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A Bischoff

Publications and source records attributed to A Bischoff.

At least 73 records · Page 4Linked to original sources
PubMed1998

Neuropeptide Y lowers blood glucose in anaesthetized rats via a Y5 receptor subtype.

We have investigated the receptor subtype mediating effects of neuropeptide Y (NPY) on blood glucose concentrations. In anaesthetized rats a 120 min i.v. infusion of 2 microg/kg/min NPY lowered blood glucose by 26 mg/dl. This was mimicked by the same dose of peptide YY (PYY), NPY2-36, PYY3-36 and [Leu31,Pro34]NPY but not by NPY13-36, PYY13-36 or rat or human pancreatic polypeptide. The effects of NPY and [Leu31,Pro34]NPY were not inhibited by 10 microg/kg/min BIBP 3226. Neither treatment significantly altered plasma insulin concentrations. We conclude that NPY lowers blood glucose concentrations via a Y5 receptor subtype, i.e. a subtype which has also been implicated in stimulation of food intake.

Animals↗
PubMed1998

Indomethacin inhibits the natriuretic effects of neuropeptide Y in anesthetized rats.

Neuropeptide Y (NPY) is a unique modulator of renal function that enhances urine flow and sodium excretion despite marked reductions in renal blood flow. We investigated whether the cyclooxygenase inhibitor indomethacin alters the renal NPY effects in anesthetized rats. Treatment with 5 mg/kg indomethacin i.p. lowered urinary prostaglandin excretion by approximately 85%. Systemic infusion of NPY elevated mean arterial pressure by approximately 15 mm Hg and renovascular resistance by approximately 8.0 mm Hg/ml/min, whereas the related peptide YY3-36 (PYY3-36) did not. Nevertheless, both peptides enhanced urine flow rate by approximately 250 and approximately 100 microl/15 min, respectively, and sodium excretion by approximately 15 micromol/15 min. Treatment with indomethacin did not affect NPY- and PYY3-36-induced alterations of systemic and renovascular hemodynamics but completely abolished NPY- and PYY3-36-induced diuresis and natriuresis. Endogenous creatinine clearance was not affected by any treatment. We conclude that cyclooxygenase-derived arachidonic acid metabolites are not involved in the systemic or renal hemodynamic effects of NPY and PYY3-36 but mediate NPY- and PYY3-36-induced diuresis and natriuresis.

Anesthesia↗
PubMed1997

The Y1 antagonist BIBP 3226 inhibits potentiation of methoxamine-induced vasoconstriction by neuropeptide Y.

We investigated the interaction of neuropeptide Y (NPY) with the alpha 1-adrenoceptor agonist, methoxamine, in control of mean arterial pressure, renovascular resistance and mesenteric vascular resistance in anaesthetized rats. Infusion of 3.0 but not 0.3 microgram/kg/min NPY enhanced the elevations of all three haemodynamic parameters caused by bolus injections of methoxamine (10-100 micrograms/kg). These enhancements largely involved a prolongation of the methoxamine effects. While infusion of the Y1 NPY receptor-selective antagonist, BIBP 3226 (10 micrograms/kg/min), alone did not alter methoxamine-induced vasoconstriction, it inhibited the potentiation by NPY. We conclude that NPY can potentiate methoxamine-induced vasoconstriction in vivo. This is mediated predominantly, if not exclusively, via the Y1 receptor. Endogenously released NPY does not appear to reach sufficient concentrations to cause tonic systemic vasoconstriction or potentiation thereof in the anaesthetized rat.

Animals↗
PubMed1997

Renovascular and tubular effects of neuropeptide Y are discriminated by PP56 (D-myo-inositol 1,2,6-triphosphate) in anaesthetized rats.

