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Biomedical subjects

H Rasmussen

Publications and source records attributed to H Rasmussen.

At least 217 records · Page 12Linked to original sources
PubMed1981

Hyperbaric oxygen toxicity and ribosome destruction in Escherichia coli K12.

The viability of resting suspensions of Escherichia coli K12 Ymel exposed to air plus 300 psi (1 psi = 6.895 kPa) oxygen (hyperbaric oxygen) decreased as an apparent first-order process after an initial period of constant viability. Control suspensions exposed to air plus 300 psi nitrogen (hyperbaric nitrogen) did not lose viability over the 96 h of the experiment. It was observed that a decrease in the refractive index of the cells preceded the loss of viability in hyperbaric oxygen. This finding together with electron micrographs, which showed extensive loss of ribosomal particles in bacteria incubated in hyperbaric oxygen, led us to suspect that ribosome injury or disassociation might be important in hyperbaric oxygen toxicity. In support of this we found that cellular RNA, labeled with [5-3H]uridine, was much more rapidly and more completely degraded in hyperbaric oxygen than in hyperbaric nitrogen. Furthermore, a far greater proportion of RNA was degraded than was DNA or protein. A direct assay for ribosome particles by sucrose gradient centrifugation showed that only 34% of the 70S ribosome particles was lost during the first 24 h in hyperbaric nitrogen whereas in hyperbaric oxygen 99.6% of the 70S particles was degraded during the same period. In hyperbaric oxygen the rate of viability loss between 24 and 72 h was equal to the rate of 70S ribosome degradation during the first 24 h. If 70S ribosome disassociation in hyperbaric oxygen continues at the same rate after first 24 h, then cumulative 70S ribosome disassociation or injury may lead to and provide an explanation for irreversible bacterial cell injury and the loss of viability.

Atmospheric Pressure↗
PubMed1981

Disordered breathing during sleep in hypothyroidism.

A 58-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 microIU/ml (normal, less than 12 microIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (VE/VCO2), and the ventilatory response to exercise (delta VE/delta VCO2) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38 to 33 mm Hg), and an increase in VE/VCO2 (17%), mouth occlusion pressure (50%), and AVE/VCO2 (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and VE/VCO2 despite a 23% increase in VE. Mouth occlusion pressure increased 37% but delta VE/delta VCO2 was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted completed relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.

Carbon Dioxide↗
PubMed1981

Calcium: its role in the mechanism of action of angiotensin II and potassium in aldosterone production.

The role of calcium in the angiotensin II- or potassium-mediated increase in aldosterone production was analyzed in isolated glomerulosa cells prepared from bovine adrenal glands. The response to potassium was highly dependent on the extracellular calcium concentration, and a maximal response was observed at 0.5 mM calcium. The response to angiotensin II was also a function of the calcium concentration between 0 and 0.5 mM Ca but was independent of calcium concentration above this value. The divalent ionophore A23187 also increased aldosterone production in a calcium-dependent manner. Methoxyverapamil blocked the stimulation of steroidogenesis due to angiotensin II and potassium. Calcium fluxes were studied during angiotensin II and potassium stimulation of aldosterone production. Incubation of zona glomerulosa cells with either angiotensin II or potassium at a concentration for maximal stimulation in the presence of radioactive calcium showed a significant increase in calcium uptake. Angiotensin II at a concentration for maximal stimulation increased the calcium uptake measured, using two techniques. Methoxyverapamil inhibited the angiotensin-mediated increase in calcium uptake without affecting the basal rate of calcium uptake. It is concluded that angiotensin II and potassium activate the cells of the glomerulosa by increasing the entry of calcium into the cell, which serves an important messenger function in the response of this cell to angiotensin II and potassium.

Adrenal Glands↗
PubMed1980

Effect of 1,25-dihydroxyvitamin D-3 on phosphate uptake into chick intestinal brush border membrane vesicles.

