whole study period. Duplex scanning was performed at diagnosis and 1 and 3 months later to measure thrombus mass and reflux. The supine venous pump function test was used to assess calf muscle pump function. 3. Three months follow-up was completed in 60 patients. In total 218 (28%) out of 780 vein segments were initially thrombosed and 134 (17%) could not be traced. A statistically significant reduction of thrombus mass was recorded throughout the study period. Total resolution of thrombosis in all vein segments occurred in 25% of the patients within 1 month and in 40% in 3 months. There was no difference in regression between the various proximal vein segments. Distal segments showed more regression than proximal segments. Reflux occurred in 27% of the initially thrombosed veins and in 15% of the patent veins. Patients who showed total resolution after 1 month had a significantly higher calf muscle pump function than patients without total resolution (70%pf vs 61%pf, P < 0.05). Patients with reflux in two or more segments had a significantly lower calf muscle pump function than patients with reflux in less than two segments (58%pf vs 69%pf, P < 0.05). 4. Using duplex scanning and the supine venous pump function test 3 months after an acute deep venous thrombosis, overall haemodynamic abnormalities and local site of valve incompetence could readily be identified. Patients with haemodynamic abnormalities might be at risk to develop the post-thrombotic syndrome. There was no difference in thrombus regression between the various proximal vein segments. Reflux was significantly more often seen in initially thrombosed veins. Thirty-five percent of the patients developed an abnormal calf muscle pump function after 3 months. Patients with early resolution of thrombus had a higher calf muscle pump function after 3 months.

Adult↗
PubMed1998

Relevance of erythrocyte Na+/Li+ countertransport measurement in essential hypertension, hyperlipidaemia and diabetic nephropathy: a critical review.

In this review the usefulness of the measurement of erythrocyte Na+/Li+ countertransport (Na+/Li+ CT) activity is evaluated. In particular, the association between enhanced erythrocyte Na+/Li+ CT activity and essential hypertension, hyperlipidaemia and diabetic nephropathy is discussed. The conclusion of this review is that elevated erythrocyte Na+/Li+ CT activity is associated with essential hypertension and hyperlipidaemia. A relationship between Na+/Li+ CT activity and diabetic nephropathy is less evident. Despite a significant link of Na+/Li+ CT activity with hypertension and hyperlipidaemia, the diagnostic significance of Na+/Li+ CT activity is low. This is due to the large overlap between the results of control subjects and patients. The factors that contribute to this broad range are discussed in detail.

Animals↗
PubMed1998

The effect of renin-angiotensin system inhibitors on pro- and anti-inflammatory cytokine production.

The balance between pro- and anti-inflammatory cytokines has been implicated in the pathogenesis of infectious and auto-immune diseases, and its modulation has been proposed as a potential therapeutic target. The results reported in the present study show that modulators of the renin-angiotensin system, such as the angiotensin-converting enzyme (ACE)-inhibitor captopril and the angiotensin II receptor type I antagonist valsartan, have potent inhibitory effects on the lipopolysaccharide (LPS)-stimulated production of pro-inflammatory cytokines tumour necrosis factor (TNF) and interleukin-1 (IL-1) in vitro. The anti-inflammatory cytokine IL-1Ra is increased by captopril, whereas IL-6 production is decreased by valsartan. These effects are exerted mainly at high concentrations of the drugs. Administration of one dose of captopril or valsartan in therapeutic dosages to patients with essential hypertension did not influence LPS-stimulated production of cytokines by whole blood. In conclusion, despite inhibitory effects on pro-inflammatory cytokine production in vitro, it is unlikely that captopril or valsartan could be used in anticytokine therapeutic strategies in vivo.

Angiotensin II↗
PubMed1998

Does it matter whether blood pressure measurements are taken with subjects sitting or supine?

BACKGROUND: Several guidelines for the management of hypertension do not give special preference to a specific position of the patient during blood pressure measurement, suggesting that blood pressure readings taken with patients sitting and with patients supine are interchangeable. OBJECTIVE: To test whether there is any difference between the blood pressure readings with patients sitting and supine. DESIGN AND METHODS: Blood pressure and heart rate were measured three times each for 245 subjects (171 hypertensives), with subjects both sitting and supine, simultaneously on both arms, with a Hawksley random-zero sphygmomanometer on the right arm and a semi-automatic oscillometric device (Bosomat) on the left arm. The sequence of the two positions was randomized. The procedure was repeated on a second occasion for 49 subjects (41 hypertensives) with the sequence of the positions reversed. Because there was no systematic difference among the three readings per position, the averages of the three blood pressure and heart rate readings with subjects sitting and supine were compared and the influences of age, body mass index, hypertension and medication on the difference were examined. RESULTS: We found no influence of the subject's body posture on the systolic blood pressure. We found a higher diastolic blood pressure [by 5.2+/-0.4 mmHg (mean+/-SEM), P< 0.001 with Hawksley random-zero sphygmomanometer] and a greater heart rate [by 1.5+/-0.3 beats/min (mean+/-SEM), P< 0.001] with subjects sitting. The sitting minus supine differences for diastolic blood pressure and heart rate decreased significantly with increasing age (P< 0.001). We found no effect of body mass index, hypertension and medication on the sitting - supine differences. CONCLUSIONS: The subject's body posture influenced especially the diastolic blood pressure and heart rate, both of them being significantly higher with patients sitting rather than supine. This effect decreased with age. Thus, for indirect blood pressure measurement, diastolic blood pressure values obtained with subjects sitting and supine cannot automatically be regarded as equivalent.