Systemic infusion of neuropeptide Y (NPY; 1 microg kg-1 min-1) for 120 min rapidly reduced renal blood flow and increased mean arterial pressure and renovascular resistance and, at later time points (> 30 min), enhanced diuresis, natriuresis and calciuresis in anaesthetized rats. Infusion of the reported NPY antagonist PP56 (D-myo-inositol 1,2,6-triphosphate, 333 mg kg-1 min-1) slightly but significantly enhanced renal blood flow and reduced renovascular resistance over the course of the infusion period. Infusion of PP56 together with NPY (starting 30 min prior to the NPY infusion) significantly inhibited NPY-induced alterations of mean arterial pressure, renal blood flow and renovascular resistance. Coinfusion of PP56 also attenuated the renovascular effects of bolus injections of NPY (0.1-10 microg/kg) but at the highest NPY dose the antagonistic effect of PP56 could partially be overcome. In contrast to the antagonism of the vascular NPY effects, infusion of PP56 did not significantly affect NPY-induced enhancements of diuresis, natriuresis and calciuresis. Thus, PP56 is a surmountable antagonist of vascular but not tubular NPY effects. We conclude that tubular NPY effects occur largely independently of alterations of renal haemodynamics.

Anesthesia↗
PubMed1997

Receptor subtypes Y1 and Y5 are involved in the renal effects of neuropeptide Y.

1. Systemic infusion of neuropeptide Y (NPY) reduces renal blood flow and can concomitantly increase diuresis, natriuresis and calciuresis in anaesthetized rats. The present study was designed to investigate whether the apparently contradictory NPY effects on renal blood flow and urine formation and composition are mediated by distinct NPY receptor subtypes. 2. NPY and its analogues, peptide YY (PYY), [Leu31, Pro34]NPY and NPY13-36, were infused in incremental doses of 0.3, 1 and 3 micrograms kg-1 min-1 for 45 min each and the results compared to those obtained in vehicle-infused rats. Renal blood flow was monitored in 1-5 min intervals, while urine excretion and composition were determined in 15 min collection periods. Plasma renin activity and aldosterone concentrations were measured at the end of the final infusion period. 3. Relative to vehicle NPY, PYY and [Leu31, Pro34]NPY dose-dependently reduced renal blood flow and increased diuresis, natriuresis and calciuresis with roughly similar potency; NPY13-36 slightly but significantly increased renal blood flow but had no effect on diuresis, natriuresis and calciuresis. None of the peptides significantly affected endogenous creatinine clearance or kaliuresis. 4. Plasma renin activity was significantly reduced by PYY. Quantitatively similar reductions were observed with NPY and [Leu31, Pro34]NPY but failed to reach statistical significance with the given number of experiments. NPY13-36 did not reduce plasma renin activity. None of the peptides significantly affected plasma aldosterone concentrations. 5. In another series of experiments infusion of PYY3-36 (2 micrograms kg-1 min-1 for 120 min) did not reduce renal blood flow but significantly enhanced diuresis and natriuresis to a similar extent as the NPY 2 micrograms kg-1 min-1. 6. In a final series of experiments the Y1-selective antagonist, BIBP 3226 (1 or 10 micrograms kg-1 min-1) dose-dependently antagonized reductions of renal blood flow elicited by bolus injections of NPY (0.1-30 micrograms kg-1). BIBP 3226 (10 micrograms kg-1 min-1) also inhibited the effects of a 120 min infusion of NPY (2 micrograms kg-1 min-1) on renal blood flow but had only minor inhibitory effects on enhancements of diuresis and did not significantly affect enhancements of natriuresis. 7. We conclude that NPY reduces renal blood via a classical Y1 subtype of NPY receptor. In contrast enhancements of diuresis, natriuresis and calciuresis occur via a distinct subtype which resembles the receptor that mediates NPY-induced enhancement of food intake.

Animals↗
PubMed1997

Vasoconstriction of rat renal interlobar arteries by noradrenaline and neuropeptide Y.

