The mechanism of beta-adrenergic preconditioning: roles for adenosine and ROS during triggering and mediation.

The aim of this study was to investigate the mechanism of beta-adrenergic preconditioning (BPC). The roles of adenosine and its receptor subtypes, the generation of oxygen free radicals (ROS) and activation of the K(ATP) channels as well as the phosphoinositide-3-kinase (PI(3)K)/PKB/Akt and extracellular signal-regulated kinase (ERK) signal transduction pathways during the triggering and mediation phases were evaluated. Using the isolated working rat heart, BPC was elicited by administration of denopamine (beta1 adrenergic receptor agonist, 10(-7) M), isoproterenol (beta1/beta2 adrenergic receptor agonist, 10(-7) M) or formoterol (beta2 adrenergic receptor agonist, 10(-9) M) for 5 min followed by 5 min washout.

The role of β-adrenergic receptors in the cardioprotective effects of beta-preconditioning (βPC).

Aim: To determine the mechanism whereby transient stimulation of the β-adrenergic receptor subtypes (β-AR) elicit cardioprotection against subsequent ischaemia.

Methods: Isolated rat hearts were subjected to 35 min regional ischaemia (RI) and reperfusion and infarct size (IS) determined. Hearts were preconditioned with 5 min isoproterenol (β1/β2-AR agonist), denopamine (β1-AR agonist), formoterol hemifumarate (β2-AR agonist) or BRL37344 (β3-AR agonist) and 5 min reperfusion.

Bilateral ostial coronary stenosis and rheumatic aortic valve stenosis.

A 49-year-old patient presented with angina pectoris and clinical findings of aortic valve stenosis and regurgitation. Rheumatic aortic valve stenosis and regurgitation was diagnosed on echocardiography. Coronary angiography findings showed severe calcification in the aorta root with right coronary ostial occlusion, and were suggestive of left main ostial stenosis and proximal main stem stenosis, which was confirmed on CT angiography.

Inhibition of myocardial apoptosis by ischaemic and beta-adrenergic preconditioning is dependent on p38 MAPK.

Introduction: Apoptosis occurring during ischaemia /reperfusion contributes independently to tissue damage, and involves activation of the stress-kinase, p38 MAPK during reperfusion. Ischaemic preconditioning (IPC) protects against ischaemia/reperfusion mediated necrosis and apoptosis. The role of p38 MAPK in the protective effect of preconditioning against apoptosis is unknown.