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Biomedical subjects

A H van den Meiracker

Publications and source records attributed to A H van den Meiracker.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Hypertensive crisis: definition, pathophysiology and treatment].

Hypertensive crises are currently subdivided into hypertensive emergencies and urgencies depending on the acuteness with which the elevated blood pressure has to be lowered. Malignant hypertension, defined as severe hypertension and a hypertensive fundus grade III or IV, can present itself as an emergency or an urgency. For a hypertensive emergency intravenously acting blood pressure lowering agents are almost always required, whereas an urgency can usually be treated with oral agents. In view of the danger of cerebral hypoperfusion, blood pressure reduction during the initial treatment phase of a hypertensive crisis should not be more than 20 to 25%. Agents that exert a controllable blood pressure lowering action are preferred. Controllable blood pressure lowering cannot be achieved with nifedipine capsules. The practice of biting and swallowing a nifedipine capsule for the treatment of a hypertensive crisis therefore is to be discouraged.

Acute Disease↗
PubMed1999

Sensitive and specific method for the simultaneous determination of natural and synthetic catecholamines and 3,4-dihydroxyphenylglycol in microdialysis samples.

The relatively new technique of microdialysis provides new possibilities for investigating in vivo the functioning of the sympathetic nervous system. The small sample volumes obtained, however, are a great challenge for analytical chemists. We report here a HPLC method for measuring in one run both natural and synthetic catecholamines [dopamine, (nor)epinephrine, alpha-methylnorepinephrine, isoproterenol and epinine] and the intraneuronal metabolite 3,4-dihydroxyphenylglycol in small microdialysis samples after derivatization with the fluorogenic agent 1,2-diphenylethylenediamine. No prior clean-up step is necessary. N-Ethylmaleimide is necessary for preventing an inhibitory action on derivatization occurring in in vivo microdialysis samples. The method can handle large numbers of samples, is sensitive (on-column detection limits 30 to 200 fg) and reproducible (RSD 1 to 7%). Recovery characteristics of the commercial microdialysis probe used (CMA/20) were extensively investigated both in vitro and in vivo at various perfusion rates; for practical purposes a rate of 2 microl/min and sampling at 10-min intervals was found to be workable and to give good and reproducible recoveries (50 to 70%).

Animals↗
PubMed1999

Endothelin-1 and blood pressure after inhibition of nitric oxide synthesis in human septic shock.

BACKGROUND: The systemic hypotension during human sepsis has been ascribed to increased production of nitric oxide (NO). Therefore, inhibitors of NO synthesis have been used in the treatment of hypotension in patients with septic shock. In addition, NO production may inhibit the synthesis and vasoconstrictor effects of endothelin-1 (ET-1). In this study, we tested whether ET-1 contributed to the vasopressor action of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in patients with severe septic shock. METHODS AND RESULTS: Compared with healthy volunteers, patients with septic shock had increased plasma levels of nitrite/nitrate (37+/-5 [SEM] versus 12+/-5 mmol/L, P<0.01), the stable end products of NO metabolism, and ET-1 (45+/-7 versus 3+/-2 pg/mL, P<0.001). Plasma ET-1 concentration was not related to plasma nitrite/nitrate concentration or blood pressure. Continuous infusion of L-NAME (1 mg. kg-1. h-1 IV) for 12 hours increased mean arterial pressure by 43+/-5% and systemic vascular resistance by 64+/-10% (both P<0.01). The increase in blood pressure and systemic vascular resistance correlated positively with the level of ET-1 (both P<0. 005) but not with plasma nitrite/nitrate level. L-NAME infusion did not result in significant changes in the plasma concentrations of ET-1 or nitrite/nitrate. CONCLUSIONS: NO and ET-1 may both play a role in the cardiovascular derangements of human sepsis. Although L-NAME does not increase ET-1 concentration in patients with septic shock, the vasopressor response induced by L-NAME depends on the plasma level of ET-1. These findings may indicate that inhibitors of NO synthesis unmask a tonic pressor response of ET-1 in human septic shock.

Blood Pressure↗
PubMed1999

Circulating semicarbazide-sensitive amine oxidase is raised both in type I (insulin-dependent), in type II (non-insulin-dependent) diabetes mellitus and even in childhood type I diabetes at first clinical diagnosis.