1. We have studied the contractile effects of noradrenaline and neuropeptide Y given alone and in combination on isolated rat renal interlobar arteries. 2. Noradrenaline contracted proximal and distal intrarenal microvessels in a concentration dependent manner, with similar potency (EC50 approximately equal to 550 nM), but maximal effects were greater in the proximal than in the distal vessel segments (approximately equal to 10 and 6 nM, respectively). 3. The noradrenaline-induced contraction was inhibited by low prazosin concentrations (3-10 nM) but not by 1 microM yohimbine indicating involvement of alpha(1)-but not alpha(2)-adrenoceptors. The alpha(1)A-adrenoceptor-selective antagonist, 5-methylurapidil and tamsulosin, had high potency (apparent affinities of approximately equal to 8 nM and 57 pM, respectively) while the alpha(1)D-adrenoceptor-selective antagonist, BMY 7378, had only low potency (apparent affinity approximately equal to 300 nM). The alpha(1)B-adrenoceptor-alkylating agent, chloroethylclonidine (10 microM for 30 min at 37 degrees C), had no inhibitory effects. The Ca2+ entry blocker, nitrendipine (300 nM), reduced the potency and maximal effects of noradrenaline. 4. Neuropeptide Y (1-100 nM) also contracted interlobar arteries in a concentration dependent manner, with greater effects in the proximal than in the distal segments, but maximal effects were only small in either segment (< 2 mN). In addition, neuropeptide Y also potentiated the response to noradrenaline, i.e. lowered its EC50 but this enhancement was also small. 5. We conclude that noradrenaline contracts rat interlobar arteries by an alpha(1)A-adrenoceptor; its co-transmitter, neuropeptide Y, affects the response only marginally in this vascular bed.

Adrenergic alpha-Antagonists↗
PubMed1996

Neuropeptide Y-enhanced diuresis and natriuresis in anaesthetized rats is independent of renal blood flow reduction.

1. Neuropeptide Y (NPY) has been reported to enhance diuresis and natriuresis in anaesthetized rats although it is a potent renal vasoconstrictor in vitro in vivo in several species. Therefore, we have investigated anaesthetized rats to see whether reduction in renal blood flow (RBF) and enhancement of diuresis and natriuresis can occur concomitantly, and how diuresis and natriuresis might be enhanced despite reduced RBF. 2. Systemic or intrarenal NPY infusion (0.03-3 micrograms kg-1 min-1) had only a small effect on mean arterial pressure (maximal increase 15-20 mmHg) and heart rate (maximal decrease 30 beats min-1) but dose-dependently reduced RBF (maximal peak reduction 3 ml min-1) Endogenous creatinine clearance was not significantly altered. 3. In anaesthetized rats systemic infusion of 1 or 3 micrograms kg-1 min-1 NPY enhanced urine formation and sodium and calcium excretion by a maximum of 110, 110 and 45%, respectively, but did not alter potassium excretion. Enhancement of diuresis was also detectable in conscious rats. 4. The diuretic and natriuretic effects of systemically infused NPY were at least partly maintained in rats with decapsulated kidneys and in rats where NPY-induced increase of renal perfusion pressure was excluded mechanically by an adjustable clamp placed on the abdominal aorta. 5. Intrarenal infusion of 0.3 or 1 microgram kg-1 min-1 NPY reduced RBF to a greater extent than systemic infusion (maximal peak reduction 4 ml min-1) but caused a smaller enhancement or even a reduction of urine formation and sodium excretion. 6. We conclude that systemic infusion of NPY reduces RBF by a direct effect on the renal vasculature. Systemic NPY infusion enhances urine formation and sodium and calcium excretion. This occurs independently (at least in part) of pressure natriuresis by formation and/or release of an extrarenal factor which might act on distal tubules and/or collecting ducts.

Anesthesia, General↗
PubMed1996

Corundum, rutile, periclase, and CaO in Ca,Al-rich inclusions from carbonaceous chondrites.

