Search PubMed⌕ Search

Biomedical subjects

K Rasmussen

Publications and source records attributed to K Rasmussen.

At least 379 records · Page 21Linked to original sources
PubMed1982

Haemodynamic effects of alpha-receptor blockade during acute administration and chronic treatment.

Acute administration of relatively large doses of the postsynaptic alpha-adrenoceptor blocking agent prazosin results in a marked vasodilatation and blood-pressure reduction, often combined with tachycardia. Chronic administration results in a decrease in total peripheral resistance and blood pressure at rest and during exercise. Cardiac output is unchanged at rest but shows a slight increase during exercise. Peripheral blood flow is increased during chronic treatment. It is concluded that alpha-receptor antagonists may be able to normalize - completely or partly - the pathological haemodynamics of the hypertensive patient.

Adrenergic alpha-Antagonists↗
PubMed1982

Antiarrhythmic efficacy of amiodarone in recurrent ventricular tachycardia evaluated by multiple electrophysiological and ambulatory ECG recordings.

Thirty-three patients with recurrent drug-refractory ventricular tachycardia were treated with oral amiodarone during an average period of 6.1 months. In-hospital monitoring for two weeks or more, electrophysiological tests and ambulatory ECG were used to evaluate the results. Twenty patients are still using the drug with complete control of the arrhythmia. Eleven have failed the drug, ten due to recurrence of documented ventricular tachycardia. Only three patients failed after the first month of therapy. Two patients died, one suddenly. The drug was discontinued in a further two patients due to side-effects. Other side-effects were tolerable or manageable by dose adjustments alone. Five patients showed evidence of inadequate arrhythmia control between days 15 and 32 of therapy but subsequently responded to the drug for 4-9 months, giving further support to the concept that in some patients at least 30 days of therapy is necessary for the full effect of the drug to appear. In 16 of the 20 patients tested by arrhythmia induction study while on the drug, ventricular tachycardia could still be induced. Seven (44%) of these eventually failed the drug. Arrhythmia recurred in one of those four in whom tachycardia could not be induced. Amiodarone is a valuable drug in the management of recurrent ventricular tachycardia, refractory to other antiarrhythmic drugs.

Adult↗
PubMed1982

The prevalence of chromosome abnormalities among mentally retarded persons in a geographically delimited area of Denmark.

A cytogenetic survey of an unselected group of mentally retarded persons in a geographically limited area was made in order to establish the frequency of chromosome abnormalities within this group. In the area there were 2,157 patients, both institutionalized and living at home. A chromosome analysis was performed in 1905 cases; 359 (18.8%) of these had a chromosome anomaly: 281 (14.7%) Down's syndrome, 45 (2.4%) autosomal anomaly other than Down's, and 33 (1.8%) sex chromosome anomaly. The frequency of chromosome aberrations in relation to the whole group was higher compared with similar surveys, which leads to the conclusion that the total number of mentally retarded persons living within a limited area is determined by many factors. This means that a comparison between frequencies of abnormal chromosomes in an unselected group of mentally retarded persons is only relevant when related to the whole population living in the investigation area.

Chromosome Aberrations↗
PubMed1982

C6-C10-dicarboxylic aciduria: investigations of a patient with riboflavin responsive multiple acyl-CoA dehydrogenation defects.

The abnormal metabolites-adipic, suberic, and sebacic acids-were detected in large amounts in the urine of a boy during a Reye's syndrome-like crisis. Substantial amounts of 5-OH-caproic acid, caproylglycine, glutaric acid, and 3-OH-butyric acid and moderately elevated amounts of ethylmalonic acid, methylsuccinic acid, 3-OH-isovaleric acid, and isovalerylglycine were also found. These metabolites were consistently present in urine samples collected in the boy's habitual condition after the attack. 1-[14C]-Palmitic acid was oxidized at a normal rate, whereas U-[14C]-Palmitic acid was oxidized at a reduced rate in cultured skin fibroblasts from the patient, thus indicating a defect at the level of medium- and/or short-chain fatty acid oxidation. Riboflavin medication (100 mg three times a day) significantly reduced the excreted amounts of pathologic metabolites, suggesting a flavineadeninedinucleotide-related acyl-CoA dehydrogenation defect as the cause of the disease. Carnitine in plasma was low in the patient (6 mumole/liter, controls 26-74 mumole/liter), suggesting carnitine deficiency as a secondary effect of the acyl-CoA dehydrogenation deficiency. The present patient, who presented with a Reye's syndrome-like attack, suffers from impaired dehydrogenation of acyl-CoA resulting in accumulation of acyl-CoA in the cells. Attacks with similar symptoms are seen in other acyl-CoA dehydrogenation deficiencies, such as glutaric aciduria types I and II, other types of C6-C10-dicarboxylic acidurias and isovaleric acidemia. Reduced flow through the acyl-CoA dehydrogenation steps may therefore be an ethiologic factor in Reye's syndrome. Several of the accumulated acyl-CoA's are toxic and may be responsible for some of the symptoms. The low carnitine level in plasma and the elevated esterified carnitine excretion in the present patient indicate that acyl-CoA accumulation may cause a functional carnitine deficiency by sequestration of carnitine as acyl-carnitines. As the inborn defect, systemic carnitine deficiency may exhibit symptoms like those of Reye's syndrome, it may be speculated whether functional carnitine deficiency in patients with accumulated acyl-CoA is another causal factor in the development of the symptoms during attacks.

