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Biomedical subjects

M Hausberg

Publications and source records attributed to M Hausberg.

At least 37 records · Page 2Linked to original sources
PubMed2001

Acute effects of haemodialysis on endothelial function and large artery elasticity.

BACKGROUND: Disturbances of functional properties of large arteries contribute to increased cardiovascular morbidity and mortality in patients with end-stage renal disease. However, it is not clear whether haemodialysis per se acutely affects mechanical vessel wall properties or endothelial function. METHODS: Twenty-five chronic haemodialysis patients (mean+/-standard error of the mean (SEM): age 52+/-5 years; time on dialysis 63+/-7 months; blood pressure 132+/-4/72+/-2 mmHg) were studied before and immediately after a haemodialysis (HD) session using a polysulphone dialyser (ultrafiltration 1460+/-54 ml), as well as on the following day. Blood pressure was measured with an automatic sphygmomanometer and applanation tonometry. End-diastolic diameter and distension of the brachial and carotid arteries were measured by Doppler frequency analysis of vessel wall movements in M-mode using a multigate pulsed Doppler system and aortic pulse wave velocity (PWV) by an automatic device (Complior). Endothelial function was determined as brachial artery flow-mediated dilation (FMD) and compared with endothelium-independent nitroglycerine-induced dilation (NMD). RESULTS: FMD was 7.9+/-1.8% in patients before HD and did not change significantly after HD or in the dialysis-free intervall (6.7+/-2.1 and 7.1+/-2.0%, respectively; NS). The same was true for NMD and PWV (12.6+/-0.8 m/s before HD, 12.8+/-0.8 m/s after HD, and 11.9+/-0.7 m/s on the HD-free day). Carotid distensibility coefficients decreased significantly during HD (from 18.1+/-1.9 x 10(-3)/kPa to 16.7+/-2.2 x 10(-3)/kPa, P<0.05) and increased again on the HD-free day (19.8+/-2.4 x 10(-3)/kPa). However, when corrected for blood pressure by tonometry, isobaric carotid distensibility did not change significantly. Brachial artery distensibility also did not show significant acute changes. CONCLUSIONS: Haemodialysis per se did not have a significant effect on endothelial function or large artery mechanical vessel wall properties in patients on maintenance dialysis therapy.

Arteries↗
PubMed2001

A novel assay for determination of diadenosine polyphosphates in human platelets: studies in normotensive subjects and in patients with essential hypertension.

OBJECTIVE: Diadenosine polyphosphates (APnAs, n = 3-6) are a family of endogenous vasoactive purine dinucleotides which have been isolated from thrombocytes. Diadenosine pentaphosphate (AP5A) and diadenosine hexaphosphate (AP6A) are more potent than diadenosine tetraphosphate (AP4A) and diadenosine triphosphate (AP3A) and cause skeletal muscle vasoconstriction in rats. Little is known about their physiological and pathophysiological significance in humans. The aims of the present study were to compare thrombocyte APnA concentrations in patients with essential hypertension (HYP) and in healthy normotensive humans (CON) using a novel quantitative assay and to assess a possible relationship between thrombocyte APnA concentrations and skeletal muscle vascular resistance. DESIGN AND METHODS: We describe a novel assay for quantification of APnAs in human platelets, involving platelet isolation from human blood, a solid-phase extracting procedure with a derivatized resin, desalting and quantitative determination of the substances with an ion-pair reversed-phase high-performance liquid chromatography (HPLC) system. The structural integrity of the isolated APnAs was confirmed by mixed assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) measurements and co-elution with added standards. The detection threshold for all four APnAs was 1 pmol/l and the inter-assay coefficients of variation were < 11% (n = 12). After venous blood sampling, mean arterial blood pressure (MAP) and forearm blood flow (FBF, using venous occlusion plethysmography) were measured in HYP and CON. Forearm vascular resistance (FVR) was calculated as MAP/FBF. significantly differ in platelet AP3A and AP4A content, but HYP had significantly higher thrombocyte concentrations of AP5A (56 +/- 7 versus 32 +/- 3 ng/microg beta-thromboglobulin, P = 0.003) and AP6A (10 +/- 1 versus 6 +/- 1 ng/microg beta-thromboglobulin, P = 0.015) than CON. HYP had significantly elevated FVR (50 +/- 6 versus 33 +/- 2 arbitrary units, P = 0.01) compared to CON. Significant correlations were found between AP5A and FVR (p = 0.38, P = 0.04) as well as between AP6A and FVR (p = 0.42, P = 0.02). In contrast, there were no significant correlations between APnAs and MAP. CONCLUSIONS: The study shows that thrombocyte concentrations of AP5A and AP6A are elevated in patients with essential hypertension. Vasoconstriction caused by release of AP5A and AP6A from thrombocytes may contribute to the increase of vascular resistance in hypertensive patients.

