Because ischaemia preconditioning is a general phenomenon - it is present in almost all tissues and organs - we must look for a mechanism which involves cell types common to all organs. The hypothesis outlined below is that endothelial cells, in response to a brief ischaemic stimulus, release protective mediators which (in the heart) diffuse to cardiac myocytes to increase resistance to a subsequent ischaemic stress. These substances include nitric oxide, generated through initial bradykinin release, and prostacyclin. The evidence includes measurement of mediator release and the pharmacological attenuation of the antiarrythmic effects of preconditioning by blockade of bradykinin receptors and inhibition of nitric oxide production.
|Number of pages||16|
|Journal||Journal of Physiology and Pharmacology|
|Publication status||Published - Dec 1 1999|
- Endothelial-myocyte interactions
- Myocardial protection
- Nitric oxite
ASJC Scopus subject areas