Induction of anesthesia with propofol decreased blood pressure, entropy, and HF in a BIS-dependent manner, indicating that propofol reduces cardiac parasympathetic tone depending on the depth of hypnosis. Conversely, sevoflurane did not show the BIS-dependent decreases in heart rate, blood pressure, HF, and entropy, indicating that sevoflurane has little or no effect on cardiac parasympathetic tone.

P Pu ur rp po os se e: : Beta blockers are thought to exert beneficial effects on the ischemic heart. The authors examined the effects of landiolol (ONO 1101), a highly selective ß1 antagonist, propranolol, a nonspecific ß blocker, and esmolol, a selective ß1 antagonist, on postischemic contractile recovery. Drugs were given prophylactically.M Me et th ho od ds s: : Ischemia-reperfusion in isolated guinea pig hearts was induced by stopping the perfusion for 45 min and reperfusing for 60 min. Hearts (n = 7 in each group) were treated with or without propranolol (1 or 10 µM), esmolol (5 or 50 µM), or landiolol (20, 100 or 500 µM) ten minutes before inducing ischemia.R Re es su ul lt ts s: : At the end of reperfusion, left ventricular pressure (LVP) recovered to 64 ± 3% of the baseline value in the control group. With 1 and 10 µM propranolol, LVP recovered to 90 ± 5% and 100 ± 6% of the baseline value at 60 min after reperfusion, respectively. Fifty µM but not 5 µM of esmolol resulted in restoration of LVP to 97 ± 17% of the pre-ischemic value at 60 min after reperfusion. In hearts pretreated with 100 and 500 µM landiolol, LVP was restored to 109 ± 5% and 104 ± 5% of the baseline value, respectively. Landiolol 100 µM did not depress LVP in the pre-ischemic period.C Co on nc cl lu us si io on ns s: : The present study shows that landiolol, an ultrashort-acting cardioselective ß1 blocker, has cardioprotective effects on ischemia-reperfusion injury in isolated guinea pig hearts. All three ß blockers were equally protective but the intermediate dosage of landiolol preserved LVP during the pre-ischemic period. Objectif Méthode : L'ischémie-reperfusion a été induite dans des coeurs de cobaye isolés en stoppant la perfusion pendant 45 min et en reperfusant pendant 60 min. Les coeurs (n = 7 dans chaque groupe) ont été traités avec ou sans propranolol (1 ou 10 µM), esmolol (5 ou 50 µM) ou landiolol (20, 100 ou 500 µM) dix minutes avant l'induction de l'ischémie. Résultats

Important information may not be obtained if the pulse oximetry signal is lost during inflation of a cuff for blood pressure measurement, particularly in patients with hemodynamic instability. In the present study, we compared the failure times of pulse oximeters during cuff-induced hypoperfusion in volunteers. A pulse oximeter sensor was attached to the index finger, and a blood pressure cuff was attached to the same arm of each volunteer. MasimoSET Radical (Masimo), Nellcor N-395 (N-395), Nellcor N-20PA, and Nellcor D-25 were tested. To evaluate the failure time of each pulse oximeter, time to peak of cuff pressure, time to loss of signal, time to recovery of signal, and failure interval were measured. All measurements were performed three times for each pulse oximeter and were averaged. There were no differences in hemodynamic measurements among the groups. Time to loss of signal was longer in Masimo than the other pulse oximeters. Masimo and N-395 showed significantly shorter times to recovery of signal than those of the other two pulse oximeters. Failure interval was in the order of Masimo << N-395 < Nellcor D-25 = Nellcor N-20PA. Masimo did not lose a signal as rapidly as the other oximeters studied. Masimo was similar in performance to the N-395 at providing useful data sooner than conventional technology after a loss of the signal. These observations suggest that data will be more available with fewer false-positive alarms when using the Masimo oximeter followed by the N-395 when compared with conventional oximeters.

Recent clinical neuroimaging studies have suggested that morphological brain changes occur and progress in the course of schizophrenia. Although the neurogenetic and neurotrophic effects of antipsychotics are considered to contribute to the prevention of reduction in brain volume, the cellular molecular mechanisms of action of antipsychotics have not yet been elucidated. We examined the effects of antipsychotics on the endoplasmic reticulum (ER) stress-induced damages of neurons and neural stem cells (NSCs) using cultured cells. In the neuronal cultures, the atypical antipsychotic olanzapine protected neurons from thapsigargin (1 microM)-induced injury. It was observed that a low concentration of thapsigargin (10 nM) that did not affect the neuronal survival could reduce neuronal differentiation of cultured NSCs, suggesting a role of ER stress in the differentiation function of NSCs. Treatment with olanzapine increased the neuronal differentiation suppressed by the exposure to thapsigargin (10 nM). The thapsigargin-induced ER chaperones, GRP78, which indicate the ER stress condition of the cell, were decreased by the treatment with the atypical antipsychotics olanzapine and quetiapine but not by the typical antipsychotic haloperidol. These results indicate that the amelioration of ER-stress might be involved in the cellular mechanisms of atypical antipsychotics to produce neuroprotective and neurogenetic actions in neurons and NSCs, suggesting potential roles of these drugs for treatment of schizophrenia.

Induction of anaesthesia with thiopental increased heart rate and decreased high frequency, entropy and low frequency in a BIS-dependent manner, indicating that thiopental reduces cardiac parasympathetic tone depending on the depth of hypnosis.