Four calcium,aluminum-rich inclusions from four carbonaceous chondrites-Allende, Acfer 082, Acfer 086, and Acfer 094-were studied by transmission electron microscopy. All inclusions contained at least two of the oxides periclase (MgO), rutile (TiO2), calcium oxide (CaO), and corundum (Al2O3). The oxides (50 to 200 nanometers in size) were found inside and at grain boundaries of the constituent minerals of the inclusions. Determining how these oxides formed may provide insight about condensation processes in the early solar nebula and the origin of refractory inclusions in chondrites. Formation of these oxides by exsolution is considered unlikely. An origin by kinetically controlled condensation appears more probable.

Journal Article↗
PubMed1996

Early aqueous activity on primitive meteorite parent bodies.

The interstellar material from which the solar system formed has been modified by many processes: evaporation and condensation in the solar nebula, accretion into protoplanetary bodies and post-accretion processes within these bodies. Meteorites provide a record of these events and their chronology. Carbonaceous CI chondrites are among the most primitive, undifferentiated meteorites, but nevertheless show evidence of post-accretion alteration; they contain carbonates that are believed to have formed by reactions between anhydrous CI precursor materials and circulating fluids in the meteorite parent body (or bodies), yet little is known about the nature of these reactions or the timescale on which they occurred. Here we report measurements of excess 53Cr--formed by the decay of short-lived 53Mn--in five carbonate fragments from the CI chondrites Orgueil and Ivuna. Our results show that aqueous alteration on small protoplanetary bodies must have begun less than 20 Myr after the time of formation of the oldest known solar-nebula condensates (Allende refractory inclusions). This upper limit is much shorter than that of 50 Myr inferred from previous studies, and clearly establishes aqueous alteration as one of the earliest processes in the chemical evolution of the solar system.

Carbonates↗
PubMed1996

[Trends in autologous blood transfusion in the old states of the Federal Republic of Germany, 1989-1993. 1. A panel study of 143 hopitals].

Increased perception of the risks of homologous blood transfusion has focused substantial interest on autologous blood transfusion (ABT). To evaluate the role of ABT in the Federal Republic of Germany (FRG), we conducted postal surveys of German hospitals in 1989 and 1993. In the present study, the responses of 143 hospitals in the "old" federal states (former West Germany) that replied to both of our surveys were analysed. The objective was to examine trends in ABT practice in the FRG from 1989 to 1993. The study was restricted to the "old" federal states because data for the "new" federal states (former German Democratic Republic) were not available for that period. METHODS. Data presented in this study were obtained by postal surveys of German hospitals in 1989 and 1993. Because of German reunification (3 October 1990), only hospitals in the "old" federal states were surveyed in 1989, while hospitals in both the "old" and "new" states were included in 1993. Four hundred randomly selected hospitals in the "old" federal states were included in both surveys, 143 of which responded to both. The completed questionnaires of these 143 hospitals were analysed. In addition, to estimate the magnitude of positive selection bias, the data provided by these 143 hospitals were compared with data provided by another set of 162 hospitals in the "old" federal states that replied to the 1993 but not to the 1989 survey. RESULTS. There were no significant changes from 1989 to 1993 in the 143 hospitals with respect to hospital size by number of beds and spectrum of surgical specialties. The proportion of hospitals that performed preoperative autologous blood donation grew by 20% (from 74% to 89%) and the proportion that used this technique regularly ("frequently" and "mostly") rose by 80% (from 25% to 45%). The percentage of hospitals that performed preoperative plasmapheresis had more than doubled (from 8% to 19%). The proportion that used acute isovolaemic haemodilution grew by 32% (from 62% to 82%), while those doing so regularly ("frequently" and "mostly") increased by only 17% (from 23% to 27%). The fraction of hospitals equipped with cell-washing devices grew by 29% (from 35% to 45%). General transfusion practice, as measured by acceptance of postoperative haemoglobin levels of less than 10.0 g/dl, had changed but little. CONCLUSIONS. Although the 143 hospitals are not representative on a national level, the findings of our study allow some conclusions on general trends in the "old" states of the FRG. The potential for ABT has substantially grown in the "old" states from 1989 to 1993, although more consistent advantage of this potential could be taken.

Blood Transfusion, Autologous↗