Adult↗
PubMed2001

Arterial distensibility and pulse wave velocity in patients with primary hyperparathyroidism before and after parathyroidectomy.

AIMS: There is evidence that secondary hyperparathyroidism alters arterial vessel wall properties. However, it is unclear whether effects of parathyroid hormone (PTH) on the vascular wall are direct or permissive and related to hypertension and renal failure. To assess early direct effects of PTH on large artery wall properties isobaric distensibility (DC), pulse wave velocity (PWV) and intima-media thickness (IMT) were studied before and after parathyroidectomy (Ptx) in patients with primary hyperparathyroidism (pHPT). METHODS: DC and IMT of the brachial and carotid artery were measured by echo-tracking and tonometry, PWV by the automatic Complior-device at baseline and 6 months after Ptx in 20 patients with pHPT (data mean +/- SEM, age 45+/-5 years, PTH 240+/-61 ng/l). Cardiovascular risk factors like diabetes, hypertension, renal insufficiency and hypercholesterolemia were excluded. Twenty healthy volunteers matched for age, sex and blood pressure served as controls. RESULTS: Six months after Ptx, PTH decreased to normal; however, blood pressure levels and vessel wall parameter remained unchanged. At baseline, there were no significant differences in brachial and carotid IMT (0.48+/-0.04 and 0.62+/-0.04 mm vs. 0.47+/-0.06 and 0.61+/-0.06 mm), radial and aortic PWV (9.1+/-0.4 and 9.9+/-0.7 m/s vs. 9.2+/-0.5 and 10.0+/-0.6 m/s), brachial and isobaric carotid DC (10.1+/-1.4 and 19.5+/-3.4 10(-3)/kPa vs. 9.1+/-0.9 and 20.4+/-3.2 10(-3)/kPa) or artery diameter between patients and controls. CONCLUSIONS: Structural and viscoelastic properties of large arteries are not disturbed and not influenced by parathyroidectomy in patients with early pHPT devoid of hypertension and renal disease. We conclude that increased PTH levels per se are not associated with alterations of mechanical arteriall wall properties; permissive factors like renal insufficiency may be necessary to mediate vessel wall alterations in patients with hyperparathyroidism.

Blood Flow Velocity↗
PubMed2001

Antihypertensive treatment in renal transplant patients--is there a role for ACE inhibitors?