Adult↗
PubMed1998

Haemodynamic actions of insulin.

Several lines of evidence indicate a significant association between insulin and cardiovascular disease. This association might be explained by direct (cardio) vascular effects of insulin. Two hemodynamic actions of insulin are discussed in this review; it induces direct vasodilation in skeletal muscle and stimulation of the sympathetic nervous system. These closely linked effects normally offset each other. Although more insight has been obtained into responses in insulin-resistant individuals and possible mechanisms, direct evidence to support a causative role for insulin is not yet available.

Animals↗
PubMed1998

Thiazide-induced vasodilation in humans is mediated by potassium channel activation.

-Hydrochlorothiazide and indapamide are thought to exert their hypotensive efficacy through a combined vasodilator and diuretic effect, but in vivo evidence for a direct vascular effect is lacking. The presence and mechanism of a direct vascular action of hydrochlorothiazide in vivo in humans were examined and compared with those of the thiazide-like drug indapamide. Forearm vasodilator responses to infusion of placebo and increasing doses of hydrochlorothiazide (8, 25, and 75 microg. min-1. dL-1) into the brachial artery were recorded by venous occlusion plethysmography. Dose-response curves were repeated after local tetraethylammonium (TEA) administration to determine the role of potassium channel activation and, in patients with the Gitelman syndrome, to determine the role of the thiazide-sensitive Na-Cl cotransporter in the vasodilator effect of hydrochlorothiazide. Vascular effects of hydrochlorothiazide were compared with those of indapamide in both normotensive (mean arterial pressure, 85+/-7 mm Hg) and hypertensive (mean arterial pressure, 124+/-16 mm Hg) subjects. At the highest infusion rate, local plasma concentrations of hydrochlorothiazide averaged 11.0+/-1.6 microg/mL, and those of indapamide averaged 7. 2+/-1.5 microg/mL. In contrast to indapamide, hydrochlorothiazide showed a direct vascular effect (maximal vasodilation, 55+/-14%; P=0. 013), which was inhibited by TEA (maximal vasodilation after TEA, 13+/-10%; P=0.02). The response was not dependent on blood pressure and was similar in patients with Gitelman syndrome, indicating that absence of the Na-Cl cotransporter does not alter the vasodilatory effect of hydrochlorothiazide. The vasodilator effect of hydrochlorothiazide in the human forearm is small and only occurs at high concentrations. The mechanism of action is not mediated by inhibition of vascular Na-Cl cotransport but involves vascular potassium channel activation. In contrast, indapamide does not exert any direct vasoactivity in the forearm vascular bed.

Antihypertensive Agents↗
PubMed1998

Adenosine-induced renal vasodilatation is prolonged in renal artery stenosis.

OBJECTIVE: The objective of this study was to determine whether the response of renal blood flow (RBF) to adenosine infusions differs between hypertensive patients with and without renal artery stenosis (RAS). DESIGN AND METHODS: Twenty-one hypertensive patients who underwent diagnostic angiography of the renal arteries were studied. Nine patients (median age 51 years; 45-61 interquartile ranges) were diagnosed as having essential hypertension (EH). Twelve patients (median age 52 years; 50-58) had hypertension and renal artery stenosis. In all patients three stepwise increasing doses of adenosine (1, 3 and 10 (microg/kg/min) were infused into the renal artery. RBF was measured before and during infusions by means of the 133xenon wash-out method. Arterial and venous plasma samples for renin concentration were obtained from the renal artery and renal vein. Intraarterial blood pressure and heart rate were monitored continuously. RESULTS: Both groups were similar with respect to age, body mass index, mean arterial pressure and baseline RBF (EH: median 428; RAS 343 ml/min/100 g). Both groups showed a similar dose-related increase in RBF during adenosine infusions (normal kidneys: 9, 21 and 34% change vs baseline; stenotic kidneys: 16, 39 and 52% change vs baseline). Ten minutes after discontinuation of the adenosine infusion, RBF returned to baseline in the normal kidney group, but increased further in the stenotic kidney group (71% vs baseline; P = 0.033). Adenosine infusion did not affect the renin secretion in either group. CONCLUSION: Both essential hypertensive patients and patients with renal artery stenosis show a dose-dependent vasodilatation following adenosine infusion. This vasodilatation is sustained after discontinuation of the adenosine infusion in patients with renal artery stenosis, suggesting a potentiated mechanism for vasodilatation induced by adenosine.

