Preconditioning
In medicine, preconditioning describes a mechanism in which brief stimuli (e.g. lack of oxygen or medication ) trigger the body's own processes that protect against the effects of later damage of a similar nature.
Depending on the time of preconditioning, a distinction is made between:
- early preconditioning: stimulus and damage at short intervals (1–2 hours)
- late preconditioning: stimulus and damage in large time intervals (12-24 hours)
Depending on the type of preconditioning stimulus, one differentiates:
- ischemic preconditioning (also ischemic preconditioning (IPC) or ischemic tolerance )
- pharmacological preconditioning
Ischemic preconditioning
Heart muscles
Brief reduced blood flow to the heart muscles leads to a lack of oxygen (= preconditioning stimulus ). The heart is now protected against the effects of a heart attack for a certain period of time through remodeling processes in the muscle cells . This protection is noticeable in the fact that less heart muscle tissue dies and fewer cardiac arrhythmias occur during a heart attack .
This effect was first demonstrated in 1986 by Charles E. Murry et al. described in animal experiments.
The underlying mechanisms are not yet fully understood. It has been shown that potassium channel openers enable these processes, while potassium channel blockers prevent them. An example is diazoxide , which in low concentrations opens the mitochondrial potassium channels , but leaves those in the sarcolemma unaffected.
Observations on patients show evidence of preconditioning also in the human heart:
- The effects of the subsequent myocardial infarction are less in patients who already have a low blood supply 24 hours before a heart attack ( pre-infarct angina ).
- An exercise interrupted due to heart problems ( angina pectoris ) can be repeated after a few minutes with the same intensity without any symptoms (“warm-up” phenomenon).
brain
The phenomenon occurs not only in the heart muscle, but also in the brain, where it can protect against or during cerebral infarction. A 20–30% reduction in the infarct volume was demonstrated in focal cerebral ischemia. In global cerebral ischemia, damage to the CA1 region of the hippocampus is reduced by up to 90%.
This phenomenon is explained on the one hand by rapid mechanisms such as the release of neurotransmitters and neuromodulators (for example GABA and adenosine , which ultimately cause vasodilation ) and on the other hand by (slower) changes in the gene expression of the cells to reduce growth factors such as hypoxia-induced factor (HIF) , erythropoietin and vascular endothelial growth factor to produce (VEGF) enhanced the tissue, for example, by stimulating increased growth of blood vessels more resistant to localized lack of oxygen.
See also
- Preconditioning (mathematics)
- Conditioning (psychology)
- Hormesis (including radiation biology)
literature
- RF Sharp et al: Hypoxic preconditioning protects against ischemic brain injury . In: The American Society for Experimental Neurotherapeutics, Inc . tape 1 , no. 1 , 2004, p. 25-36 .
- M. Weih et al: Ischemia Tolerance - Model for Research, Hope for the Clinic? In: The neurologist . tape 72 , no. 4 , 2001, p. 255-260 .
Web links
- How blood pressure cuffs protect bypass patients , Deutsches Ärzteblatt 10/2007
- Ischemic and pharmacological preconditioning of pig hearts in the working heart model ( Memento from June 10, 2007 in the Internet Archive ) Dissertation by Jens Stefan Haas, Medical Faculty of the Eberhard Karls University Tübingen