During the past two decades great progress was achieved with regards to short-term kidney graft survival. However, long-term graft survival did not improve similarly. Many factors contribute to chronic graft nephropathy eventually resulting in late graft loss, among these arterial hypertension is of major importance. In patients with chronic renal disease of diabetic and non-diabetic origin, angiotensin converting enzyme inhibitors have been convincingly shown to slow the progression of renal failure. The achieved nephroprotection correlates with the reduction of proteinuria by ACE inhibitor treatment. Also in renal transplant patients, ACE inhibitors have been shown unequivocally to reduce urinary protein excretion. The prevention of hyperfiltration, particular in the context of a reduced number of functional nephrons in patients with chronic graft nephropathy, could be important to prolong graft survival after renal transplantation. Moreover, ACE inhibitors may exert beneficial effects on immunologic processes contributing to chronic graft nephropathy. Many studies published in the last decade show convincingly that ACE inhibitors are safe and effective for the treatment of hypertension in renal allograft recipients. However, no data exist so far showing that ACE inhibitors are superior to other antihypertensive drugs in renal transplant patients and that they prolong graft survival. Studies investigating this issue are warranted. Apart from effects on the graft, ACE inhibitors may improve alterations of the cardiovascular system generally observed in renal transplant patients, such as structural alterations of large arteries, left ventricular hypertrophy, disturbed mechanical vessel wall properties and endothelial dysfunction. Therefore, angiotensin converting enzyme inhibitors could reduce cardiovascular morbidity and mortality in kidney transplant patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Comparison of quinapril versus atenolol: effects on blood pressure and cardiac mass after renal transplantation.

Based on epidemiologic facts on elevated cardiovascular mortality in renal allograft recipients, an echocardiographic 2-year follow-up in hypertensive renal allograft recipients was conducted. This study provides evidence that, in contrast to atenolol, quinapril, independent of blood pressure reduction, reduces left ventricular hypertrophy and improves left ventricular diastolic function in this population.

Adrenergic beta-Antagonists↗
PubMed2000

[Alterations of arterial vessel wall properties in hyperparathyroidism].

Alterations of arterial vessel wall function are associated with increased cardiovascular morbidity and can be measured by noninvasive ultrasound techniques. There is increasing evidence that hyperparathyroidism contributes not only to structural changes of the cardiovascular system but to disturbances in functional arterial vessel wall properties. It has been shown that elevated concentrations of parathyroid hormone are associated with decreased arterial distensibility and increased intima-media thickness in patients with renal insufficiency. A permissive role of parathyroid hormone in the pathogenesis of uremic vessel wall changes has been discussed. The endothelium is a newly recognized target organ of parathyroid hormone. In patients with primary hyperparathyroidism endothelial dysfunction has been demonstrated, that seems to be reversible after parathyroidectomy. Effects on arterial vessel wall function may contribute to increased blood pressure observed in hyperparathyroidism. The complex cardiovascular effects of parathyroid hormone and changes in vascular tone, arterial distensibility and endothelial function in hyperparathyroidism are discussed.

Arteriosclerosis↗
PubMed2000

[Alterations of the arterial vessel wall in renal failure].

Cardiovascular events are the main cause of death in patients with end-stage renal disease. Functional and structural alterations of the arterial system substantially contribute to the high cardiovascular mortality in these patients. Structural alterations of the arterial wall comprise intima-media thickening and atherosclerotic plaque formation. Moreover, mechanical vessel wall properties of large arteries are significantly disturbed. This is already observed in young patients. Reduced arterial distensibility impairs large artery cushioning function. This results in increased ventricular afterload promoting left ventricular hypertrophy and in reduced coronary perfusion. After renal transplantation, structural alterations of the arterial wall and disturbed mechanical vessel wall properties persist. Moreover, renal failure is characterized by a severe impairment of endothelial function. Disturbed endothelial function results from reduced production of endothelium-dependent endogenous vasodilators and/or blunted vascular effects of these substances. Uremia is associated with the accumulation of an endogenous inhibitor of the endothelial nitric oxide synthase. Impaired endothelial function in renal failure promotes the progression of structural lesions of the arterial wall. Also in renal transplant recipients, substantially impaired endothelial function is observed despite correction of uremia. Hyperparathyroidism commonly observed in renal failure contributes to the disturbed functional vessel wall properties of large arteries. In patients with end-stage renal disease, decreased large artery distensibility is an independent risk factor for increased cardiovascular mortality. This may apply also to intima-media thickening and to impaired endothelial function.

Arteriosclerosis↗
PubMed2000

[Diagnosis and therapy of renovascular hypertension].

