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Biomedical subjects

U Helmchen

Publications and source records attributed to U Helmchen.

At least 127 records · Page 7Linked to original sources
PubMed1984

Glomerular prostaglandin formation in two-kidney, one-clip hypertensive rats.

In vitro prostaglandin (PG) and thromboxane B2 (TXB2) formation by isolated glomeruli from normotensive (N) and two-kidney, one-clip hypertensive (2K,1C) rats was determined. When calculated on the basis of glomerular protein content, PGE2, 6-keto-PGF1 alpha and TXB2 production of glomeruli from clipped kidneys was significantly greater than PG and TXB2 formation of glomeruli from the untouched kidneys. When PG and TXB2 formation was calculated per amount of glomeruli, only PGE2 formation was found to be significantly greater in clipped kidneys. No severe damage of glomerular structure was found in the kidneys when studied by light microscopy. In additional in vivo studies, the effect of the cyclooxygenase inhibitor indomethacin on blood pressure and glomerular filtration rate (GFR) was evaluated. Following indomethacin GFR in 7 of 13 clipped kidneys of 2K,1C rats decreased from 363 +/- 77 to 188 +/- 51 microliter/100 g body wt, whereas six kidneys developed anuria. No effect of cyclooxygenase inhibition on GFR was found in N rats and in untouched kidneys of 2K,1C rats. Mean arterial blood pressure in 2K,1C hypertension fell significantly, from 158 +/- 10 to 135 +/- 7 mmHg, after cyclooxygenase inhibition. No effect was seen in N rats. The data suggest that increased glomerular PG formation in the clipped kidneys of 2K,1C rats is involved in the pathogenesis of hypertension in this animal model.

Animals↗
PubMed1984

Favourable outcome of hepatic veno-occlusive disease in a renal transplant patient receiving azathioprine, treated by portacaval shunt. Report of a case and review of the literature.

Veno-occlusive disease (VOD) developed in a 45-year-old white male 2 years after cadaveric kidney transplantation while receiving combined immunosuppressive therapy with prednisone and azathioprine. Early clinical signs at presentation included ascites and tender hepatomegaly. The diagnosis of VOD was established at laparoscopy and by histological examination of liver biopsies. Azathioprine was discontinued. Gross ascites refractory to medical treatment and decreasing liver function required surgical treatment by portacaval shunt. Transient postoperative complications were hepatic encephalopathy and considerable hyperbilirubinaemia. 8 months later the patient is well, with stable renal function and no clinical signs of hepatic disease.

Azathioprine↗
PubMed1982

The intrarenal renin-angiotensin-system. An immunocytochemical study on the localization of renin, angiotensinogen, converting enzyme and the angiotensins in the kidney of mouse and rat.

The localization of renin, converting enzyme (CE) and angiotensin II (ANG II) in the kidneys of rats and mice was investigated with immunocytochemical methods. According to the presence and specific intrarenal localization of these components of the renin-angiotensin-system (RAS) our results suggest that in addition to the well known systemic effects of the RAS, there are interactions of its components inside the kidney. These interactions may lead to the generation of an extra portion of ANG II in the renal blood stream with its target cells determined by the localization of CE at the luminal side of well defined endothelial areas. These intrarenal-intravasal reactions may or may not reinforce the action of "systemic" ANG II, generated prerenally. In addition, the existence of true intrarenal-interstitial interactions, with the different components and actions of this intrarenal RAS restricted entirely to the kidney is suggested by our results, particularly the demonstration of ANG II within epitheloid cells and the dissociation of systemic renin and ANG II from their local concentrations in renal hypertensive rats.

Angiotensinogen↗
PubMed1982

Contrasting renal effects of different antihypertensive agents in hypertensive rats with bilaterally constricted renal arteries.

Systemic and renal effects of the vasodilators dihydralazine and minoxidil were compared with those of the converting-enzyme inhibitor captopril (SQ 14225) and the AII antagonist sarisoleucin (Sar1Ile8-AII) in chronically sodium-depleted, two-kidney, two-clip hypertensive rats. Arterial blood pressure normalized in all experimental groups within 24 hours and remained normal until the end of the experiment. By day 4, plasma concentrations of creatinine and urea in animals treated by captopril or sarisoleucin were significantly higher than those measured after the administration of dihydralazine or minoxidil. Renal tubular lesions were also more frequently observed after the renin-angiotensin system (RAS) was blocked than they were after vasodilatation was induced by direct smooth muscle relaxation. Captopril and sarisoleucin stimulated the RAS more extensively than dihydralazine and minoxidil did. The results indicate that, in the presence of bilateral renal artery stenosis and sodium deprivation, systemic blood pressure normalization after the blockade of the RAS may be accompanied by acute renal failure. This may be explained partially by poststenotic renal hypotension, but it may also reflect a reduction of the GFR because of the blockade of intrarenal actions of AII.

