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Biomedical subjects

F Reubi

Publications and source records attributed to F Reubi.

At least 19 recordsLinked to original sources
PubMed1987

[On the history of kidney disease].

Except for infections (pyelonephritis, abscess of the kidney), which cause symptoms such as pyuria, pain and fever, most diseases of the renal parenchyma were unknown in Greek and Roman antiquity. Even in the Renaissance they were not yet properly identified. Edema was generally thought to be related to liver disease. Proteinuria was discovered at the end of the 18th century. In 1827 Bright provided the first, almost complete clinical description of the various forms of acute and chronic glomerulonephritis and showed that they were accompanied by macroscopic changes in the kidneys. Between 1850 and 1885, Frerichs, Klebs and Langhans described the primary glomerular lesions. The amount of new knowledge acquired during the 20th century has been tremendous, and covers the mechanism of urine formation, the role of sodium retention in edematous states, the physiology and physiopathology of the renin-angiotensin-aldosterone system, the glomerular origin of the nephrotic syndrome, new methods of investigation, progress in histology and immunology, the discovery of many tubular syndromes, the introduction of antibiotics and antihypertensive drugs, and the development of dialysis and transplantation.

Europe↗
PubMed1985

[History of blood circulation].

Until the beginning of the 17th century it was assumed that the arteries carried a subtle kind of air or spirit to the organs, and the veins the nutrient blood. No one seems to have seriously considered that a backflow was necessary. The circulation of the blood was discovered in 1628 by William Harvey. Blood pressure was first measured in animals by Hales (1733). Reliable blood pressure measurements in humans were rendered possible at the beginning of the 20th century through the efforts of Mahomed, von Basch, Potain, Riva-Rocci and Korotkoff. In 1903 electrocardiography was introduced by Einthoven. In 1941 the use of venous catheterization by Cournand initiated the giant forward strides of modern cardiovascular research, diagnosis and therapy.

Blood Circulation↗
PubMed1985

Effect of nitroglycerin on blood rheology in healthy subjects.

Transdermal nitroglycerin (Nitroderm TTS 5) and a placebo were applied to 10 healthy male volunteers for 10 days. Before the first application and 6, 24, 48, 96, and 240 h thereafter, the viscosity of plasma and whole blood was measured and the packed-cell volume determined. During nitroglycerin application, the viscosity of plasma and whole blood was significantly diminished, and after 10 days it averaged 5% below the initial value. The greater the initial viscosity, the more marked was the drug-induced reduction: in 5 subjects with plasma and whole-blood viscosities near the lower limit of the normal range, there was only a temporary decrease and the values reverted to their initial levels after 4 days; in the other 5 subjects, whose whole-blood viscosities were near the upper limit of the normal range, a 10% reduction was still demonstrable after 10 days. In those subjects all values measured throughout the 10-day observation period were significantly below the initial values. The haematocrit readings followed the same pattern as the alterations in viscosity. It can be assumed, therefore, that the decrease in viscosity induced by nitroglycerin results from "internal haemodilution". The clinical relevance of the changes observed is discussed. The improvement in the rheological properties of the blood may contribute to the anti-anginal effect of Nitroderm TTS.

Adult↗
PubMed1978

[Simultaneous comparative renal clearances and renal iodo (I125)-hippurate in man (author's transl)].

In 111 Patients with a wide range of renal function (normal to advanced renal failure) the renal clearances of Na-paraaminohippurate (CPAH) and of Na-orthojodohippurate--J125(COJ(J125(H) have been simultaneously determined under standardized clearance conditions. We found a significant correlation between the 2 parameters, defined by the equation CPAH = 1.11.COJ(J125)H. The scatter of the single observations however is considerable and hence the +/- 2Sy range is very large. The difference between the 2 clearances is not die to a competition at the same tubular carrier, since adding inactive carrier of OJH does not improve the ratio of the 2 clearances: CPAH = 1.13.COJ(J125)H. Rather the renal extraction of OJ(J125)H(EOJ(J125)H is considerably lower (74% than EPAH (90%). Our datas suggest that OJ(J125)H is not a suitable indicator to replace PAH for measurements of real renal plasma flow.

Humans↗
PubMed1978

Hepatic metabolism of aminopyrine in patients with chronic renal failure.

1. To evaluate potential alterations in hepatic metabolism of drugs occurring in patients with renal insufficiency the fate of aminopyrine was studied in 17 patients with chronic renal failure and in 27 normal subjects. 2. Although patients with chronic renal failure exhibited large variations, their aminopyrine plasma disappearance times (mean 0.62 +/- SD 0.24 h-1) were significantly higher than those found in normal subjects (0.30 +/- 0.07 h-1, P less than 0.002). 3. 14CO2 derived from [dimethylamine-14C]aminopyrine disappeared from breath more rapidly in patients with chronic renal failure and a history of analgesic abuse (0.40 +/- 0.04 h-1) than in control subjects (0.22 +/- 0.03 h-1, P less than 0.01) and in other patients with chronic renal failure (0.24 +/- 0.04 h-1). 4. Dialysis treatment and serum creatinine concentrations were not correlated with the rates of aminopyrine metabolism. Two additional patients, however, with combined renal and hepatic disease, exhibited markedly slowed rates of aminopyrine demethylation. 5. Although chronic renal failure by itself might not alter microsomal drug metabolism it is concluded that, in patients with a history of abuse of phenacetin-containing analgesics, marked acceleration in aminopyrine N-demethylation may be observed.

Adult↗
PubMed1976

[Renal hypertension].

In about 15% of cases hypertension is caused by renal diseases, including unilateral and bilateral parenchymatous nephropathies, renal artery stenosis and renin producing tumors. Important pathogenic determinants are the sodium volume status and the renin angiotensin system. The level of the blood pressure may also depend on the duration of hypertension. An increase in peripheral resistance plays a more important role than an increase in cardiac index. Simultaneous determination of the renin activity in both renal veins is of decisive importance in the diagnosis of renal artery stenosis. Drug treatment of renal hypertension is not essentially different from that of essential hypertension. Surgical procedures include revascularization, uninephrectomy and, in uncontrollable hemodialysis patients, binephrectomy.

Aldosterone↗
PubMed1976

Hypertension associated with early stage kidney disease. Complementary roles of circulating renin, the body sodium/volume state and duration of hypertension.

Interrelations among blood pressure, exchangeable sodium, blood volume and plasma renin activity were studied in 40 normal subjects and in 40 patients with early stage kidney disease (mean plasma creatinine, 2 mg/100 ml). Findings in eight normotensive patients did not differ significantly from those in normal subjects. However, 32 hypertensive patients showed increases (p less than 0.05) in mean exchangeable sodium and in the products of the logarithm of plasma renin activity and exchangeable sodium or blood volume. In normal subjects, blood pressure did not correlate with any of the parameters measured. In the patients, it correlated significantly (p less than 0.05) with duration of hypertension (r = 0.70), exchangeable sodium (r = 0.34) and with sodium-renin (r = 0.38) or volume-renin (r = 0.30) products, but not with blood volume or circulating renin individually. Multiple regression analysis with blood pressure as a dependent variable, and duration of hypertension and the sodium-renin or volume-renin products as independent variables, revealed correlation coefficients of 0.77 and 0.76, respectively. These findings suggest that hypertension accompanying early stage kidney disease may depend at least partly on subtle abnormalities in the sodium volume-renin feedback mechanism as well as on a factor related to the duration of preexisting hypertension.

Adult↗