BACKGROUND: Renovascular hypertension as a secondary form of hypertension can be improved or cured in many cases by interventional radiology or vascular surgery. BASIS: The renin-angiotensin-aldosterone system and the development of hypertension are linked in renovascular hypertension. CLINICAL APPEARANCE: Early clinical symptoms are of special interest in diagnosing renovascular hypertension. DIAGNOSIS AND THERAPY: Nowadays, angioplasty or stenting have mostly replaced surgery in view of treatment of renovascular hypertension. CONCLUSION: Renovascular hypertension, if diagnosed early, can be improved or cured in many cases regarding hypertension and/or renal insufficiency.

Angioplasty, Balloon↗
PubMed2000

Impaired flow-mediated vasodilation of the brachial artery in patients with primary hyperparathyroidism improves after parathyroidectomy.

OBJECTIVE: The endothelium is a newly recognised target tissue of parathyroid hormone (PTH). It is not clear whether hyperparathyroidism affects endothelial function and whether parathyroidectomy (Ptx) has an influence on arterial vessel wall properties. We studied brachial flow-mediated vasodilation (FMD) and brachial and carotid intima-media thickness (IMT) in patients with primary hyperparathyroidism (pHPT) before and after Ptx and in healthy controls. METHODS: 19 patients with pHPT (mean+SEM, age 45+/-4.7 years, PTH 238+/-52 ng/l) were studied. Diabetes, hypertension and vascular disease were excluded. Twenty healthy volunteers matched for age, sex and blood pressure served as controls. Enddiastolic diameter, FMD and nitroglycerine-induced (NMD) dilation of the brachial artery were measured by a multigate pulsed doppler system (echo-tracking), IMT was determined using automatic analysis of the M-line signal. Healthy volunteers where studied on one occasion, patients were studied at baseline and 6 months after Ptx. RESULTS: Six months after Ptx PTH had decreased to normal, blood pressure levels remained unchanged. Endothelium dependent FMD at baseline was impaired in patients compared to controls (4.7+/-1.2 vs. 18.2+/-3.7%, P<0.01), however, FMD improved significantly after Ptx (16.7+/-3.0%, P<0.01). Nitroglycerine-induced dilation, IMT and artery diameter were not different between groups and did not change after Ptx. CONCLUSIONS: Impaired endothelium dependent vasodilation in patients with primary hyperparathyroidism improves after successful parathyroidectomy. Endothelial dysfunction associated with primary hyperparathyroidism occurs without detectable structural wall alterations of the brachial artery and appears therefore to be an early and reversible arterial alteration.

Adult↗
PubMed2000

Membrane, intracellular, and plasma magnesium and calcium concentrations in preeclampsia.

Changes in intracellular calcium and magnesium concentrations seem to be involved in the pathogenesis of preeclampsia, whereas the role of cell membranes has not been studied in detail yet. To investigate the changes in calcium and magnesium metabolism in normal pregnancy and preeclampsia, plasma, intracellular, and membrane calcium and magnesium concentrations were determined in a clinical study. Twenty-five control, 18 untreated healthy pregnant, and 16 nulliparas preeclamptic women were investigated. Plasma, cellular, and membrane (erythrocytes) calcium and magnesium contents were measured by atomic absorption spectroscopy. Plasma and intracellular magnesium concentrations were significantly lower in the healthy pregnant group and the preeclamptic group as compared to controls (P < .01). In erythrocyte membranes magnesium content was found significantly decreased in the preeclamptic women as compared to healthy subjects (P < .001). There was a significant decrease in the plasma calcium concentration in the preeclamptic group compared to controls or healthy pregnant women (P < .05). Membranous calcium content was significantly increased in the preeclamptic group versus controls or healthy pregnant women (P < .001) and an inverse correlation with membranous magnesium content was found (r = -0.79,P < .01). Lowered plasma, intracellular, and membrane magnesium concentrations in preeclampsia may contribute to the development in hypertension in pregnancy. In addition, a disturbed calcium homeostasis is observed in preeclampsia.