Plasma semicarbazide-sensitive amine oxidase is raised in patients with Type I (insulin-dependent) diabetes mellitus. It has been suggested that this enzyme is involved in the development of microvascular damage through its ability to convert amines (e.g. methylamine and aminoacetone) into aldehydes, hydrogen peroxide and ammonia. Plasma semicarbazide-sensitive amine oxidase was found to be equally raised both in patients with Type I diabetes (n = 73) and Type II (non-insulin-dependent) diabetes mellitus (n = 88) compared with control subjects (621 +/- 209 and 619 +/- 202 vs 352 +/- 102 mU/l, p < 0.0001) and to correlate in multiple regression analysis with HbA1c. Since the enzyme could protect the islets from the inhibitory effects of methylamine on insulin secretion, we also tested sera of 100 children, collected consecutively at first diagnosis of Type I diabetes, for semicarbazide-sensitive amine oxidase. The activity was greatly increased compared with serum values of 76 control (siblings) children (757 +/- 300 vs 455 +/- 138 mU/l, p < 0.0001), but not associated with HbA1c. Our study confirms the increase of plasma semicarbazide-sensitive amine oxidase in Type I diabetes and extends this finding to Type II diabetes as well as to childhood Type I at first clinical diagnosis. In the last case increased enzyme activities could serve to protect the islets from inhibitory effects of methylamine but cause damage by generation of hydrogen peroxide, aldehydes and ammonia. In the long run the increased enzyme activities could also contribute to vascular damage by direct cytotoxic action on endothelial cells, including increased oxidative stress and glycosylation of proteins.

Adolescent↗
PubMed1999

Role of sympathetic nervous system in cyclosporine-induced rise in blood pressure.

To clarify the role of the sympathetic nervous system in the development of cyclosporine A (CsA)-induced rise in blood pressure (BP), the effects of CsA on 24-hour ambulatory BP (ABP) were studied in patients with familial amyloid polyneuropathy (FAP) who underwent a liver transplantation. On the basis of autonomic function tests, patients with absent or mild-to-moderate sympathetic damage (Group A, n=11, age 29 to 43 years, disease duration 2 to 6 years) and patients with severe sympathetic damage (Group B, n=9, age 27 to 38 years, disease duration 3 to 9 years) were identified. Both groups were followed for 1 year. The daily doses of CsA and the CsA whole blood trough levels between the groups did not differ. Pretransplantation values of daytime and nighttime ABP were, respectively, 117+/-8/76+/-7 mm Hg and 108+/-12/68+/-9 mm Hg in group A and 107+/-6/66+/-4 mm Hg (P<0.05 group A versus group B) and 102+/-6/62+/-4 mm Hg in group B. In response to CsA, BP increased in all patients, but more so in patients of group B than in patients of group A. One year after transplantation, daytime and nighttime ABP had increased by 6+/-9/3+/-11% and 12+/-10/14+/-14% in group A and by 12+/-6/13+/-10% (P<0.05) and 21+/-11/27+/-21% (P<0.01) in group B. In both groups, the increase in nighttime ABP was greater than the increase in daytime ABP, which resulted in an attenuation or, even, a reversal of the diurnal BP rhythm. Because the rise in BP was greater in patients with more advanced sympathetic dysfunction, the sympathetic nervous system appears to counteract the CsA-induced rise in BP rather than causing it. This implies involvement of factors other than sympathetic activation in the pathogenesis of CsA-induced rise in BP in patients with familial amyloid polyneuropathy.

Adult↗
PubMed1998

Forearm vasorelaxation in hypertensive renal transplant patients: the impact of withdrawal of cyclosporine.

