Replacing animal use in physiology and pharmacology teaching in selected universities in Eastern Europe--charting a way forward.

The aims of this study were to explore the use of animals in teaching and the implementation of innovative technology-based teaching practices across a small sample of universities in Eastern Europe. The research methods used were a questionnaire circulated four weeks before a workshop took place (in October 2009, in Belgrade, Serbia), as well as focused, face-to-face group discussions, led by one of the authors during the workshop. Twenty-two faculty (physiologists and pharmacologists), from 13 Eastern European countries, attended the meeting.

The impact of introducing computer-based alternatives to the use of animals in the teaching of physiology and pharmacology at Balkan universities - a pilot study.

Balkan universities use a substantial number of small mammals and amphibians in the teaching of physiology and pharmacology. This project investigated whether making computer-based alternatives readily available, and combining this availability with a staff development workshop focusing on methods of integrating such resources into undergraduate curricula, would have any effect on animal use. Teachers from 20 Institutes (from five Balkan countries) participated in the workshop.

[Animal models in the study of atherosclerosis].

When selecting an animal species for atherosclerosis research, the most important issue is matching the model to the experiment. In choosing the atherosclerosis model there is a wide variety of choices. Genetic hyperlipidemic disorders are best studied in Watanabe rabbits and in transgenic (knockout or overexpressed) mice.

Endothelial NO formation does not control myocardial O2 consumption in mouse heart.

To test whether endothelium-derived nitric oxide (NO) regulates mitochondrial respiration, NO was pharmacologically modulated in isolated mouse hearts, which were perfused at constant flow to sensitively detect small changes in myocardial O2 consumption (MVO2). Stimulation of NO formation by 10 microM bradykinin (BK) increased coronary venous nitrite release fivefold to 58 +/- 33 nM (n = 17). Vasodilatation by BK, adenosine (1 microM), or papaverine (10 microM) decreased perfusion pressure, left ventricular developed pressure (LVDP), and MVO2.