Adenosine↗
PubMed1997

[Left ventricular hypertrophy; differences in the diagnostic and prognostic value of electrocardiography and echocardiography].

OBJECTIVE: To compare the electrocardiogram (ECG) and the echocardiogram for demonstration of left ventricular hypertrophy (LVH) and the prognostic values of these methods. DESIGN: Literature study. SETTING: Department of General Practice, Social and Nursing Home Medicine, R.C. University of Nijmegen, the Netherlands. METHOD: Using articles retrieved by means of a search action in Medline (1962-January 1996), a study was made of the differences between determination of LVH by ECG and by echocardiography with regard to the sensitivities and specificities for measuring anatomical LVH, and their predictive values concerning cardiovascular morbidity and mortality. RESULTS: The sensitivity of echocardiography for the prediction of anatomical LVH (88-93%) exceeded that of ECG (21-54%), while both methods had a high specificity (77-97%). ECG-LVH seemed a better predictor of cardiovascular complications than echo-LVH. CONCLUSION: Echocardiography is the better instrument for screening for LVH, but ECG should keep its place in the diagnostics of LVH in view of its high predictive value for morbidity and mortality and its availability to primary health care. In regard to LVH, echocardiography measures only morphological disorders, while ECG also detects functional disorders.

Electrocardiography↗
PubMed1997

Direct vascular effects of furosemide in humans.

BACKGROUND: In humans, hemodynamic changes observed within minutes after systemic administration of furosemide are often referred to as direct vasoactivity. However, these immediate changes do not per se imply a direct vascular effect. We examined the genuine direct vascular effects of furosemide on the human forearm vascular bed and dorsal hand vein. METHODS AND RESULTS: Forearm blood flow in response to infusion of increasing dosages of furosemide into the brachial artery was recorded by venous occlusion plethysmography. Local plasma concentrations of furosemide reached a maximum of 234+/-40 microg/mL during the highest infused dose but did not significantly affect the ratio of flow in the infused/noninfused arms. Venous distensibility of a dorsal hand vein was measured with a linear variable differential transformer. During precontraction with norepinephrine, five increasing dosages of furosemide (1 to 100 microg/min) were administered locally. Additional experiments using local administration of indomethacin or N(G)-monomethyl-L-arginine (L-NMMA) were carried out to determine whether effects were dependent on local prostaglandin or nitric oxide synthesis, respectively. Also, the effects of systemic administration of furosemide were examined. Local administration of furosemide led to a dose-dependent venorelaxation of 18+/-6% at the first to 72+/-16% at the last dose. Indomethacin almost completely abolished furosemide-induced venorelaxation, whereas L-NMMA had no effect. Systemic administration of furosemide resulted in a time-dependent increase of hand vein distensibility, reaching 45+/-11% after 8 minutes. CONCLUSIONS: Furosemide does not exert any direct arterial vasoactivity in the human forearm, even at supratherapeutic concentrations. In contrast, at concentrations estimated to be in the therapeutic range, we observed a dose-dependent direct venodilator effect on the dorsal hand vein that appears to be mediated by local vascular prostaglandin synthesis.

Adult↗
PubMed1997

New developments in the treatment of deep venous thrombosis.

An initial course of standard heparin (SH) or low-molecular-weight heparins (LMWH) is regarded as the treatment of choice for patients with deep venous thrombosis (DVT). LMWH have better bioavailability after subcutaneous administration, have a longer half-life, and show higher and more predictable anticoagulant activity. As a result they can be given subcutaneously and without laboratory control, using a dose that is determined by bodyweight. Because of these multiple advantages of LMWH they will replace SH in the future and subsequently home treatment with LMWH of selected patients seems feasible. The currently accepted approach is to start with SH or LMWH therapy combined with oral anticoagulant therapy. (OAT) at the time of diagnosis. The course of SH or LMWH should continue for at least 5 days, provided that international normalized ratio (INR) is in the therapeutic range on 2 consecutive days. OAT should be continued for at least 3 months to prolong the prothrombin time to an INR of 2-3. When oral anticoagulants are either contraindicated or inconvenient, SH or LMWH can be used at the middosing interval. The role of anti-platelet treatment is not yet established and should be compared with coumarin therapy in the future.

Anticoagulants↗