Acyl Coenzyme A↗
PubMed1982

C6-C10-dicarboxylic aciduria: biochemical considerations in relation to diagnosis of beta-oxidation defects.

By means of gas chromatographic methods substantial amounts of the C6-C10-dicarboxylic acids, i.e. adipic, suberic and sebacic acids, have been found in the urine from children with unexplained attacks of lethargy and hypotonia, presumably related to episodes of fever and/or insufficient food intake. The course have once been fatal and is often characterized by severe hypoglycemia without ketonuria. Systematic gas chromatographic/mass spectrometric determinations of selected organic acid metabolites in the urine, together with enzymatic measurements in fibroblasts and clinical data from 4 patients of this category, have shown that the biochemical basis of this syndrome can be inborn errors of the beta-oxidation of fatty acids, localized to the medium-chain acyl-CoA dehydrogenation system. The biosynthesis of adipic, suberic and sebacic acids was studied using ketotic rats as the model, since ketosis in rats and humans is accompanied by excessive urinary excretion of adipic and suberic acids. A probable pathway for the production of the three dicarboxylic acids was found to be an initial omega-oxidation of the medium-chain C10-C14-monocarboxylic acids followed by beta-oxidation of the resulting medium-chain dicarboxylic acids. It is argued that the source of the omega-oxidizable monocarboxylic acids in ketosis most probably is the fat deposites, and it is speculated that the patients with beta-oxidation defects supplement this source with beta-oxidation intermediate medium-chain monocarboxylic acids, accumulated as a result of the defect. The ratio between the excreted amounts of adipic acid and sebacic acid in the urine from the patients with beta-oxidation defects is less than 50. This is in contrast to the ratio in urine from ketotic patients, where it is greater than 100. Adipic acid/sebacic acid ratio-measured by means of a gas chromatographic analysis-is therefore suggested as a tool in the diagnosis of dicarboxylic acidurias. Based on the clinical picture and the pattern of a series of organic acids in the urinary metabolic profile our four patients can be divided in two types of dicarboxylic aciduria. The two types have different therapeutic implications.

Adipates↗
PubMed1981

Comparative efficiency of quinidine and verapamil in the maintenance of sinus rhythm after DC conversion of atrial fibrillation. A controlled clinical trial.

Fifty-three patients with chronic atrial fibrillation participated in a randomized cross-over trial in order to compare the ability of two drug regimens to establish and maintain sinus rhythm. The patients were given orally either sustained release quinidine 0.4 g twice day or verapamil 80 mg three times a day. Thirty-one patients tried both regimens. Quinidine was found to have a greater ability to induce conversion to sinus rhythm by drug alone (p less than 0.05) and also a greater ability to maintain sinus rhythm after conversion (after 3 months p less than 0.05). There was, however, also a significantly larger proportion of patients on quinidine who were withdrawn from the study due to side effects and two patients on quinidine died outside hospital. The study indicate that quinidine is somewhat superior to verapamil both in the establishing and preserving of sinus rhythm in subjects who are able to tolerate the drug.

Arrhythmias, Cardiac↗
PubMed1980

Non-ketotic C6-C10-dicarboxylic aciduria: biochemical investigations of two cases.

Two boys, who are not related, with hypoglycemia and C6-C10-dicarboxylic aciduria were investigated. Besides substantial amounts of adipic, suberic and sebacic acids, the urinary metabolic profile of organic acids contained 5-OH-caproic acid and caproylglycine. During acute attacks the concentrations of adipic, suberic and sebacic acids were 300--530, 160--200 and 35--200 micrograms/mg creatinine, respectively, and the excretions of 5-OH-caproic acid and caproylglycine were 75--330 and 41--260 micrograms/mg creatinine, respectively. It is argued that the biosynthesis of adipic acid passes through an omega-oxidation, that the production of 5-OH-caproic acid is caused by an omega-1-oxidation, and that caproylglycine formation passes through a glycine-N-acylase catalysed conjugation of accumulated caproic acid in the patients. Suberic acid and sebacic acid are in the same way omega-oxidation products of accumulated caprylic acid and capric acid, respectively. From the excretion pattern presented it is hypothesized that the patients suffer from a defect in the dehydrogenation of fatty acids in the beta-oxidation pathway. The biological significance of the findings is discussed.

Adipates↗