[Blood pressure control in the home].
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Blood Pressure Determination↗
Biomedical subjects
J Elmgreen
Publications and source records attributed to J Elmgreen.
Elevated serum parathyroid hormone concentration during treatment with high ceiling diuretics.
Serum concentrations of parathyroid hormone (s-PTH) calcium, phosphorus and alkaline phosphatase were measured during treatment with furosemide or bumetanide for congestive heart failure. Significant elevations both of s-PTH and alkaline phosphatase were found, whereas serum calcium concentration was decreased. The changes were not related to the dose of drug or to the duration of treatment. It is concluded that treatment with furosemide or bumetanide may cause hypocalcaemia, resulting in elevation of s-PTH. The increased concentration of alkaline phosphatase may indicate accelerated bone remodelling, as found in primary hyperparathyroidism.
Adult↗
Adrenal scintigraphy in primary aldosteronism caused by an aldosterone producing adenoma.
Adrenal scintigraphy with 131I-19-iodo-cholesterol was performed in 13 hypertensive patients with biochemical disturbances suggesting an aldosterone-producing adenoma. The actual presence of an adenoma was subsequently confirmed in all cases. An asymmetrical tracer uptake (lateralization) was seen in 7 patients and in 6 of these the adenoma was located in the adrenal with the higher uptake. In one patient a large necrotic tumour was not visualized and a faint contralateral accumulation was wrongly taken to represent a tumour. In 6 patients the scintigram was non-lateralizing. In these highly selected patients a lateralizing scintigram had a high diagnostic specificity and at present adrenal scintigraphy should be the method of first choice in the preoperative side prediction. However, the sensitivity is low: a non-lateralizing scintigram does not exclude the presence of an aldosterone-producing adenoma.
Adenoma↗
The relationship of urinary prostaglandins and plasma renin to sodium balance and diuresis in normal man.
The significance of changes in sodium balance and urinary sodium excretion for renal PG excretion was studied in normal man. In protocol B a strongly negative sodium balance was produced in 5 healthy young subjects by a low sodium diet given for 7 days (lo mmol Na/day) with 80 mg furosemide p.o. added on the last two days. 24 hour urinary PGE2 excretion remained constant, while plasma renin increased. In protocol A the effect of i.v. furosemide (1 mg/kg bwt) on urinary PGE2 and PGF2 alpha excretion rates was examined in 5 healthy young subjects. Rapid but short-lasting increases in PG excretion rates ran in parallel with the changes in urine flow rate. The study suggests that PGE2 is not of importance for the sodium homeostasis in normal man. Renal prostaglandins may play a modifying role for the renal response to loop diuretics but are hardly instrumental for the diuretic effect.
Adult↗
Sodium balance, urinary prostaglandin E2 and renin in normal man.
1. Urinary prostaglandin (PG) E2 excretion and plasma renin were measured in five healthy volunteer subjects for 2 h after intravenous injection of frusemid (protocol A) and during salt restriction for 7 days with frusemide added on the 2 last days (protocol B). 2 In protocol A, peak values in PGE2 and urine flow were reached in 10-20 min, after which the values rapidly subsided. Plasma renin increased twofold in 60 min. 3. In protocol B, even during severe antinatriuresis (day 5) and during maximal negative sodium balance (day 7), no change in urinary PGE2 excretion was observed. Plasma renin increased twofold on day 5 and increased tenfold on day 7. 4. The result of protocol B does not suggest any essential role of renal PGE2 for sodium excretion or sodium homeostasis in man. The result of protocol A may point to a role of renal prostaglandins for the diuretic action of frusemide.
Adult↗
The effect of syngeneic peripheral blood cells on the formation of colonies by normal human bone marrow cells in diffusion chambers in mice.
This paper describes the influence of cells capable of releasing colony stimulating activity (CSA) in vitro on the formation of granulocytic colonies by normal human bone marrow in diffusion chambers in mice. A carbonyl iron method was used to remove phagocytic cells from normal human bone marrow. This treatment prevented spontaneous colony and cluster formation when the cells were cultured in agar in vitro at initial concentrations of 2-5 x 105 cells per ml. However, non-phagocytic bone marrow cells formed granulocytic colonies when inoculated into diffusion chambers at 105 cells per chamber and cultured in 450 R-irradiated or non-irradiated mice. The formation of granulocytic colonies by carbonyl iron treated marrow in diffusion chamber cultures was not consistently enhanced by the admixture of 1.4 x 105 1500 R-irradiated syngeneic light density blood cells (less than 1.077 g/ml) to the chamber inoculum. In contrast, these cells induced cluster or colony formation when added in the same proportion to the marrow cells in agar cultures in vitro. Addition of 1.4 x 105 1500 R-irradiated high density blood cells(greater than 1.077 g/ml) to the inoculum resulted in a slight, non-significant decrease in the number of colonies in diffusion chambers. The stimulating effect of host irradiation on neutrophilic colony formation was independent of the presence of CSA releasing cells in the chamber inoculum.
Animals↗
Influence of hyposensitization of ATP level and CO2 production of mast cells in anaphylaxis.
Anaphylaxis in a glucose-free medium containing pyruvate caused a release of histamine and a significant decrease in the ATP level of rat mast cells. The fall was maximal after 10 min and it was found to reverse after 22 min. Glucose completely counteracted the ATP fall without changing the anaphylactic histamine release. Furthermore, the oxidative metabolism of exogenous pyruvate to CO2 was stimulated in the mast cell. A high level of protection of mast cells to antigen challenge was obtained following hyposensitization and only a small amount of the intracellular histamine was released in contrast to non-hyposensitized cells. Hyposensitization counteracted the ATP fall by antigen challenge but the increase in oxidative metabolism remained unchanged. The results indicate that hyposensitization exerts effects in the mast cell consistent with a reduced ATP utilization or with a reduced uncoupling of oxidative phosphorylation. The mechanism of the hyposensitization must be due to inhibition of one or more of the cellular steps leading to histamine release and subsequent morphological changes of the cell or to uncoupling of oxidative phosphorylation.
Adenosine Triphosphate↗