OBJECTIVE: To determine whether cyclosporine A-induced hypertension in renal transplant recipients is accompanied by impairment of endothelium-dependent vasodilatation, which has been suggested by in-vitro and in-vivo animal experiments. DESIGN AND METHODS: In-vivo endothelium-dependent and endothelium-independent vasodilatation, and plasma concentrations of vasoactive hormones in 16 renal transplant patients were determined while they were being treated with cyclosporine A, and 16 weeks later, after their treatment had been changed to azathioprine therapy. The vasodilator response of the forearm vascular bed was measured by strain gauge venous occlusion plethysmography during intra-arterial infusion of acetylcholine (endothelium-dependent vasodilatation) and nitroprusside (endothelium-independent vasodilatation). Postischemic reactive flow was measured after 10 min of arterial occlusion. In addition, plasma concentrations of norepinephrine, and the prostanoids prostaglandin E2 and thromboxane B2, and also concentration of cyclosporine A in blood, were measured. Glomerular filtration rate and renal blood flow were estimated 1 day before the plethysmography study during each treatment period. RESULTS: Upon changing from cyclosporine A to azathioprine treatment, mean arterial pressure fell significantly by 12+/-3% (P< 0.05). Glomerular filtration rate and renal blood flow increased by 13+/-5 and 19+/-8%, respectively (both P< 0.05), while renal vascular resistance fell by 48+/-11% (P< 0.01). Both baseline forearm blood flow and baseline forearm resistance did not change after conversion (5.7+/-0.7 versus 4.9+/-0.6 ml/100 ml/min, and 27.3+/-4.2 versus 26.2+/-3.2 arbitrary units). The absolute and relative forearm blood flow responses, and forearm vascular resistance responses to infusions of acetylcholine and nitroprusside were similar during treatments with cyclosporine A and azathioprine. Peak postischaemic forearm blood flow was 42+/-12% higher during cyclosporine A treatment than it was during azathioprine treatment (P< 0.05), but the minimal postischaemic forearm vascular resistance did not differ for these treatments. Plasma prostaglandin E2 and thromboxane B2 levels decreased by 34+/-7 and 45+/-8%, respectively, after changing treatment, but norepinephrine levels did not change. CONCLUSIONS: Our data indicate that cyclosporine A-induced hypertension in renal transplant recipients is not accompanied by an increase in forearm vascular resistance. In addition, changing from cyclosporine A to azathioprine treatment did not cause changes in endothelial vasodilator functioning, although mean arterial pressure decreased significantly. Our results do not support the hypothesis that attenuation of endothelial vasodilator functioning contributes to the development of cyclosporine A-induced hypertension.

Adult↗
PubMed1998

Effect of diaspirin cross-linked hemoglobin on endothelin-1 and blood pressure in acute ischemic stroke in man.

OBJECTIVE: For almost 50 years it has been known that hemolysed blood can increase blood pressure. Although preclinical studies suggest that this pressor response is due to an interaction of hemoglobin with endothelium-derived vasoactive substances, its mechanism in humans is unknown. We investigated the involvement of endothelin-1 in the blood pressure response to the oxygen carrier diaspirin cross-linked hemoglobin (DCLHb) in stroke patients. DESIGN: In a randomized phase II study, increasing doses of DCLHb (25, 50 and 100 mg/kg, n=8, 8 and 11, respectively) or placebo (n=26) were infused intravenously every 6 h for 72 h to patients with an acute ischemic stroke. Blood pressure and heart rate were measured every 15 min and plasma concentrations of endothelin-1, catecholamines, renin, vasopressin and atrial natriuretic peptide were measured before and 24 and 66 h after the start of the infusions. RESULTS: In the placebo group, mean arterial pressure (MAP) was 112 (109-115) mmHg (mean and 95% confidence interval) at baseline and decreased spontaneously by 11.4 (5.4-17.5) and 12.5 (5.4-19.5) mmHg after 24 and 66 h, respectively. This decrease in MAP was attenuated in patients treated with DCLHb, reaching statistical significance in the highest dose group. The plasma endothelin-1 concentration decreased slightly in the placebo group, from 4.2 (3.1-5.3) pg/ml (median and range) at baseline to 2.4 (1.9-3.7) pg/ml after 24 h (P=0.0044) and 2.8 (1.9-3.7) pg/ml after 66 h (P=0.0042), but increased dose-dependently in response to DCLHb infusion. With the highest dose of DCLHb, the plasma endothelin-1 concentration rose from 4.8 (0.1-7.8) pg/ml at baseline to 21.2 (13.4-53.2) pg/ml after 24 h (P< 0.001) and to 27.6 (11.9-47.8) pg/ml after 66 h (P< 0.001). The increases in the plasma endothelin-1 concentration and in MAP were correlated (r=0.30, P=0.02). Other vasoactive hormones were not affected by the DCLHb infusion. CONCLUSIONS: Infusion of DCLHb in patients with acute ischemic stroke was associated with a dose-dependent increase in plasma endothelin-1 concentration. This may underlie the attenuation by DCLHb of the natural decrease in blood pressure that we observed in these patients.