Brush border membrane vesicles prepared from the vitamin D-deficient chick duodenum take up phosphate and show an overshoot phenomenon in the presence of NaCl. Substitution of choline chloride for NaCl reduces phosphate uptake. Prior treatment of vitamin D-deficient chicks with 1,25-dihydroxy-vitamin D-3 increases the initial rate of Na+-dependent phosphate uptake into the brush border vesicles. This Na+-dependent phosphate uptake is a saturable process, exhibiting an apparent Km of 0.31 mM and a V of 385 pmol/mg per 15 s. Pretreatment of chicks with 1,25-dihydroxyvitamin D-3 leads to an increase in V (750 pmol/mg per 15 s) without significantly altering the apparent Km (0.33 mM). Addition of Ca2+, either in the presence or absence of the polyene antibiotic, filipin, or of calmodulin, has no effect on Na+-dependent phosphate uptake. Pretreatment of the vitamin D-deficient chick with a dose of cycloheximide sufficient to inhibit membrane protein synthesis blocks the 1,25-dihydroxyvitamin D-3-induced increase in alkaline phosphatase activity, but does not affect the stimulation of Na+-dependent phosphate uptake. From these data, it is concluded that 1,25-dihydroxyvitamin D-3 stimulates Na+-dependent phosphate transport at the brush border membrane of the enterocyte, that alkaline phosphatase is not directly involved in this process, and that this effect of 1,25-dihydroxyvitamin D-3 is independent of new protein synthesis.

Alkaline Phosphatase↗
PubMed1980

Selective stimulation of erythrocyte membrane phospholipid fatty acid turnover associated with decreased cell volume.

Treatment of erythrocytes with the divalent cation ionophore A23187 results in net uptake of calcium and a calcium-dependent decrease in cellular potassium content and cell volume. These changes in membrane properties are associated with a selective stimulation of fatty acid incorporation into membrane phosphatidylethanolamine (PE). In this study the relationship between this selective stimulation of phospholipid fatty acid turnover and changes in calcium uptake, cellular potassium content, and cell volume has been examined by 1) preventing the calcium-dependent loss of potassium without abolishing calcium uptake and 2) altering cellular potassium content and cell volume without increasing net uptake of calcium by utilizing the monovalent cation inonophore nigericin or increasing the osmolarity of the buffer. It has been shown that treatment of erythrocytes with A23187, nigericin, or hypertonic buffer results in a selective stimulation of fatty acid incorporation into PE. These results suggest that a mechanical or conformational change in the membrane is associated with a selective stimulation of fatty acid turnover in phosphatidylethanolamine.

Biological Transport, Active↗
PubMed1980

The importance of circulating 1,25-dihydroxyvitamin D in the pathogenesis of hypercalciuria and renal-stone formation in primary hyperparathyroidism.

Fifty patients with primary hyperparathyroidism were studied with an oral calcium-tolerance test, measurements of plasma levels of vitamin D metabolites, and determination of calcium excretion on both a low-normal (400 mg) and high-normal (1000 mg) calcium intake. There were strong positive correlations between plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)2D) and both the calciuric response to the calcium-tolerance test (r = +0.75, P less than 0.001) and calcium excretion on the 1000-mg calcium diet (r = +0.65, P less than 0.001). The patients were classified into two subpopulations: 30 patients showed hyperabsorption with the calcium-tolerance test, striking hypercalciuria, marked elevations in plasma 1,25(OH)2D, and a high incidence (19 of 30 patients) of renal stones; 20 patients had a normal response to the tolerance test, normocalciuria, normal or high-normal plasma 1,25(OH)2D, and a low incidence of stones (three of 20 patients). The findings emphasize the importance of circulating 1,25(OH)2D in the pathogenesis of hypercalciuria and stone formation in primary hyperparathyroidism.

Calcium↗
PubMed1980

1,25(OH)2D3 is not the only D metabolite involved in the pathogenesis of osteomalacia.

