[Can environmental noise be injurious to health?].
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Biomedical subjects
Publications and source records attributed to H Ising.
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Magnesium concentrations in the blood plasma of patients with ventricular arrhythmias were found to be significantly lower than in controls, whereas the sodium and calcium concentrations of the erythrocytes were significantly higher than in the controls. Intensive magnesium therapy resulted in an increase of the plasma magnesium concentration and in significant changes of Na, K, Ca and Mg in the erythrocytes. By means of long-term ECG recordings, it was shown that the therapy may result in a quantitative decrease of the ventricular arrhythmias.
Rats maintained for 12 weeks on diets moderately or more severely deficient in magnesium showed significant elevations in arterial blood pressure compared to control animals. Examination of the mesenteric microcirculation in situ revealed that dietary magnesium deficiency resulted in reduced capillary, postcapillary, and venular blood flow concomitant with reduced terminal arteriolar, precapillary sphincter, and venular lumen sizes. The greater the degree of dietary magnesium deficiency the greater the reductions in microvascular lumen sizes. These findings may provide a rationale for the etiology, as well as treatment, of some forms of hypertensive vascular disease.
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Noise-induced hearing loss (NIHL) is significantly greater in rats fed a magnesium-deficient diet than in rats on a magnesium-rich diet. The hearing loss was found to be negatively correlated with the magnesium concentration of the perilymph. It is suggested that also in man, the magnesium concentration in the perilymph may be of importance in determining susceptibility to NIHL.
Mg-deficient guinea pigs developed significantly increased hearing loss during 4 weeks of noise exposure [95 dB(A)] as compared to animals fed a Mg-rich diet. The hearing loss was negatively correlated to the Mg content of the perilymph (r = -0.86). Besides this auditory effect, there was a decrease of intracellular Mg and an increase of collagen in the myocardium, both of which were correlated to the hearing loss and caused by Mg deficiency and noise stress.
Pregnant rats an mice received a magnesium (Mg)-deficient diet with different Mg contents from 40 t 360 ppm. The control received 2,000 ppm. At the end of gestation, the Mg concentration in the maternal serum was found to have decreased by up to 0.3 mmole/liter, depending on the Mg content of the food. Mg-dose-dependent embryotoxic effects (resorptions, retardation, disturbed bone development, and skeletal malformations) were observed only below a threshold value of 0.7 mmole/liter of the maternal serum Mg concentration. Noise stress in rats, in addition to a mild Mg deficiency (360 ppm Mg), which by itself had no effects, increased the rate of resorptions only.
The present study investigated the distribution of HLA-antigens and Bf alleles in a group of 21 patients suffering from biopsy proven Idiopathic Membranous Nephropathy (IMN). A statistically significant increase of HLA-DR3 (76.2%) was detected in the patient group as well as an increase of MT-2 (86%), which is a new supertypic specificity defined within the 8th International Histocompatibility Workshop 1980. No association between BfF1 and IMN can be deduced from this study. Only the common Bf alleles (BfFF, BfFS, BfSS) were found in the patient group presented here. Also the previously reported association between HLA-B18 and IMN was not corroborated by this study. Not a single IMN-patient typed positive for HLA-B18. Thus the presence of two different HLA-DR-Bf-B linkage groups (HLA-DR3/BfF1/HLA-B18 and HLA-DR3/Bf; all alleles/HLA-B8) may point to at least two different immunological mechanisms underlying IMN.
A feedback mechanism between noise stress and Mg decrease is postulated. The two sides of the interaction between noise stress as a model of general stress and cellular Mg decrease with possible Ca increase are demonstrated in laboratory and field studies with rats and human test persons.
In 57 test persons having worked 1 day under traffic noise (Leq = 85 dB(A) and 1 day without noise (Leq < 50 dB(A), blood pressure and pulse frequency were measured at 1 h intervals and total urine was collected during working hours. Additionally, blood was sampled at the end of each working day. Psychological parameters were assessed by means of questionnaires. Statistically significant reactions to noise were found in the following fields: 1. Ergnomics--decrease of working quality; 2. Psychology--increase of psychical tension; 3. Blood circulation--increase of blood pressure and pulse frequency; 4. Biochemistry--increase of epinephrine, cAMP, urine and serum Mg, protein, cholesterol plus decrease of erythrocyte Na, and renin. Hypothetical mechanisms of the action of traffic noise are discussed.
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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.
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.
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.
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.
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.
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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).