[Intraoperative cardiac arrest due to coronary vasospasm after tourniquet release--a case report].

A 55-year-old man with no past history of ischemic heart disease underwent open reduction and internal fixation of the right arm because of an open fracture. Under general anesthesia with brachial plexus block, the operation was started after the upper arm had been pressurized at 280 mmHg by tourniquet. The patient had cardiac arrest 15 min after the tourniquet release, and was resuscitated by CPR. Postoperative intracoronary infusion of acetylcholine revealed that the coronary artery is sensitive to the agent, indicating that the intraoperative cardiac arrest might have been due to coronary vasospasm. Although the similar case is rare, attention should be taken during the anesthetic management with the use of tourniquet.

The anticonvulsant action of propofol on epileptiform activity in rat hippocampal slices.

We used extracellular electrophysiological recordings from the CA1 region in rat hippocampal slices to investigate the effects of propofol on the field excitatory postsynaptic potential (fEPSP), population spike, and epileptiform activity induced by a Mg(2+)-free condition. Propofol depressed the population spike, fEPSP, and epileptiform activity. Both aminophylline, a nonselective adenosine receptor antagonist, and 8-cyclopentyl-1,3-dipropylxanthine, an A(1) receptor antagonist, significantly reduced the effect of propofol on fEPSP amplitude. However, 3,7-dimethyl-1-propagylxanthine, an A(2) receptor antagonist, did not alter the effect of propofol on fEPSP amplitude. Picrotoxin, a specific chloride channel blocker, partly reduced the effect of propofol on epileptiform activity, but bicuculline, a competitive gamma-aminobutyric acid(A) receptor antagonist, failed to antagonize it. Aminophylline significantly reduced the action of propofol on the epileptiform activity. The anticonvulsant action of propofol was partly reduced by 8-cyclopentyl-1,3-dipropylxanthine, whereas 3,7-dimethyl-1-propagylxanthine failed to affect it. Adenosine depressed the amplitude of fEPSPs in a dose-dependent manner, and propofol enhanced this inhibition. The results demonstrated that, in rat hippocampal slices, propofol inhibits epileptiform activity. In addition, adenosine neuromodulation through the A(1) receptor may contribute to the anticonvulsant action of propofol.