Adult↗
PubMed2000

Studies on flow-mediated vasodilation and intima-media thickness of the brachial artery in patients with primary hyperparathyroidism.

The endothelium is a newly recognized target organ of parathyroid hormone (PTH) and may contribute to its effects on vascular tone and blood pressure regulation. Flow-mediated vasodilation (FMD), brachial and carotid intima-media thickness (IMT) were studied in patients with primary hyperparathyroidism (pHPT) and controls to evaluate endothelial function and structural arterial vessel wall alterations. Sixteen patients with pHPT (mean +/- SEM, age 44 +/- 5 years; PTH 229 +/- 72 ng/L; serum calcium 3.0 +/- 0.06 mmol/L; serum phosphate 2.0 +/- 0.2 mg/L) and 16 normocalcemic control subjects matched for age, sex, and blood pressure were included. Diabetes, hypertension, and vascular disease were excluded in both groups. End-diastolic diameter, flow-mediated (FMD) and nitroglycerin-mediated (NMD) dilation of the brachial artery were measured by a multigate pulsed Doppler system (echo-tracking). IMT was determined using automatic analysis of the M-line signal. Endothelium-dependent FMD was impaired in patients compared to controls (4.6 +/- 1.6% v 19.2 +/- 3.9%, P < .001). NMD (23.8 +/- 3.1% v. 22.4 +/- 2.8%, P = NS), carotid and brachial IMT (0.60 +/- 0.04 mm v 0.64 +/- 0.06 mm, P = NS, and 0.46 +/- 0.04 mm v 0.47 +/- 0.08 mm, P = NS, respectively) and artery diameters were not different. Endothelium-dependent vasodilation is impaired in patients with primary hyperparathyroidism despite normal IMT. Endothelial dysfunction may contribute to increased cardiovascular morbidity and mortality in pHPT.

Adult↗
PubMed2000

Intracellular Mg++ concentrations in smooth and striated muscle cells in spontaneously hypertensive rats.

Decreased intracellular Mg++ concentrations seem to be involved in the pathogenesis of primary hypertension. Of special interest is the smooth muscle cell with its electrolyte metabolism in primary hypertension, but also heart muscle cells and their Mg++ concentrations are of growing interest. Therefore, in aortic smooth muscle cells and striated heart muscle cells (left ventricle) from 20 spontaneously hypertensive rats (SHR) of the Münster strain and 20 normotensive Wistar-Kyoto rats (WKY), the intracellular Mg++ content was measured. The electron probe x-ray microanalysis technique was used to determine intracellular Mg++ concentrations under nearly in vivo conditions in aortic cryosections 3 microm thick and striated heart muscle cells 4 microm thick (Camscan CS 24 apparatus). Vascular smooth muscle Mg++ content was 36.4 +/- 3.1 mmol/kg dry weight in SHR versus 48.6 +/- 3.7 mmol/kg dry weight in WKY (P < .001). In striated heart muscle cell Mg++ concentrations, there was no significant difference in SHR and WKY (79.9 +/- 5.6 versus 80.3 +/- 5.9 mmol/ kg dry weight). In conclusion, the present study revealed that genetic hypertension in the spontaneously hypertensive rat is accompanied by significantly decreased intracellular Mg++ concentrations in vascular smooth muscle cells. In striated heart muscle cells, Mg++ content was not significantly different in SHR and WKY. Mg++ handling is different in vascular smooth muscle and striated heart muscle cells in WKY and SHR (P < .01).

Animals↗
PubMed2000

Alterations of plasma calcium and intracellular and membrane calcium in erythrocytes of patients with pre-eclampsia.

