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Angela Bischoff

Publications and source records attributed to Angela Bischoff.

5 recordsLinked to original sources
PubMed2006

Indomethacin differentiates the renal effects of sphingosine-1-phosphate and sphingosylphosphorylcholine.

The sphingomyelin breakdown products sphingosine-1-phosphate (S1P) and sphingosylphosphorylcholine (SPC) constrict intrarenal microvessels in vitro in a pertussis toxin (PTX) sensitive manner, and S1P also reduces renal blood flow in vivo. Nevertheless, both S1P and SPC have been reported to enhance diuresis and natriuresis. This pattern is similar to that of neuropeptide Y, which also reduces renal blood flow and enhances diuresis and natriuresis. The latter effects are inhibited by the cyclooxygenase inhibitor indomethacin, and various S1P and SPC responses have also been linked to the cyclooxygenase pathway. Therefore, we have investigated whether indomethacin can alter the renal effects of S1P and SPC in anaesthetised rats in vivo. In line with earlier experiments S1P bolus injections dose-dependently reduced renal blood flow (by up to 4.8 +/- 0.5 ml min(-1)), and this was not significantly affected by indomethacin treatment (5 mg kg(-1) i.p.). Infusion of S1P but not of SPC (30 microg kg(-1) min(-1) each) for 60 min reduced renal blood flow by up to 0.8 +/- 0.2 ml min(-1), and this was not markedly altered by indomethacin. Despite the differential renovascular effect, both S1P and SPC enhanced diuresis by up to 215 +/- 65 and 201 +/- 58 microl 15 min(-1) respectively, and natriuresis by up to 25 +/- 9 and 29 +/- 11 micromol 15 min(-1) respectively. While indomethacin abolished the SPC-induced diuresis and natriuresis, it, if anything, slightly enhanced the diuretic and natriuretic effect of S1P. To determine whether tubular SPC effects are receptor-mediated, PTX experiments were performed. SPC-induced enhancements of diuresis and natriuresis were abolished by PTX. We conclude that S1P, SPC and neuropeptide Y exhibit distinct patterns of modulation of renal function and that indomethacin allows such effects to be differentiated.

Animals↗
PubMed2002

Problem- vs. lecture-based pharmacology teaching in a German medical school.

We have compared the effectiveness of problem-based learning (PBL) and classical lecture-based learning (LBL) in conveying medical facts in a general pharmacology class of third year medical students ( n=107). Three groups with a total of 31 students were randomly assigned to PBL. The PBL groups (9-12 students each) received ten 2-h sessions in which a clinical case was discussed and ten 2-h sessions in which areas of pharmacology not covered by the case discussions were presented in an LBL format (one group with all 31 students). The other students were assigned to groups of 14-15 students and received 20 2-h sessions in an LBL format. At the end of the semester all students received a questionnaire and participated in the same 30-question multiple-choice exam. The mean number of false answers was 7.6+/-4.0 and 9.7+/-4.7 in the PBL and LBL groups, respectively ( P<0.05 in a two-tailed t-test), and the percentage of failing students (>10 false answers) was 27% and 38%, respectively. Both groups were asked to rate their pharmacology class on a scale of 1 (lowest) to 10 (highest). In this questionnaire, PBL students by average rated generated interest in pharmacology, conveyed knowledge in pharmacology and understanding of medical questions approximately 1 point higher than LBL students. In an additional questionnaire given to the PBL students only, they reported to have prepared themselves 0.9+/-1.1 h for their lecture sessions but 3.0+/-1.4 h for their case discussions. The above findings were largely confirmed in the next semester when students were allowed to decide whether to participate in PBL or LBL classes. Moreover, PBL students did not score worse than LBL students in nation-wide pharmacology exams (523+/-76 vs. 500+/-91 points, P=0.09). We conclude that a switch from LBL to PBL teaching of pharmacology does not occur at the expense of factual knowledge transmission.

Education, Medical, Undergraduate↗
PubMed2002

Comparison of problem-and lecture-based pharmacology teaching.

Problem-based learning (PBL) is gaining interest in many medical schools. Although various approaches have been labelled PBL, it remains unclear which approach is most appropriate for pharmacology courses. Moreover, some teachers remain sceptical about whether PBL is adequate to convey the numerous facts medical students need to memorize about drugs. However, comparisons of PBL methods with conventional lecture-based learning (LBL) methods within general pharmacology courses for medical students show that PBL students are at least as successful in standardized tests but enjoy their course to a greater extent than do LBL students.

Education, Medical↗
PubMed2002

Transient relaxation of rat mesenteric microvessels by ceramides.

We have investigated the vasodilating effects of D-erythro-C2-ceramide (C2-ceramide) in methoxamine-contracted rat mesenteric microvessels. C2-ceramide (10 - 100 microM) caused a concentration-dependent, slowly developing relaxation which reached maximum values after approximately 10 min and partially abated thereafter. Endothelium removal or inhibitors of guanylyl cyclase (3 microM ODQ), protein kinase A (10 microM H7, 1 microM H89) and various types of K(+) channels (10 microM BaCl(2), 3 mM tetraethylammonium, 30 nM charybdotoxin, 30 nM iberiotoxin, 300 nM apamine, 10 microM glibenclamide) had only small if any inhibitory effects against C2-ceramide-induced vasodilation, but some of them attenuated vasodilation by sodium nitroprusside or isoprenaline. A combination of ODQ and charybdotoxin almost completely abolished C2-ceramide-induced vasodilation. A second administration of C2-ceramide caused a detectable but weaker relaxation. L-threo-C2-ceramide (100 microM), which should not be a substrate to ceramide metabolism, had no biphasic time course. The ceramidase inhibitor (1S,2R)-D-erythro-2-(N-myristoylamino)-1-phenyl-1-propanol (100 microM) alone caused some vasodilation, indicating vasodilation by endogenous ceramides, and also hastened relaxation by exogenous C2-ceramide. The late-developing reversal of C2-ceramide-induced vasodilation was absent when alpha-adrenergic tone was removed by addition of 10 microM phentolamine. We conclude that C2-ceramide relaxes rat resistance vessels in an endothelium-independent manner which is prevented only by combined inhibition of guanylyl cyclase and charybdotoxin-sensitive K(+) channels. The vasodilation abates with time partly due to desensitization of the ceramide response and partly due to metabolism of C2-ceramide to an inactive metabolite.

Animals↗