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Biomedical subjects

K H Rahn

Publications and source records attributed to K H Rahn.

At least 37 records · Page 2Linked to original sources
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

[Classic case of benign recurrent intrahepatic cholestasis (Summerskill-Halshe-Tygstrup syndrome)].

BACKGROUND: The benign recurrent intrahepatic cholestasis is an autosomal recessively inherited liver disease. The gene was mapped to a region on chromosome 18q21-22. Because of its rareness this disease is first considered in the differential diagnosis of cholestasis after many years of extensive investigations. CASE REPORT: We report about a 17-year-old patient, who suffered from intermittent attacks of cholestatic jaundice and pruritus. Clinical course, laboratory data and invasive investigations led to the diagnosis of a typical case of benign recurrent intrahepatic cholestasis (Summerskill-Walshe-Tygstrup syndrome). CONCLUSION: This disease is remarkable for a discrepancy between a rise of serum bile acids at the onset of each attack and a later rise of bilirubin. Typically high bilirubin levels are noted, and bilirubin can even reach more than 50 mg/dl. The serum alkaline phosphatase is increased, too, whereas the values for the transaminases and gamma GT are normal or only slightly elevated. Histological studies reveal a cholestasis, bile plugs in the bile canaliculi, a perilobular fibrosis and inflammatory infiltrations of the periportal zones. Differential diagnosis includes an abundance of diseases with cholestasis. Treatment is difficult, purely symptomatic and often without marked effect. Nevertheless prognosis is good, histories of about 50 years were without evidence of progression to cirrhosis.

Adolescent↗
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

Effect of homocysteine on carotid intima-media thickness after renal transplantation.

The common carotid intima-media thickness (CC IMT) is a strong predictor for cardiovascular disease in patients with end-stage renal failure. However, little is known about possible associations between potential cardiovascular risk factors such as serum total homocysteine concentrations (tHcy) and the CC IMT. Thus, we investigated (a) the course of tHcy levels after renal transplantation (RTX) and (b) the relationship between CC IMT and tHcy in 53 renal allograft recipients with chronic renal failure before transplantation and 3, 6, and 12 months after transplantation. Exclusion criteria were volume overload, symptomatic coronary artery disease, symptomatic cerebrovascular disease, peripheral artery disease, heart failure, valvular heart disease, diabetes mellitus, severe hypercholesterolemia, and blood pressure above 159/89 mmHg at the time of the investigation. In all renal allograft recipients, a carotid high-resolution B-mode ultrasound measurement of the CC IMT was performed. Eighteen patients had normal ( < 20 micromol/L) pre-transplant (U0) tHcy, 25 had moderately elevated (20-40 micromol/L) pre-transplant (U0) tHcy, and 10 had severely elevated (> 40 micromol/L) pre-transplant (U0) tHcy. After 12 months of follow-up time (U12), no statistically significant differences concerning the tHcy levels could be detected between the groups (average serum tHcy 16.4 micromol/L +/- 1.1 micromol/L). The CC IMT did not differ significantly between the three tHcy groups at any time within the present follow-up. This was also true for the 'wall-to-lumen ratio'. A multiple forward stepwise regression analysis showed that the reduction of the CC IMT was positively correlated with gender (p < 0.01), glucose levels at U12 (p < 0.05; r2 = 0.96), systolic arterial blood pressure at U12 (p < 0.05; r2 = 0.97), and with the intact parathyroid hormone levels at U0 (p < 0.01; r2 = 0.98). In conclusion, (a) tHcy decreases significantly after RTX, but (b) does not influence the CC IMT thickness independently.

Adult↗
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

In vivo effects of diadenosine polyphosphates on rat renal microcirculation.

BACKGROUND: Diadenosine polyphosphates (APXA) are vasoactive nucleotides that elicit effects via purinoceptors. Recent data suggest differential effects of APXA on kidney vasculature. METHODS: The in vivo effects of AP3A, AP5A, and adenosine on renal microvessels and the role of purinoceptors were investigated by the application of agonists to the hydronephrotic rat kidney and preincubation with respective antagonists. RESULTS: The addition of the agonists (10-7 mol/L up to 10-4 mol/L) resulted in a concentration-dependent transient vasoconstriction [interlobular artery (ILOB): adenosine 30 +/- 7%, N = 7, AP3A 35 +/- 10%, N = 5; AP5A 66 +/- 19%, N = 5; 10-5 mol/L each] lasting up to one minute, followed by a concentration-dependent vasodilation (ILOB: adenosine 10 +/- 3%, N = 6; AP3A 19 +/- 4%, N = 5; AP5A 12 +/- 5%, N = 6; 10-5 mol/L each). In ILOB and in the afferent arteriole (AFF), the constrictory effects of AP5A were more pronounced than those of AP3A and adenosine. In the efferent arteriole (EFF), vascular tone was only slightly affected by all agonists. The dilatory potency was comparable for all agonists in ILOB and EFF. No significant vasodilation occurred in AFF. The application of the selective A1 receptor antagonist DPCPX (10-5 mol/L) completely abolished the adenosine-induced vasoconstriction, whereas the A2 receptor antagonist DMPX and the P2 purinoceptor antagonists PPADS and A3P5P (all 10-5 mol/L) did not affect adenosine-induced constriction. The AP3A-induced constriction was abolished by DPCPX and was partially inhibited by PPADS. The constriction induced by AP5A was less sensitive to DPCPX but more sensitive to PPADS. In ILOB and EFF, DMPX or A3P5P abolished dilation after the addition of the agonists. The dilation after AP5A was not significantly reduced. In AFF, no significant dilation was observed with these agonists alone, but it was clearly visible in the presence of DPCPX or PPADS. CONCLUSIONS: APXA evoke transient constrictions in vessels of the hydronephrotic rat kidney, which are mediated by A1 and P2 purinoceptors. The length of the phosphate chain determines the degree of vasoconstriction and the extent to which the substances exert effects on the P2 purinoceptor subtypes. ILOB and AFF are more potently affected by APXA than EFF. Afferent vasodilation is partially overridden by sustained vasoconstriction.