BACKGROUND: Changes in plasma and intracellular calcium levels have been suggested in the pathogenesis of pre-eclampsia, however, membrane calcium content has not been studied so far. We compared intracellular and membrane calcium concentrations in erythrocytes of women with pre-eclampsia, healthy pregnant woman and controls to determine a possible alteration of membrane calcium in pre-eclampsia. SUBJECTS AND METHODS: Eighteen untreated, healthy pregnant woman and 16 pregnant nulliparous women with manifest pre-eclampsia were included, 25 healthy, age-matched woman served as controls. Atomic absorption spectroscopy was used for measurement of intracellular and membrane calcium content in erythrocytes and plasmalemmal preparations. RESULTS: Plasma Ca++ concentrations were significantly lower in pre-eclamptic women (1.96 +/- 0.15 mmol/l, P < 0.01, mean +/- s.e.m.) compared to healthy controls (2.43 +/- 0.14 mmol/l) or women with uncomplicated pregnancies (2.20 +/- 0.10 mmol/l). Intracellular Ca++ concentrations were not different between groups, however, membrane Ca++ content was significantly increased in the pre-eclamptic patients (1.23 +/- 0.36 micromol/g membrane protein, P < 0.01) compared to control subjects (0.83 +/- 0.16 micromol/g) and healthy pregnant women (0.77 +/- 0.13 micromol/g). CONCLUSION: Membrane calcium content is significantly increased in pre-eclamptic women despite low plasma Ca++ concentrations. This finding suggests an altered membrane ion transport and may be of importance for the pathogenesis of pre-eclampsia.

Adult↗
PubMed2000

Effects of bicarbonate- and lactate-buffered replacement fluids on cardiovascular outcome in CVVH patients.

BACKGROUND: Bicarbonate-buffered replacement fluid (RF-bic) in continuous venovenous hemofiltration (CVVH) may be superior to lactate-buffered replacement fluid (RF-lac) in acute renal failure. In an open, randomized, multicenter study, we investigated the effects of RF-bic and RF-lac on cardiovascular outcome in patients requiring CVVH following acute renal failure. METHODS: One hundred seventeen patients between the age of 18 and 80 years were randomized to CVVH either with RF-bic (N = 61) or RF-lac (N = 56). Patients were treated with CVVH for five days or until either renal function was restored or the patient was removed from the study. Data were analyzed on day 5 or according to the "last observation carried forward" (LOCF) option. Adverse events were classified according to the WHO-Adverse Reaction Terminology system. RESULTS: Blood lactate levels were significantly lower and blood bicarbonate levels were significantly higher in patients treated with RF-bic than in those treated with RF-lac (lactate, 17.4 +/- 8.5 vs. 28.7 +/- 10.4 mg/dL, P < 0.05; bicarbonate, 23.7 +/- 0.4 vs. 21.8 +/- 0.5 mmol/L, P < 0. 01). The number of hypotensive crises was lower in RF-bic-treated patients than in RF-lac-treated patients (RF-bic 14 out of 61 patients, RF-lac in 29 out of 56 patients; 0.26 +/- 0.09 vs. 0.60 +/- 0.31 episodes per 24 h, P < 0.05). Nine out of 61 patients (15%) treated with RF-bic and 21 out of 56 patients (38%) treated with RF-lac developed cardiovascular events during CVVH therapy (P < 0. 01). A multiple regression analysis showed that the occurrence of cardiovascular events was dependent on replacement fluid and previous cardiovascular disease and not on age or blood pressure. Patients with cardiac failure died less frequently in the group treated with RF-bic (7 out of 24, 29%) than in the group treated with RF-lac (12 out of 21, 57%, P = 0.058). In patients with septic shock, lethality was comparable in both groups (RF-bic, 10 out of 27, 37%; RF-lac, 7 out of 20, 35%, P = NS). CONCLUSIONS: The results show that the administration of RF-bic solution was superior in normalizing acidosis of patients without the risk of alkalosis. The data also suggest that the use of RF-bic during CVVH reduces cardiovascular events in critically ill patients with acute renal failure, particularly those with previous cardiovascular disease or heart failure.

APACHE↗