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Biomedical subjects

U Kneissler

Publications and source records attributed to U Kneissler.

At least 19 recordsLinked to original sources
PubMed1996

Antibody and complement reduce renal hemodynamic function in isolated perfused rat kidney.

To evaluate the effect of antibody and complement on renal hemodynamic changes, glomerular injury was induced in isolated perfused kidneys by an anti-thymocyte antibody (ATS) and rat serum (RS). Glomerular filtration rate (GFR), renal vascular resistance (RVR), and renal perfusate flow (RPF) were assessed over an 80-min period. The possible role of thromboxane (Tx) was tested by the application of the Tx synthesis inhibitor UK-38485 and the Tx receptor blocker daltroban. Perfusion of kidneys with ATS and RS significantly reduced GFR at 10 min (control, 501 +/- 111; ATS + RS, 138 +/- 86 ml.g kidney-1.min-1, significance of F = 0.000) after RS. Similarly, RPF (ml.g kidney-1.min-1) fell from 19.2 +/- 1.8 to 6.1 +/- 2.0 (significance of F = 0.000), whereas RVR (mmHg.ml-1.g.min) increased threefold from 5.2 +/- 0.4 to 17.9 +/- 5.0 at 10 min. These changes were ameliorated by the pretreatment of the rats with daltroban and UK-38485. Addition of erythrocytes to the perfusate increased RVR and GFR, whereas RPF decreased compared with cell-free perfused kidneys. ATS and RS in this preparation also decrease GFR and RPF. The hemodynamic alterations appeared without changes in filtration fraction. Compared with untreated, perfused control kidneys, glomerular Tx formation was significantly increased in ATS and RS perfused kidneys. These data demonstrate that antibody and RS induce impairment of renal hemodynamics, which are mediated by increased Tx formation.

Absorption↗
PubMed1996

[ANCA-associated forms of vasculitis].

Among the various types of primary systemic vasculitides, which were recently newly classified (Chapel Hill Classification, 1994), in two forms of small vessel vasculitis, i.e. in Wegener's granulomatosis and in microscopic polyangiitis, the diagnostic utility of anti-neutrophil cytoplasmic antibodies (ANCA) is now well established. In most cases of Wegener's granulomatosis and microscopic polyangiitis the target antigens of these autoantibodies are proteinase 3 (c-ANCA) or myeloperoxidase (p-ANCA), respectively. Both of these autoantibodies are probably not only diagnostic tools but also contribute to the pathogenic mechanisms causing the vascular damage. In Wegener's granulomatosis and in microscopic polyangiitis the upper and lower respiratory tract and the kidneys are preferentially affected. The lesions of Wegener's granulomatosis show an extremely wide morphologic spectrum. In the oropharynx, nasal sinuses, trachea, and large bronchi, they appear for the most part as ulcerations in which a granulomatous response may or may not be evident. Thus in the absence of granulomas, especially in small biopsy material, the diagnosis of Wegener's granulomatosis should by no means be excluded. In the kidneys a focal and segmental necrotizing glomerulonephritis, often associated with crescent formation, is the typical lesion in Wegener's granulomatosis and in microscopic polyangiitis, as well. Histologically, this glomerulonephritis does not differ from the forms also seen in Schoenlein-Henoch disease, in Goodpasture's syndrome and in some cases of systemic lupus erythematosus, but in Wegener's granulomatosis and in microscopic polyangiitis immune glomerular deposits are uncommon. In fact, by analysis of our biopsy material, these "pauci immune" type of necrotizing glomerulonephritis account for nearly 70%. In the past, Wegener's granulomatosis was usually fatal within 5 months of diagnosis. After introduction of the combined therapy with steroids and cyclophosphamide the prognosis improved considerably. Nevertheless, a further improvement is necessary. This could be reached, without any doubt, by an earlier detection of the disease.

Anti-Glomerular Basement Membrane Disease↗
PubMed1984

Adaptation and decompensation of intrarenal small arteries in experimental hypertension.

In the presence of hypertension, the arterial and arteriolar vessel walls may undergo adaptive, destructive, and reparative changes. These different types of hypertensive alterations were studied simultaneously in the intrarenal vascular bed of two-kidney, one-clip hypertensive rats. After constriction of one renal artery, focal medial necrosis of the interlobular arteries developed in the untouched kidneys after the first 24 h. These earliest signs of vascular decompensation could be explained by short-lasting hypertensive episodes that were only detectable by continuous blood pressure recording in conscious animals. Two weeks after the experiment was started, owing to a widening of the media, a substantial increase in the wall-to-lumen ratio was observed in the interlobular arteries. At the same time, the frequency of focal medial necrosis began to fall significantly. Therefore we concluded that the structural vascular adaptation might be responsible for the disappearance of focal medial necrosis in spite of still rising blood pressure values. This assumption was confirmed by an additional experiment in previously chronically two-kidney, one-clip hypertensive rats: 24 h after removing the renal artery clip, a short, severely hypertensive period, induced by infusions of angiotensin II, caused hypertensive vascular lesions almost exclusively in the primarily clipped kidneys with a nonadapted vascular bed. Early intimal changes, which are known to lead to malignant nephrosclerosis, were not only absent in the beginning of two-kidney, one-clip hypertension, but also did not occur during the angiotensin-induced accelerated hypertension. Thus, even extremely high blood-pressure values per se may not be enough to initiate this crucial renal vascular disease.

Adaptation, Physiological↗
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

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↗
PubMed1975

Tubular dimensions and juxtaglomerular granulation index in rat kidneys after unilateral obstruction of the ureter. A study of the morphogenesis of hydronephrosis.

The effect of ligation of a ureter on the tissues in the kidneys in male Wistar rats was studied by morphometry. Dilation of the lumen in the obstructed kidney persisted after ligation only in distal convolutions and collecting ducts. Swelling of epithelial cells in the obstructed kidney was noted only in the distal convolutions and collecting ducts. The Juxtaglomerular Granulation Index (JGI) in the obstructed kidney increased to a maximum 7 days after ligation of the ureter. In the control kidney the lumen of Bowman's space was expanded, epithelial cells in both proximal and distal parts of the nephron were swollen, and the JGI was increased after ligation of the contralateral ureter. The morphological findings support the assumption that reduced cortical blood flow and decreased intratubular flow are the cause of proximal tubular atrophy rather than a persisting increase of proximal intratubular pressure.

Animals↗