Acute Disease↗
PubMed1998

Fatigue in primary Sjögren's syndrome.

OBJECTIVE: To assess fatigue in relation to depression, blood pressure, and plasma catecholamines in patients with primary Sjögren's syndrome (SS), in comparison with healthy controls and patients with rheumatoid arthritis. METHODS: For the assessment of fatigue the Multidimensional Fatigue Inventory (MFI) was used, a 20 item questionnaire, covering the following dimensions: general fatigue, physical fatigue, mental fatigue, reduced motivation, and reduced activity. Furthermore, the Zung depression scale was used to quantify aspects of depression. Forty nine female primary SS patients, 44 female patients with rheumatoid arthritis (RA), and 32 healthy women filled in both questionnaires. In addition, supine values of blood pressure and plasma catecholamines were measured in the patients with primary SS. RESULTS: Primary SS patients were more fatigued compared with the healthy controls on all the five dimensions of the MFI. When the analyses were repeated using depression as a covariate, group differences disappeared for the dimensions of reduced motivation and mental fatigue. In the primary SS patients, significant positive correlations between depression and the dimensions of reduced motivation and mental fatigue were found. Comparing patients with primary SS with those with RA, using depression as covariate, no statistically significant differences were found between these groups. No relation between fatigue and blood pressure was found, but a negative correlation was observed between the general fatigue subscale of the MFI and plasma noradrenaline. CONCLUSION: Patients with primary SS report more fatigue than healthy controls on all the dimensions of the MFI and when controlling for depression significant differences remain on the dimensions of general fatigue, physical fatigue, and reduced activity. The negative correlations between levels of noradrenaline and general fatigue in patients with primary SS may imply the involvement of the autonomic nervous system in chronic fatigue.

Adult↗
PubMed1997

[Hypertension in the acute phase of cerebral infarction; not always to be treated].

Hypertension is observed in three-fourths of the patients in the acute phase of a cerebral infarction. Treatment of an elevated blood pressure in the acute phase of a cerebral infarction is discouraged for the following arguments: In most instances the elevated blood pressure decreases spontaneously in the first few days after the infarction and stabilisation of the blood pressure is usually seen within 4 to 7 days. The elevated blood pressure in the acute phase of the cerebral infarction may be considered a favourable adaptation mechanism aimed at maintaining cerebral perfusion in the region surrounding the infarction. As a consequence lowering of the elevated blood pressure may be harmful because it can lead to expansion of the infarction. No controlled prospective studies to determine if treatment of hypertension in the acute phase of a cerebral infarction might be of benefit have been performed. There are, however, several case reports showing that treatment of an elevated blood pressure in the acute phase of a cerebral infarction is associated with dramatic progression of the neurological deficit. Exceptions can be made for situations where diastolic blood is repeatedly higher than 130-140 mmHg or where there are concomitant cardiovascular diseases, such as myocardial infarction, heart failure or a dissecting aneurysm requiring immediate antihypertensive treatment.

Antihypertensive Agents↗
PubMed1997

Improved orthostatic tolerance in familial amyloidotic polyneuropathy with unnatural noradrenaline precursor L-threo-3,4-dihydroxyphenylserine.

Disabling orthostatic hypotension, due to insufficiency of the autonomic nervous system, is a common complication of type I familial amyloidotic polyneuropathy (FAP). We investigated whether oral treatment with L-threo-3,4-dihydroxyphenylserine (L-threo-Dops), a noradrenaline precursor, might be of therapeutical benefit. In twenty untreated FAP patients, aged 33 to 44 years, who, because of severe orthostatic hypotension, were bedridden or constrained to a sitting life, supine and erect blood pressure (BP), plasma noradrenaline and tilting time, defined as the interval (s) between the beginning of a 60 degrees head-up tilt and the occurrence of orthostatic symptoms (dizziness, blurred vision or near syncope) were determined before and at repeated intervals during oral treatment with L-threo-Dops, 100 mg bid, for 6 months. Before treatment supine mean BP was 80 (76-85) mmHg (mean and 95% CI), supine plasma noradrenaline was low, 59 (41-77) pg/ml and tilting time ranged from 38 to 118 s. In response to tilt, mean BP immediately fell by 36 (31-41) mmHg, whereas plasma noradrenaline increased by only 11 (0-21) pg/ml (p = 0.05). After 3 to 5 days of treatment with L-threo-Dops all patients experienced marked improvement of their orthostatic tolerance as reflected by their ability to walk freely around. This effect sustained throughout the six months of treatment. Plasma noradrenaline increased moderately by 37 (11-63) pg/ml (p = 0.02) and supine mean BP increased by 8.6 (5.8-12.4) mmHg (p < 0.001) during chronic treatment. Supine or nocturnal hypertension did not develop, the fall in mean BP in response to tilt diminished by 12.5 (6.5-17.3) mmHg (p < 0.001) and tilting time became longer than 600 s in all patients. Because of its efficacy, its sustained duration of action and the lack of side effects, L-threo-Dops is advocated to improve orthostatic tolerance in patients with autonomic insufficiency due to FAP.

