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Biomedical subjects

H Ising

Publications and source records attributed to H Ising.

At least 73 records · Page 4Linked to original sources
PubMed1978

Thiouracil-induced myocardial fibrosis.

Rabbits were fed with thiouracil for 8 months. Subsequently their hearts were examined electron microscopically as well as biochemically for collagen and hexosamine content. Chronic treatment with thiouracil induced an increase in interstitial connective tissue collagen and hexosamine without visible necrosis. As seen by electron microscopy, the increase in collagen content might have been caused by stimulation of the fibrocytes. Furthermore, the heart muscle cells showed deep indentations and bulges of the cell membrane and an enlargement of the T-system.

Animals↗
PubMed1978

[Electrolyte and collagen content of rat heart in chronic Mg-deficiency and stress (author's transl)].

In chronic Mg-deficiency, there is a decrease in the content of Mg and K+ in the heart muscle. The contents of Ca, Na+ and hydroxyproline increase. There is also an increased urinary excretion of adrenaline and especially noradrenaline. With simultaneous noise stress, these changes are even greater. The magnitude of the changes increases with the degree of Mg-deficiency. The changes in the contents of Na+, K+, Ca, Mg and hydroxyproline correlate with the excretion of noradrenaline. The increase in the collagen content can be verified by electron microscopy, and it is due to a stimulation of the fibrocytes.

Calcium↗
PubMed1976

[Increase of connective tissue in rat hearts under exposure to noise and with magnesium deficiency (author's transl)].

Only a small amount of noise caused, combined with a nutritional Mg deficiency, a significant increase of collagen in the myocard of rats. While Mg deficiency or noise each for its own had no effect, the combination of both had a noxious effect. The results of these experiments give a hint to a correlation between collagen-increase in the myocard and an increase of urinal Catecholamine during the same time.

Animals↗
PubMed1975

[The development of intramyocardial haemorrhages or fluidaccumulation in the extracellular space].

Isolated rat hearts according to Langendorff and rabbit hearts after orthostatic collapse were studied under the light and electron microscope. The light-micrographs were also quantitatively analysed. Changes in the vessels are noticeable, especially those in the sinusoid's. Vessel ruptures occur, also isolated endothelial ruptures with intact basement membranes and perfusion fluid enters the extracellular space. Numerous 0.06-01 mu large vesicles appear in the cytoplasma of the endothelial cells. A large number of vesiculation processes can be demonstrated along the cell membrane. The extracellular space is strongly-dilated. Changes in the colloid osmotic pressure and a rise in perfusion pressure have no clearly demonstrable influence on the extent of extravasation under the experimental conditions. The mechanism possible inducing such vessel changes is discussed.

Animals↗
PubMed1975

[Coronaro-myocardial interplay determining the instantaneous mean ventricular shape (author's transl)].

A working hypothesis on the mechanism of diastolic chamber expansion based on functional anatomy and physiology is developed. It should be a major determinant of the momentary average chamber width. The sum of all intramyocardial fluid-filled spaces and the myocardium itself are considered in the working hypothesis as the hydraulic medium of a process which can be summarised under the term "cavernous body mechanism". The most important factor of this hydraulic system should represent the intramural fluid volume (hydraulic medium) and the contractile-elastic tension development in the transmural direction of the chamber wall. Morphological analysis of myocardial structure shows that an endoepicardial direction of force in the myocardial net can be recognised. The "motor" of circular fibres of the middle layer is surrounded by the spiral course of the fibres of the inner and outer layers of the chamber wall (uvula mechanism). It is interwoven by very dense bifurcating myocardial fibres (structural principle of the tongue). By these means, the width of the chamber cone is influenced decisively by an active decrease in wall thickness. The coronary perfusion pressure is thought to have a chamber dilating influence in the sense of a "cavernous body mechanism". The hypothesis presented helps us to understand pathological chamber dilation secondary to transmural myocardial fibrosis. Such a narrow functional coronary-myocardial interaction gives the myocardium two functions; besides haemodynamic pumping, the cardial muscle must function as an internal antagonist to favour diastolic chamber dilation.

Animals↗
PubMed1975

Light- and electron microscopic investigations of pulmonary tissue after high-frequency positive-pressure ventilation (HFPPV).

Narcotisized dogs were artificially ventilated for periods of two to five hours with HFPPV. During this time the blood gases, pH and bases were controlled. In spite of sufficient oxygenation and CO2-elimination, a metabolic acidosis developed which could not be fully compensated by the addition of buffer solutions. In light and electron microscopy these lungs did not differ significantly from control lungs. Haemorrhages or atelectases were never observed. Type I cells as well as Type II cells in the alveoli are unchanged, i.e. the Type II cells were not depleted but contained numerous typical lamellar bodies with a diameter of 0.4-1 mu. The blood gas barrier was not widened and was ca. 3000 A wide. The alveolar surface was coated by an often fragmented electron-dense film (monolayer of the surfactant).

Acid-Base Equilibrium↗
PubMedDate not supplied

Oral magnesium intake reduces permanent hearing loss induced by noise exposure.

INTRODUCTION: Following animal experiments where correlations were observed between serum magnesium level and noise-induced permanent hearing threshold shifts (NIPTS), we tested the prophylactic effect of magnesium in human subjects exposed to hazardous noise. METHODS: Subjects were 300 young, healthy, and normal-hearing recruits who underwent 2 months of basic military training. This training necessarily included repeated exposures to high levels of impulse noises while using ear plugs. During this placebo-controlled, double-blind study, each subject received daily an additional drink containing either 6.7 mmol (167 mg) magnesium aspartate or a similar quantity of placebo (Na-aspartate). RESULTS: NIPTS was significantly more frequent and more severe in the placebo group than in the magnesium group, especially in bilateral damages. NIPTS was negatively correlated to the magnesium content of blood red cells but especially to the magnesium mononuclear cells. Long-term additional intake of a small dose of oral magnesium was not accompanied by any notable side effect. CONCLUSION: This study may introduce a significant natural agent for the reduction of hearing damages in noise-exposed population.

Administration, Oral↗
PubMedDate not supplied

Traffic noise and cardiovascular risk. The Caerphilly study, first phase. Outdoor noise levels and risk factors.

As part of the Caerphilly study, traffic noise exposure and risk for ischemic heart disease (IHD) were studied in a sample of 2,512 men aged 45-59 yr. The traffic noise emission level ranged between Leq = 51-70 dB(A) (6-22 hr, 10 min). No association was found between traffic noise and prevalence of IHD. Associations were found between noise and potential IHD risk factors including systolic blood pressure, oestradiol, total cholesterol, plasma viscosity, antithrombin III (increases), cortisol, and platelet count (decrease). Not all results supported the hypothesis that traffic noise increases the risk for IHD. The possibility of confounding cannot be excluded, although an extensive range of potential confounding variables were included in the analysis.

Automobiles↗
PubMedDate not supplied

Traffic noise and cardiovascular risk: the Speedwell study, first phase. Outdoor noise levels and risk factors.

As part of the Speedwell study, traffic noise exposure and risk factors for ischemic heart disease were studied in a sample of 2,348 men whose ages ranged from 45 to 63 y. The road traffic noise emission level, Leq, ranged between 51 and 70 dB(A) (6-22 h, 10-m distance). Significant associations were found between noise and potential ischemic heart disease risk factors, including total triglycerides, platelet count, plasma viscosity, glucose (increases), and systolic and diastolic blood pressure (decreases). Not all results support the hypothesis that traffic noise increases ischemic heart disease risk. The results were controlled for a number of potential confounding factors.

Automobiles↗