Three patients are described in whom there was no simple correlation between plasma 1,25(OH)2D3 concentration and the occurrence of osteomalacia. One patient had severe osteomalacia with high plasma 1,25(OH)2D3 and normal mineral ion product; the second had a normal mineral ion product and no evidence of osteomalacia even though plasma 1,25(OH)2D3 was undetectable; and the third had osteomalacia, low plasma 1,25(OH)2D3 and a reduced mineral ion product. In considering these data in the light of presently available information, it is concluded that osteomalacia can occur as a consequence of a lack of a vitamin D metabolite other than 1,25(OH)2D3, or a consequence of a reduced mineral ion product, but not as a consequence of 1,25(OH)2D3 lack if the mineral ion product is normally maintained and other D metabolites are present. However, a deficiency of 1,25(OH)2D3 normally leads to a reduction in the mineral ion product hence 1,25(OH)2D3 deficiency may play a role in the development of certain forms of osteomalacia.

Adult↗
PubMed1980

Early diagnosis of juvenile renal osteodystrophy.

Renal osteodystrophy has assumed growing importance as a major and frequently disabling complication of chronic renal failure in children since the advent of successful hemodialysis and renal transplantation programs. The frequency and severity of renal osteodystrophy appears greatest in younger children with congenital diseases of the kidney and urinary tract, who experience long intervals of chronic renal failure prior to reaching end-stage. Twenty-nine children with varying degrees of chronic renal failure were studied to learn: (1) how early renal osteodystrophy can be diagnosed; and (2) how the various clinical, biochemical, and hormonal abnormalities correlate with abnormal bone histomorphometry as determined from percutaneous transilial bone biopsies. Results showed: (1) marked-to-moderate reductions in GFR (mean = 35 ml/minute/1.73 m2; range 11 to 65 ml/minute/1.73 m2); (2) elevations of serum PTH concentrations in all patients with a GFR < 45 ml/minute/1.73 m2; (3) abnormal bone histomorphometry in all patients with elevated PTH concentrations; (4) "early" renal osteodystrophy (elevated PTH concentrations and abnormal bone histomorphometry but normal serum chemistry values and radiographs) in one quarter of the patients; (5) poor correlations of serum chemistry values and radiographs with bone histomorphometry; and (6) a wide range of histologic abnormalities including predominant osteomalacia (n = 7), predominant hyperparathyroidism (n = 6), or a mixed picture (n = 11).

Adolescent↗
PubMed1980

Primary hyperparathyroidism with intermittent hypercalcaemia: serial observations and simple diagnosis by means of an oral calcium tolerance test.

Ten patients with subtle primary hyperparathyroidism and intermittent hypercalcaemia were followed serially for periods of 2--18 months (mean 10 months). Fasting serum calcium was elevated (greater than 10.6 mg/dl) in only 20% of determinations and fluctuated widely (9.1--11.2 mg/dl), yet the patients displayed a continuous, rather than episodic, basic disease process as defined by increases in nephrogenous cyclic AMP and serum iPTH. Identical findings were noted in short-term (2--3 successive days) studies in twelve patients. In response to a 1000 mg oral calcium tolerance test, twelve patients with primary hyperparathyroidism and intermittent hypercalcaemia (basal serum calcium 10.2 +/- 0.2 mg/dl, mean +/- SD) displayed: (1) hyperabsorption of calcium (mean calciuric response twice normal); (2) induced-hypercalcaemia (mean serum calcium 11.4 mg/dl, with a mean increase of 1.2 mg/dl versus 0.2 mg/cl in normal subjects); and (3) abnormal parathyroid suppressibility (nephrogenous cyclic AMP 2.66 +/- 0.57 nmol/100 ml GF versus 0.95 +/- 0.40 nmol/100 ml GF in normal subjects, mean +/- SD). The patients demonstrated striking hypercalciuria (452 +/- 123 mg/24 h) on a 1000 mg metabolic calcium diet. Serum levels of 1,25(OH)2D3, measured in ten patients, were markedly elevated at 90 +/- 20 pg/ml (mean +/- SD), and there was a strong positive correlation between the values for 1,25(OH)2D3 and the calciuric response to the calcium tolerance test (r = 0.75, P less than 0.001). These results (1) indicate that the calcium tolerance test is a simple and reliable technique for diagnosis of patients with primary hyperparathyroidism and intermittent hypercalcaemia, and (2) emphasize the important pathophysiologic features of this subtle clinical variant of primary hyperparathyroidism.

Calcium↗