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Biomedical subjects

H Osswald

Publications and source records attributed to H Osswald.

At least 127 records · Page 7Linked to original sources

Characterization of the postocclusive response of renal blood flow in the cat.

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.

Adenosine↗

Uridine enhances the chemotherapeutic action of the 4'-demethylepipodophyllotoxin-thenylidene-glucoside (VM 26)-cyclophosphamide combination on i.m. implanted Ehrlich carcinoma.

The chemotherapeutic effectiveness of the simultaneously used combination of 4'-demethylepipodophyllotoxin-thenylidene-glucoside (VM 26) and cyclophosphamide was significantly enhanced by uridine in i.m. implanted Ehrlich carcinoma without increasing toxicity when uridine was applied sequentially at an interval of 20 h.

Animals↗

Inhibitory effect of methylxanthines on feedback control of glomerular filtration rate in the rat kidney.

Microperfusion experiments were performed in rats to assess the effect of luminal application of theophylline and the more lipophilic 3-isobutyl-1-methylxanthine (IBMX) on feedback regulation of glomerular filtration rate. Elevation of loop of Henle flow from 0 to 40 nl/min caused a 20.3 +/- 4.5% reduction of stop flow pressure (SFP) and a 32.2 +/- 3.7% reduction of early proximal flow rate (EPFR) when the perfusate was a 140 mM NaCl solution. When theophylline was added in a concentration of 5mM SFP fell by only 5.3 +/- 1.8% and EPFR by 7.9 +/- 33%, changes which were significantly smaller than in the control perfusions (P less than 0.01). An identical change of loop of Henle flow in the presence of IBMX in concentration of 1 and 5 mM was associated with a 4.5 +/- 3.9% decrease and a 12.1 +/- 2.7% increase of EPFR. In orthograde perfusion experiments full inhibition of the feedback response was noted at an IBMX concentration of about 1 mM while during retrograde perfusion a concentration of 0.4 mM was sufficient to produce the same effect. This indicates that methylxanthines diffuse out of the loop of Henle to a considerable extent. Methylxanthines reduced absolute and fractional water absorption along the loop of Henle to some extent while Cl absorption rates and early distal Cl concentrations were not significantly altered. Cyclic AMP applied from the luminal side in a concentration of 10 mM did not affect the feedback response of EPFR to flow elevation from 0 to 40 nl/min. Luminal application of dibutyryl cyclic AMP at 10 mM induced a small, but significant reduction of the feedback response when tested by paired t-test (P less than 0.05). Our results show that luminal application of methylxanthines strongly interfere with feedback regulation of glomerular filtration rate. It is unclear at present whether this effect is related to inhibition of cyclic nucleotide phosphodiesterase and a rise in tissue cyclic AMP levels or to interference with a mechanism involving the local action of adenosine or 5'-AMP.

Animals↗

Filtration dynamics in dogs: glomerular capillary pressure.

Hydrostatic pressure in the glomerular capillaries, the primary driving force for glomerular ultrafiltration, is directly measurable only in those species with glomeruli present on the capsular surface of the kidney. Accordingly, this crucial measurement must be made indirectly in species not so endowed, such as the dog. Several different methods have been utilized in the dog; unfortunately each is indirect. This review deals with an assessment of the following methods for the determination of glomerular capillary pressure in dogs: a) reduction of arterial pressure method; b) ureteral occlusion method; c) the Winton or venous occlusion method; d) fraction of arterial pressure method; e) back calculation from forces opposing filtration; f) sieving method; and g) single nephron occlusion of the Gertz stop-flow method. Recent studies in the dog, utilizing single nephron occlusion techniques, provide estimates of glomerular capillary pressures of approximately 60 mn Hg in the autoregulatory range of blood pressure.

Animals↗

Adenosine response of the rat kidney after saline loading, sodium restriction and hemorrhagia.

Experiments were performed on three groups of rats. The first group consisted of sodium loaded (SL) rats (high sodium diet, 10 meq Na/day, the second group consisted of sodium restricted (SR) rats (low sodium diet, 0.7 meq Na/day) and the third group consisted of hemorrhagic rats (HR), which were bled with 1-1,5% of the body weight. Blood pressure, glomerular filtration rate (GFR) and sodium excretion were measured. In some animals renal blood flow (RBF) was recorded with an electromagnetic flow meter. Adenosine was injected or infused into the thoracic aorta. Bolus injection of 10 nmoles adenosine resulted in a rapid and marked decrease of RBF (40%) in SR rats whereas in SL rats only a very small decrease of RBF (2%) was observed. Continuous infusion of adenosine (10(-7) moles/min) decreased GFR by 54% in SR rats and by 33% in HR rats, whereas GFR in SL rats did not change significantly. 5'-AMP decreased GFR in SR rats by 18% and in HR rats by 32%. Adenosine and 5'-AMP caused a slight fall in the systemic blood pressure, but this decrease could not account for the decrease of GFR. The sensitivity of kidney vasculature to adenosine parallelled high plasma renin activity (162 ng ang/ml-h in SR and 76 ng ang/ml-h in HR), elevated renal vascular resistance and low GFR. Simultaneous infusion of angiotensin (Hypertensin), 250 ng/min, in SL rats resulted in an increase of sensivity to adenosine infusion: GFR decreased by 21%. Our experiments demonstrated that a marked renal vasoconstriction caused by adenosine only occurs in rats in which renin-angiotensin system was stimulated.

Adenosine↗

Renal effects of adenosine and their inhibition by theophylline in dogs.

The action of adenosine on renal blood flow and kidney function in dogs was studied with bolus injections and infusion of adenosine into the renal artery. Simultaneous infusions of theophylline, 1-5 x 10(-6) mol/min into the renal artery which did not affect renal function by itself inhibited the adenosine induced vasoconstriction. From the bolus injection studies a dose response curve (DRC) was constructed. Theophylline shifted the DRC to the right in a parallel manner. pA2-pA10 was 0.98 indicating that theophylline inhibition of the adenosine effects may be interpreted as a competitive antagonism. Infusions of adenosine (0.3-1.1 mumol/min) caused a reduction of urine volume, sodium excretion and glomerular filtration rate (GFR). The decrease of GFR after adenosine infusion by 31.4% could be diminished by theophylline. It is suggested that adenosine action is based mainly on a constriction of the vasa afferentia in the outer zone of the cortex.

Adenosine↗

Potentiated chemotherapeutic activity of 3,6-diamino-10-methyl-acridinium by combination with glycine or DL-alpha-alanine on the Ehrlich carcinoma.

Glycine or DL-alpha-alanine potentiated the chemotherapeutic action of 3,6-diaminoacridinium without increasing its toxicity when these amino acids were combined with it simultaneously. On the contrary, valine in combination with 3,6-diaminoacridinium diminished slightly the chemotherapeutic effect as compared to the monotherapy with 3,6-diaminoacridinium. The monotherapy with the applied amino acids in the same dosage showed no tumor inhibition.

Acridines↗