Adult↗
PubMed1996

Reconstruction of brachial artery pressure from noninvasive finger pressure measurements.

BACKGROUND: Pulse wave distortions, mainly caused by reflections, and pressure gradients, caused by flow in the resistive vascular tree, may cause differences between finger and brachial artery pressures. These differences may limit the use of finger pressure measurements. We investigated whether brachial artery pressure waves could be reconstructed from finger pressure measurements by correcting for the pressure gradient in addition to correction for pulse wave distortion with a previously described filter. METHODS AND RESULTS: Finger artery pressure (with Finapres), intra-arterial brachial artery pressure (BAP), Riva-Rocci/ Korotkoff (RRK), oscillometric, and return-to-flow (RTF) measurements were simultaneously performed in 57 healthy elderly subjects and patients with vascular disease and/or hypertension. A generalized waveform filter was used to correct for pulse wave distortions. Correction equations for the pressure gradient, based on finger pressure, RRK, RTF, or oscillometric measurements, were obtained in 28 randomly selected subjects and tested in 29. Before reconstruction, Finapres underestimated mean and diastolic BAP (finger pressure minus BAP: systolic, -3.2 +/- 16.9 mm Hg; mean, -13.0 +/- 10.5 mm Hg; diastolic, -8.4 +/- 9.0 mm Hg [mean +/- SD]). After filtering, reconstructed BAP waves were similar to actual BAP in shape but not in pressure level. Optimal correction for the pressure gradient with an equation based on RTF measurements reduced the pressure differences to meet American Association for the Advancement of Medical Instrumentation criteria (reconstructed finger pressure minus BAP: systolic, 3.7 +/- 7.0 mm Hg; mean, 0.7 +/- 4.6 mm Hg; and diastolic, 1.0 +/- 4.9 mm Hg). CONCLUSIONS: BAP waves can be reconstructed from noninvasive finger pressure registrations when finger pressure waves are corrected for pulse wave distortion and individual pressure gradients.

Adult↗
PubMed1996

Cardiovascular variability in major depressive disorder and effects of imipramine or mirtazapine (Org 3770).

Spectral analysis of fluctuations in heart rate (HR) and blood pressure (BP) was applied to assess sympathetic and parasympathetic cardiovascular control mechanisms in patients with unipolar affective disorder before and after treatment with imipramine (IMI) or mirtazapine (MIR). In a double-blind randomized study, 10 patients received treatment with IMI and 10 patients received treatment with MIR. Cardiovascular parameters were studied before and after 4 weeks of treatment: HR and BP (Finapres) were recorded continuously during supine rest (SR) and orthostatic challenge (OC; 60-degrees head-up tilting). During SR and OC, power spectra were calculated for HR and systolic BP. Spectral density was assessed for three frequency bands: low (0.02-0.06 Hz), mid (0.07-0.14 Hz), and high (0.15-0.50 Hz). Before treatment, the depressed patients (N = 20) differed from age-matched controls (N = 20) only in their response to OC: the depressed patients showed more suppression of HR variability (both mid- and high-frequency band fluctuations), indicating stronger vagal inhibition, and a reduced increase of BP variability (mid-frequency band fluctuations), indicating reduced sympathetic activation. After 4 weeks of treatment, patients treated with either antidepressant drug showed significant changes of HR (increase) and HR variability (decrease) during SR and OC; the suppression of mid- and high-frequency fluctuations of HR was larger for IMI than for MIR. The increase in HR and decrease in HR variability may be attributed to the anticholinergic properties of IMI (strong) and MIR (weak), resulting in cardiac vagal inhibition. Whereas MIR had no effect on BP or BP variability, IMI specifically reduced mid-frequency band fluctuations of BP as the result of a suppression of central sympathetic activity. Our data confirm and extend previous observations on the presence of autonomic dysfunctions in unmedicated depressed patients: spectral analysis of HR and BP fluctuations suggested that both parasympathetic and sympathetic mechanisms are involved, specifically during OC. The preexisting autonomic cardiovascular dysfunctions were not normalized by antidepressant drugs. In fact, some of the components of the cardiovascular autonomic dysfunction were further aggravated, depending on the pharmacologic profile of the drug under investigation.