Adenosine↗
PubMed2000

Vessel wall alterations in patients with renal failure.

Cardiovascular complications are a major cause of morbidity and mortality in patients with renal failure. Death due to myocardial infarction and to stroke is more frequent in hemodialysis patients than in the total population. These cardiovascular diseases are mainly the consequence of atherosclerosis and cause decreased life expectancy in patients with renal failure. Ultrasound techniques now make it possible to measure atherosclerotic lesions in big and medium-sized arteries. Thickening of the intima-media-complex is an early sign of atherosclerosis in these vessels. It reduces the distensibility of the arteries during systole. The distensibility of big and medium-sized arteries can be determined using ultrasound-doppler-techniques. In our studies, the intima-media-thickness of the carotid artery was significantly (p< 0.01) increased in patients with chronic renal failure (1.32+/-0.49 mm, n=28) as compared with aged-matched healthy control subjects (0.75 +/- 0.20, n= 29). The distensibility coefficient was higher (p< 0.05) in healthy controls (26 +/- 1.8 10(-3)/kPa, n= 12) than in patients with renal insufficiency (19 +/- 1.7 10(-3)/kPa, n = 12). This demonstrates increased stiffness of the vessel wall resulting in loss of Windkessel function and increased work load of the heart.

Arteries↗
PubMed2000

Measurement of skeletal status after renal transplantation by quantitative ultrasound.

BACKGROUND: Osteoporosis remains a major problem following kidney transplantation. Radiographic measures of bone mass are of limited predictive value after transplantation and are complicated by preexisting renal osteopathy. Quantitative ultrasound (QUS) is a new and non-invasive method to assess skeletal status, however, no data exist on ultrasonic bone parameter after kidney transplantation. We evaluated the potential use of this novel method in renal allograft recipients and studied the accuracy compared to normal controls. METHOD: Thirty patients (NTP, age 47.5 +/- 13.0 years) were studied 4.8 +/- 3.2 years after transplantation. Twenty-five healthy control persons (CON) were matched for age and sex. The left and right os calcis were studied by QUS and speed of sound (SOS) and broadband ultrasound attenuation (BUA) were measured. Bone stiffness (BS) was calculated from these parameters and corrected for age (CBS). Differences between right and left os calcis were compared to CON to assess the side variability. RESULTS: Mean +/- SD BS was 75 +/- 22% compared to young adults, age-corrected CBS was decreased in NTP with 86 +/- 25% of normal, indicating a two-fold increased risk of fracture. SOS was 1525 +/- 47.7 m/s, BUA 105 +/- 22 dB/MHz. Mean difference between right and left os calcis was significantly higher in NTP than in CON (7.2 +/- 7.1% vs. 2.1 +/- 2.1%, p < 0.01). Limits of agreement of the measurements (MW of differences +/- 2 SD) according to a Bland-Altmann-type statistic were -16.9% and 20.7%. There was no correlation between CBS and age, cumulative steroid dose, parathyroid hormone concentrations or time after transplantation. CONCLUSION: Our data show altered bone structure expressed by low bone stiffness values measured by quantitative ultrasound in kidney transplant patients. However, because of relatively high inter-feet variance of QUS results we suggest measurement of both ossa calcis to minimize measurement error after transplantation.

Biomechanical Phenomena↗
PubMed2000

Influence of purinoceptor antagonism on diadenosine pentaphosphate-induced hypotension in anesthetized rats.

Diadenosine polyphosphates (ApnA; n = 3-6) are potent vasoactive agents in isolated vessels. Information on effects of ApnA in vivo is still limited despite the fact that these compounds are starting to be used in humans. This study was designed to compare the effects of ApnA and their possible metabolites on blood pressure in vivo and to functionally identify purinoceptors involved in their action. All four ApnA and their degradation products induced a sustained drop of mean arterial blood pressure during i.v. infusion, which was fully reversible. The rank order of potency was Ap4A > or = Ap6A > Ap5A = Ap3A = ATP = ADP > AMP > or = adenosine, suggesting that the hypotensive effect is predominantly evoked by the original dinucleotides and not by their degradation products. The hypotensive effect of Ap5A was reduced by the P2X and P2Y(1) purinoceptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid, the A(1) purinoceptor antagonist 8-cyclopentyl-1,3-dipropylxanthine, and the A(2) purinoceptor antagonist 3, 7-dimethyl-1-propargylxanthine. The hypertensive effect by the prototype P2X receptor agonist alphabeta-methylene ATP was inhibited by pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid, too. Purinoceptor antagonists reduced the maximal effects of the agonists indicating a noncompetitive inhibition. In summary, the reported vasocontractile effect of ApnA seems to be limited to isolated preparations under resting tone conditions; however, the systemic cardiovascular effects of all four ApnA are hypotensive, also making them candidates for blood pressure reduction in humans. These effects are fast in onset and easily reversible. Activation of different purinoceptors in the vasculature (most probably P2Y(1) and A(2) receptors) contributes to the Ap5A-induced decrease of mean arterial blood pressure.

Animals↗