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H Turto

Publications and source records attributed to H Turto.

At least 37 records · Page 2Linked to original sources
PubMed1979

Increased collagen prolyl hydroxylase activity in the aortic wall of rabbits exposed to chronic hypoxia.

The activity of collagen prolyl hydroxylase in aortic wall was studied in rabbits exposed to chronic 10% ambient oxygen tension for 30 days. Prolyl hydroxylase in rabbit aorta was shown to be similar to the enzyme from other sources in that it required molecular oxygen, alpha-ketoglutarate, ferrous iron and ascorbate for its activity. The activity of prolyl hydroxylase was increased to 180% of controls in the intima-media samples from rabbits exposed to hypoxia. No atherosclerotic lesions could be seen in arteries of animals kept in chronic hypoxia. If the arteries of rabbits were injured with a single mechanical dilatation, the activity of prolyl hydroxylase increased more than 2-fold, as reported previously. The exposure of these animals to chronic hypoxia further elevated the prolyl hydroxylase activity.

Animals↗
PubMed1978

The excretion of urinary N-acetyl-beta-glucosaminidase and beta-glucuronidase as a sign of impending rejection of kidney transplants.

An evaluation was made of the assay of two urinary lysosomal enzymes, N-acetyl-beta-glucosaminidase and beta-glucuronidase, in the diagnosis of impending rejection of renal transplant. The output of enzymes was measured in 34 cadaver transplant recipients, 17 of whom underwent rejection episodes. The enzyme output during the 4 days preceding the definitive diagnosis was compared with the output during a non-rejection period. The mean excretion of both enzymes increased during the period before rejection. The best distinction for diagnostic purposes was obtained by comparing the pre-rejection values with baseline values separately in each case.

Acetylglucosaminidase↗
PubMed1977

Collagen metabolism in experimental cardiac hypertrophy in the rat and the effect of digitoxin treatment.

It is generally agreed that cardiac hypertrophy is accompanied by the hyperplasia of connective tissue cells. In the present work, collagen metabolism was studied in the heart of nondigitalised and digitalised rats after the constriction of the aorta. The activity of prolyl hydroxylase was maximally increased 2 days after the operation. The incorporation of proline into collagen hydroxyproline increased without any increase in the specific radioactivity of free intracellular proline, the peak labelling of collagen occurring at 4 days. Although the treatment of the rats with digitoxin prevented the development of cardiac hypertrophy and an increase in collagen labelling, an increase in the activity of prolyl hydroxylase was observed. The intracellular free proline pool and its specific radioactivity were significantly lower in digitalised rats as compared with non-digitalised rats. The results indicate that constriction of the aorta is accompanied by an activation of connective tissue cells leading to increased synthesis of collagen. However, digitoxin treatment can prevent the increase in collagen labelling, possibly by inhibiting the amino acid transport, but it is unable to remove the stimulus for hypertrophy.

Aminoisobutyric Acids↗
PubMed1977

Experimental cardiac hypertrophy and the synthesis of poly (A) containing RNA and of myocardial proteins in the rat: the effect of digitoxin treatment.

The synthesis of poly(A) containing RNA was increased in heart of non-digitalized and digitalized rats after aortic constriction, the increase being of the same degree as that of the RNA lacking this sequence. No differences were found, either in the absence or presence of polyuridylic acid, in the incorporation of radioactivity into protein by cardiac ribosomes isolated from animals treated differently. It may be concluded, that after the constriction of the aorta the synthesis of mRNA proceeds at a similar rate as that of the bulk RNA, and that the treatment of the animals with digitoxin does not abolish the stimulus for hypertrophy.

Animals↗
PubMed1976

Heart volume and myocardial connective tissue during development and regression of thyroxine-induced cardiac hypertrophy in rats.

To determine whether development and regression of cardiac hypertrophy are accompanied by changes in heart volume and to learn whether a change in heart volume is associated with changes in the myocardial connective tissue, cardiac hypertrophy was induced in rats by administration of thyroxine. Rats were given L-thyroxine for 4 weeks. Heart volume was estimated radiologically in vivo at the start of the experiment and at 1- or 2-week intervals for 7 weeks. At each of these stages a number of rats were killed, their hearts were weighed and determinations were made of the myocardial contents of DNA, of collagen measured as hydroxyproline, and of glycosaminoglycans, measured as uronic acid. After thyroxine treatment the ratio of left heart ventricle weight to body weight and of heart volume to body weight rose significantly. The increase in heart weight was greater than the increase in heart volume. At the same time, there was a significant decrease in the concentration of hydroxyproline. After discontinuation of thyroxine treatment heart volume, heart weight and the concentration of myocardial collagen returned to normal within 2 weeks. However, the total amount of myocardial collagen was still less than normal at 2 weeks. The results suggest that the decrease in the amount of myocardial collagen associated with thyroxine-induced cardiac hypertrophy--because it results in a weakening of the supporting properties of the myocardial connective tissue framework--might contribute to a slight increase in in vivo heart volume.

Animals↗
PubMed1976

Collagen metabolism of the rat heart during experimental cardiac hypertrophy and the effect of digitoxin treatment.

In cardiac hypertrophy the total content of collagen is increased in the myocardium. The first indicator of the increased activity of connective tissue cells is an increase in the activity of prolyl hydroxylase of the myocardium. This is later followed by an increase in the rate of collagen synthesis and subsequently collagen is accumulated in the myocardium. Digitoxin treatment prevents the hypertrophy and the accumulation of proteins to the myocardium. This effect of digitoxin is, at least partly, explained by a decreased transport of amino acids into the cells, The results emphasize the importance of amino acid supply to the process of hypertrophy.

Animals↗
PubMed1975

Prostaglandins.

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Arthritis↗