High spinal anesthesia does not alter experimental myocardial infarction size or ischemic preconditioning.

Objective: The role of the central nervous system in the development of myocardial infarction and ventricular fibrillation in virgin and ischemically preconditioned myocardium was investigated.

Design: Infarct size and ventricular arrhythmias were assessed after regional ischemia-reperfusion. Animals were randomly assigned to four groups: (1) preconditioned, central nervous system intact; (2) nonpreconditioned, nervous system intact; (3) preconditioned, nervous system blocked; and (4) nonpreconditioned, nervous system blocked.

Adrenergic activation confers cardioprotection mediated by adenosine, but is not required for ischemic preconditioning.

Background: The aim of this study was to determine whether (1) adrenergic activation is cardioprotective, (2) adrenergic cardioprotection occurs via adenosine receptor activation, and (3) ischemic preconditioning requires alpha-adrenergic activation.

Methods: Anesthetised open chest rabbits underwent 30 min coronary occlusion and 3 h reperfusion. Ischemic preconditioning was elicited with 5 min coronary occlusion and 10 min reperfusion.

Dichloroacetate reduces plasma lactate levels but does not reduce infarct size in rabbit myocardium.

Dichloroacetate (DCA), an activator of pyruvate dehydrogenase (PDHC), enhances postischemic mechanical recovery of isolated hearts. It is not known whether this is secondary to reduced infarction or preservation of contractile function in viable cardiomyocytes. This study investigated the effect of DCA on myocardial infarct size.

Anaesthetics alter the magnitude of infarct limitation by ischaemic preconditioning.

Objective: The aim was to determine whether three commonly used animal anaesthetics alter the magnitude of infarct limitation achieved with ischaemic preconditioning.

Methods: Eighty four anaesthetised non-preconditioned and preconditioned open chest rabbits underwent a 30 min coronary occlusion followed by 3 h reperfusion. Ischaemic preconditioning was achieved with 5 min coronary occlusion beginning 15 min before the 30 min coronary occlusion.

Mid-latency auditory evoked potentials and circulatory response to loud sounds.

We investigated in 60 patients scheduled for elective aorto-coronary bypass grafting if loud sounds by themselves can induce cardiovascular responses and if these could be related to mid-latency auditory evoked potentials (MLAEP). Anaesthesia was induced in group I (n = 20) with flunitrazepam-fentanyl 0.01 mg kg-1 and maintained with flunitrazepam-fentanyl 1.