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Biomedical subjects

J I Nielsen

Publications and source records attributed to J I Nielsen.

12 recordsLinked to original sources
PubMed1995

[Renal function during treatment with angiotensin converting enzyme inhibitors].

The use of ACE-inhibitors has increased greatly during the last years. They were first used in treating hypertension, but nowadays cardiac diseases, mainly cardiac failure, are common indications. This means that the drugs are used in the treatment of more elderly patients who often have generalised atherosclerosis. This means that the patients must be controlled more often after initiation of treatment, especially concerning kidney function, since treatment with ACE-inhibitors can cause pronounced changes in renal haemodynamics and kidney function. This review focuses on the effects of ACE-inhibitors on renal haemodynamics and kidney function, which may be positive, with preservation of kidney function in diabetic and other chronic nephropathy, or negative, for example in cases with atherosclerotic stenosis of large or small renal arteries. It is concluded, that in cases of diabetic nephropathy an ACE-inhibitor is the "drug of choice" for treatment of hypertension. Furthermore the ACE-inhibitors seem to reduce the rate of deterioration of renal function and proteinuria in other kidney diseases. It is emphasized, that during treatment with ACE-inhibitors kidney function must be controlled before and following one to two weeks of treatment, if the dose is changed and in all cases following two to three months of treatment. Special attention should be given to patients with atherosclerotic manifestations e.g. angina.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

[Renal function during treatment of chronic renal failure with angiotensin converting enzyme inhibitors].

The effect on kidney function fo treatment of cardiac failure with ACE-inhibitors was examined retrospectively in a material of 87 consecutive patients. Furthermore, it was evaluated whether concomitant treatment with diuretics or existing generalised atherosclerosis as indicated by ongoing treatment with nitrates could be a risk factor concerning reduction of kidney function. In 11.9% of the patients an increase in S-creatinine of > 30% was observed during the first weeks of treatment. It was only necessary to stop treatment in two of these patients. In the remainder S-creatinine decreased again during ongoing treatment. In another 10.7% of patients an increase of 20-30% in S-creatinine was observed. Seventy-two point six percent of the patients had unchanged kidney function during treatment with an ACE-inhibitor. Ongoing treatment with diuretics did not seem to be a risk factor for developing reduced kidney function, whereas significantly more patients on treatment with nitrates, indicating generalised atherosclerosis, developed reduced kidney function during treatment with ACE-inhibitors. It is recommended to control kidney function before, one to two weeks and two to three months following initiation of treatment with ACE-inhibitors and to pay special attention to patients with generalised atherosclerosis.

Adult↗
PubMed1994

Characterization of the binding between tissue factor pathway inhibitor and glycosaminoglycans.

Tissue Factor Pathway Inhibitor (TFPI) is a heparin binding protein and injection of heparin causes a release of TFPI to plasma. In order to understand the binding between TFPI and heparin in more detail we have in this study looked into some of the heparin characteristics and their importance for the TFPI-heparin interaction. We have developed an assay based on the use of heparin-Sepharose micro columns in order to compare small quantities of heparin fractions as well as different glycosaminoglycans on a weight basis for their TFPI binding. In this assay a glycosaminoglycan in solution compete with heparin-Sepharose for TFPI binding. Size fractionated heparin was analyzed for binding to TFPI, and a clear dependency on the molecular weight was observed. The highest TFPI binding capacity was found for fractions with a molecular weight above 10,000 Da, while no binding was measured below 2,000 Da. No difference in TFPI binding appeared after fractionation of heparin according to its affinity towards antithrombin, thus indicating that TFPI binding does not require the specific antithrombin binding site. A heparin fraction of 10,000 Da was fractionated on a mono Q column, resulting in four fractions with different charge densities. The charge density turned out to be a very important parameter for the binding of TFPI. A number of different glycosaminoglycans were tested and the following order of TFPI affinity was found: heparin >> dermatan sulphate > heparan sulphate > chondroitin sulphate C. No binding was observed for chondroitin sulphate A or hyaluronic acid.

Animals↗
PubMed1991

Development and validation of a size exclusion chromatography method for determination of molecular masses and molecular mass distribution in low molecular weight heparin.

A precise and rugged high performance size exclusion chromatography (HPSEC) method for determination of peak maximum molecular mass (Mp), weight average molecular mass (Mw), number average molecular mass (Mn), and molecular mass distribution (MMD) in Low Molecular Weight heparin (LMW heparin) has been developed and validated on two Ultrahydrogel 250 (ID 7, 8 mm, length 30 cm) columns in series at three laboratories using different equipment. The calibration is based on four local laboratory heparin standards with relatively narrow molecular mass distribution and Mp covering the range from 3,000 to 17,000 Da. The calibration curve describing the logarithm of the molecular mass versus retention time is linear in the range 3,000 to 17,000 Da. The precision (relative standard deviation) within-run and between-run is better than 2%. The between-laboratory variation is below 5%, 3% and 8% for Mp, Mw and Mn, respectively. This method is reproducible, rugged, and fast and is suited for the determination of average molecular masses and molecular mass distribution of LMW heparins on a routine basis.

Calibration↗
PubMed1986

A comparison of the antithrombotic and haemorrhagic effects of a low molecular weight heparin (LHN-1) and conventional heparin.

The antithrombotic effects after intravenous administration of a low molecular weight heparin (LHN-1) and conventional heparin were compared in a rabbit model of experimental thrombosis, where thrombus formation was induced by a combination of endothelial damage and stasis. Both compounds were able to prevent thrombosis completely. However, LHN-1 was significantly less potent than conventional heparin, the ratio between doses with the same antithrombotic effect being 2.4:1 on a weight basis. Bleeding times after administration of LHN-1 and conventional heparin were determined by tail transsection in anaesthetized rats and by template bleeding in the ear of conscious pigs. Given intravenously at a dose ratio of 2.4:1 (w/w), LHN-1 affected APTT less than conventional heparin, whereas the effects on haemostasis were not significantly different. In conclusion, it was found that after intravenous administration LHN-1 prevented experimental thrombosis as effectively as conventional heparin. However, the correlation between antithrombotic and haemorrhagic effects of LHN-1 was the same as that of conventional heparin. The corresponding relation in man remains to be determined.

Animals↗