Repeated preconditioning with hyperbaric oxygen induces neuroprotection against forebrain ischemia via suppression of p38 mitogen activated protein kinase.

We previously reported in rats that preconditioning with hyperbaric oxygen (HBO; 100% O(2) 3.5-atomsphere absolute (ATA), 1 h/day for 5 days) provided neuroprotection against transient (8 min) forebrain ischemia possibly through protein synthesis relevant to neurotrophin receptor and inflammatory-immune system. A recent report suggested that HBO-induced neuroprotection is relevant to brain derived neurotrophic factor and its downstream event involving suppression of p38 mitogen activated protein kinase (p38) activation.

[Anesthetic management for electroconvulsive therapy in the patients with a history of neuroleptic malignant syndrome].

We report three patients with a history of neuroleptic malignant syndrome for whom modified electroconvulsive therapy (m-ECT) was scheduled. Two patients suffered from schizophrenia, and one suffered from depression. Their symptoms, such as hyperthermia, consciousness disturbance, myotonus, tremor, sweating, and tachycardia, improved gradually with administration of dantrolene and fluid infusion.

Neutrophil elastase inhibitor attenuates hippocampal neuronal damage after transient forebrain ischemia in rats.

Inflammatory responses have been known to contribute to the development of neuronal damage after brain ischemia in experimental animals. Also, neutrophil elastase activity in the plasma has been elevated in the patients with acute cerebral infarction. In order to clarify whether neutrophil elastase distributes into the brain parenchyma and exacerbates neuronal damage following ischemia, we examined the effects of specific neutrophil elastase inhibitor, ONO-5046, on hippocampal CA1 neuronal death in relation to neutrophil elastase activity in the plasma and its distribution in the brain and to caspase-3/7 activity.

The temporal profile of genomic responses and protein synthesis in ischemic tolerance of the rat brain induced by repeated hyperbaric oxygen.

Repeated hyperbaric oxygen (HBO) exposure prior to ischemia has been reported to provide neuroprotection against ischemic brain injury. The present study examined the time course of neuroprotection of HBO (3.5 atmosphere absolute, 100% oxygen, 1 h for 5 consecutive days) and the changes of gene/protein expression in rats.

Target-controlled infusion of propofol for a patient with myotonic dystrophy.

We present a patient with myotonic dystrophy (MD) who was anesthetized with propofol using a target-controlled technique for electrophysiologic examination and cardiac catheter ablation. The patient became apneic unexpectedly at the same time when he fell asleep, with effect-site propofol concentration of 1.6 microg ml(-1).

The nerve root entry zone is highly vulnerable to intrathecal tetracaine in rabbits.

It has been speculated that the nerve root entry zone in the spinal cord, known as the Obersteiner-Redlich zone, may be more sensitive to large concentrations of local anesthetics administered intrathecally. However, there has been no morphological evidence for this. In the present study, we examined morphological changes of nerve fibers at the nerve root entry zone after administration of intrathecal tetracaine in rabbits.