Adult↗
PubMed1996

Finapres tracking of systolic pressure and baroreflex sensitivity improved by waveform filtering.

OBJECTIVE: Arterial pressure waveforms distort between brachial and finger arteries, causing differences mainly in systolic pressure. Distortion, reportedly, can be removed by applying a waveform filter to the finger pressure. DESIGN: We analysed the data from two studies that detected discrepancies in systolic tracking between Finapres and brachial pressures. The first set comprised waveforms of seven volunteers during incremental bicycle exercise to exhaustion and the second set comprised waveforms of eight volunteers during increasing phenylephrine infusion. METHODS: We applied the filter and compared 1 min averaged unfiltered and waveform-filtered finger and brachial pressures. RESULTS: During exercise, finger systolic pressure overestimated brachial increasingly, from 7(SD 10) mmHg at rest to 27(17) mmHg at maximal exertion. Differences were reduced by waveform filtering from 3 (SD 9)mmHg at rest to 1 (SD 15)mmHg at maximal exertion. During phenylephrine infusion finger systolic pressure overestimated brachial pressure, but the magnitude of the overestimate decreased from 14 (SD 15)mmHg at baseline to -1(SD 16)mmHg at maximal rate. After waveform filtering overestimation was an almost constant 6(SD 11)mmHg. Median baroreflex sensitivities from brachial, unfiltered and waveform-filtered finger pressure were 5.8, 7.5 and 5.3 ms/mmHg and correlation increased after filtering. The results indicate improved systolic pressure tracking after waveform filtering. CONCLUSIONS: Finger pressure distortion follows a general pattern correctable by waveform filtering. Waveform filtering allows a 'brachial' view to be obtained from Finapres data.

Adolescent↗
PubMed1996

Cyclosporin A impairs the nocturnal blood pressure fall in renal transplant recipients.

In renal transplant recipients, hypertension and a diminished nocturnal blood pressure fall are frequently found. To investigate whether this diminished nocturnal blood pressure fall is related to the use of cyclosporin A or to other factors, such as the use of glucocorticoids, we measured 24-hour ambulatory blood pressure in 18 renal transplant recipients both before and 16 weeks after conversion from cyclosporin A to azathioprine. Renal blood flow and glomerular filtration rate were estimated from 131I-hippurate and 125I-iothalamate clearances, respectively, and plasma concentrations of renin, atrial natriuretic peptide, norepinephrine, prostaglandin E2, and thromboxane B2 were determined. During cyclosporin A treatment, mean 24-hour blood pressure was 117 +/- 3 mm Hg, and the nocturnal fall in blood pressure was 4 +/- 9 mm Hg. A nondipping diurnal blood pressure pattern was present in 13 patients. After conversion to azathioprine, mean 24-hour blood pressure decreased to 109 +/- 3 mm Hg (P < .001), the nocturnal fall increased to 9 +/- 6 mm Hg, and the number of patients with a nondipping diurnal blood pressure pattern decreased to 9. The nocturnal fall in heart rate (17 +/- 10 beats per minute) during cyclosporin A did not change after conversion. Body weight and plasma concentrations of norepinephrine and renin did not change. Plasma concentrations of prostaglandin E2 and thromboxane B2 decreased after conversion, as did plasma atrial natriuretic peptide. Renal blood flow and glomerular filtration rate increased after conversion. In conclusion, cyclosporin A appears to be involved in the disturbance of the circadian blood pressure rhythm in renal transplant recipients. Although the precise mechanism is unclear. the elevated plasma atrial natriuretic peptide and slightly suppressed plasma renin concentrations suggest that intravascular volume expansion may contribute to the observed hemodynamic alterations.