Animals↗
PubMed1981

Effect of indomethacin on blood pressure in rats with renovascular hypertension: dependence on plasma renin activity.

The effect of the cyclooxygenase inhibitor indomethacin (3.4 mg/kg/24 hr) on systolic blood pressure (PB) and plasma-renin-activity (PRA) was evaluated in normotensive and renovascular hypertensive rats receiving either a normal or low salt diet. Indomethacin reduced PRA in normal and hypertensive animals on both low and normal salt intake. Indomethacin furthermore, decreased BP in animals on low sodium diet but increased PB in sodium repleted rats. These data suggest that the effect of indomethacin on rat BP may depend on the state of extracellular volume and PRA.

Animals↗
PubMed1979

Indomethacin induced hypotension in sodium and volume depleted rats.

After a single oral dose of 4 mg/kg indomethacin (IDM) to sodium and volume depleted rats plasma renin activity (PRA) and systolic blood pressure fell significantly within four hours. In sodium repleted animals indomethacin did not change systolic blood pressure (BP) although plasma renin activity was decreased. Thus, indomethacin by inhibition of prostaglandin synthesis may diminish the blood pressure maintaining effect of the stimulated renin-angiotensin system in sodium and volume depletion.

Animals↗
PubMed1978

Correlations between the morphological and clinical findings in a patient recovering from secondary generalised amyloidosis with renal involvement. Light- and electron microscopic investigations on serial biopsies.

We report light- and electron microscopic findings in glomerular amyloidosis (secondary amyloidosis), which occurred after recurrent empyema of the pleura. After healing of the empyema, the clinical symptoms disappeared, over a period of eight years. During the acute stage of the disease (grade II-III amyloidosis) when the nephrotic syndrome was present, amyloid deposits were seen in the mesangium and on both sides of the basement membrane of the glomerular capillaries. Furthermore, denuded basement membrane areas showing the passage of amyloid into the urinary space, and invaginations of the podocyte by straightened amyloid fibrils were found. After clinical recovery (except for a trace of proteinuria), the renal amyloidosis had electronmicroscopically transformed from an active into an inactive or resting form, while the amount of amyloid present was almost the same. In the areas of amyloid deposits, reparative changes were observed, espcially in the area of the mesangial cells and of the podocytes. The podocytes were separated from the persisting amyloid deposits by newly formed basement membrane material.

Adult↗
PubMed1978

Simultaneous occurrence of perimembranous glomerulonephritis and glomerular amyloidosis.

The results of electron microscopic examination of renal biopsies from 3 patients with rheumatoid arthritis treated with penicillamine are presented. All 3 patients developed a nephrotic syndrome upon discontinuation of penicillamine therapy. When viewed with the electron microscope, segmental forms of perimembranous glomerulonephritis (Stages I-II of Ehrenreich and Churg) and glomerular renal amyloidosis Grade I-III were observed. In all three cases the nephrotic syndrome was considered to be due to the simultaneous occurrence of the two disease processes. In 2 cases perimembranous glomerulonephritis with immuno-complex-deposits was assumed to be the dominant factor in the causation of the disease, in the other case amyloidosis was the principle abnormality.

Amyloidosis↗
PubMed1978

Renal hypotension in sodium and fluid deprivation: experimental findings in renin-depleted rats.

Arterial hypotension of renal origin occurred as consequence of low plasma renin activity in the presence of sodium and extracellular fluid volume depletion. Secretory insufficiency of the renin-producing juxtaglomerular cells and sodium and volume deprivation, simultaneously, were achieved by removing the "clamped" kidneys in renal hypertensive, sodium- and volume-depleted rats leaving in situ the contralateral kidneys deprived of renin during the preceding period of hypertension. It is suggested that renal hypotension after acute losses of sodium and extracellular fluid may also develop in patients with chronically depressed renin-angiotensin system.

Animals↗
PubMed1976

Primary malignant nephrosclerosis.

1. As proposed by Schürmann & MacMahon (1933), we suggest that two types of malignant nephrosclerosis exist. 2. In the type called primary malignant nephrosclerosis, renal vascular lesions precede hypertension. 3. In the second type, called secondary malignant nephrosclerosis, renal vascular lesions are considered to be the consequence of malignant hypertension.

Basement Membrane↗