Adult↗
PubMed1996

Renal artery stenosis towards the year 2000.

FUNCTIONAL DIAGNOSTIC TESTS FOR SELECTING PATIENTS FOR RENAL ARTERIOGRAPHY: The functional diagnostic tests now available to select patients for renal arteriography, such as captopril-renal scintigraphy and the captopril-peripheral vein renin test, have a high degree of diagnostic accuracy, 70% sensitivity at 90% specificity, but they are still not good enough to assess the large population of hypertensives for renal artery stenosis. The use of the angiotensin converting enzyme (ACE) inhibitor challenge and the introduction of a new pharmacon, technetium-labelled mercapto-triglycine, have not sufficiently increased the value of scintigraphy and further improvement in the near future seems unlikely. THE USE OF CLINICAL CRITERIA TO IDENTIFY HIGH-RISK PATIENTS: A more realistic approach to the diagnosis of renal artery stenosis is to seek simple and sensible clinical criteria to identify high-risk patients. The blood pressure response to 2 months of treatment with a standardized two-drug regimen is a suitable criterion. Interim analysis of an ongoing prospective multicentre study in the Netherlands indicates that the prevalence of renal artery stenosis is as high as 25% in patients who are resistant to the combination of 10 mg amlodipine + 50 mg atenolol, compared with 15% in patients resistant to the combination of 20 mg enalapril + 25 mg hydrochlorothiazide. When drug resistance is used as the selection criterion for arteriography, the total number of cases detected with intra-arterial digital subtraction angiography does not seem to differ according to which of these drug regimens is used. FUTURE POSSIBILITIES: The current enthusiasm for percutaneous transluminal renal angioplasty (PTRA) and stenting may be premature. With further improvement of non-invasive techniques to visualize the renal arteries, such as colour Doppler ultrasound with microparticle contrast enhancement or magnetic resonance angiography, it should become more attractive to follow patients with renal artery stenosis while they are being treated with drugs rather than automatically resorting to PTRA.

Angioplasty↗
PubMed1995

Ambulatory blood pressure monitoring in clinical trials with antihypertensive agents.

Ambulatory blood pressure monitoring (ABPM) is being used increasingly for the evaluation of antihypertensive agents in clinical trials. In this brief review several aspects of ABPM are discussed. In particular, attention is paid to the extent to which ABPM is subject to a placebo response and the extent to which the sample size of the study population can be reduced with this type of measurement. In addition, some remarks are made with regard to how selection of patients with this methodology can be improved and how it may be used as a tool to evaluate the duration of action of antihypertensive agents. Finally, some potential disadvantages of ABPM as compared to conventional clinic blood pressure measurements are discussed.

Antihypertensive Agents↗
PubMed1995

Plasma semicarbazide-sensitive amine oxidase activity is elevated in diabetes mellitus and correlates with glycosylated haemoglobin.

1. Semicarbazide-sensitive amine oxidase is a common name for a group of heterogeneous amine oxidases which are present in various mammalian tissues, especially in vascular smooth muscle cells, cartilage and adipose tissue, but also in plasma. 2. Plasma semicarbazide-sensitive amine oxidase activity was elevated in a group of 104 patients with insulin-dependent diabetes mellitus compared with normal control subjects (555 +/- 172 versus 352 +/- 102 m-units/l, P < 0.0005). 3. Plasma semicarbazide-sensitive amine oxidase activity was higher in subgroups with either retinopathy or nephropathy or both [583 +/- 116 (n = 34), 581 +/- 229 (n = 10) and 646 +/- 249 m-units/l (n = 19), respectively] than in the subgroup without overt complications [486 +/- 129 m-units/l (n = 41), P < 0.005]. 4. Plasma semicarbazide-sensitive amine oxidase activity was positively correlated with plasma glycosylated haemoglobin (r = 0.40; P < 0.0001) and with log urinary albumin excretion (r = 0.26; P < 0.025). 5. The possibility that semicarbazide-sensitive amine oxidase, by its conversion of endogenous amines like methylamine and aminoacetone into cytotoxic aldehydes, plays a role in the development of microvascular complications in diabetes mellitus, needs further investigation.

Adult↗