RESUMEN
Cognitive decline is a common complication after cardiac surgery with cardiopulmonary bypass (CPB),but as such no pharmacological therapy has been shown to be efficacious in preventing the decline.However,gastrodin has been shown to have multi-pharmacological effects on neurological functions.We undertook this study to test the hypothesis that gastrodin would potentially prevent CPB-associated neurocognitive decline.We randomly assigned 200 patients undergoing mitral valve replacement surgery to receive either gastrodin (40 mg/kg) or saline after the induction of anesthesia and subsequently evaluated cognitive function before surgery,at discharge,and at 3rd month after surgery by using a battery of five neurocognitive tests,or adverse effects of gastrodin postoperatively.Neurocognitive decline in postoperative function was defined as a drop of 1 SD or more in the scores on tests of any one of the four domains of cognitive function.Cognitive decline occurred in 9％ of the patients in the gastrodin group in contrast to 42％ in the control group (P＜0.01) at discharge.Cognitive outcome could be determined at 3rd month in 87 patients in the gastrodin group and 89 in the control group.Cognitive decline was detected in 6％ in the gastrodin group and 31％ in the control group (P＜0.01).The incidences of possible adverse effects were similar between two groups.These results indicate that gastrodin is an effective and a safe drug for the prevention of neurocognitive decline in patients undergoing mitral valve replacement surgery with CPB.
RESUMEN
To explore the method of identifying nursing-related patient safety events,types,contributing factors and evaluate consequences of these events in hospitals of China,incident report program was established and implemented in 15 patient units in two teaching hospitals of China to get the relevant information.Among 2935 hospitalized patients,141 nursing-related patient safety events were reported by nurses.Theses events were categorized into 15 types.Various factors contributed to the events and the consequence varied from no harm to patient death.Most of the events were preventable.It is concluded that incident reporting can provide more information about patient safety,and establishment of a program of voluntary incident reporting in hospitals of China is not only urgent but also feasible.
RESUMEN
Isoflurane, a commonly used inhaled anesthetic, induces apoptosis in rat pheochromo-cytoma cells (PC12) in a concentration- and time-dependent manner with unknown mechanism. We hypothesized that isoflurane induced apoptosis by causing abnormal calcium release from the endo-plasmic reticulum (ER) via activation of inositol 1,4,5-trisphosphate (IP3) receptors. Alzheimer's pre-senilin-1 (PS1) mutation increased activity of IP3 receptors and therefore rendered cells vulnerable to isoflurane-induced cytotoxicity. Sevoflurane and desflurane had less ability to disrupt intraceUular calcium homeostasis and thus being less potent to cause cytotoxicity. This study examined and com- pared the cytotoxic effects of various inhaled anesthetics on PC12 cells transfected with the Alz- heimer's mutated Psi (L286V) and the disruption of intracellular calcium homeostasis. PC12 cells transfected with wild type (WT) and mutated PS1 (L286V) were treated with equivalent of 1 MAC of isoflurane, sevoflurane and desflurane for 12 h. MTT reduction and LDH release assays were per- formed to evaluate cell viability. Changes of calcium concentration in cytosolic space ([Ca2+]c) were determined after exposing different types of cells to various inhalational anesthetics. The effects of IP3 receptor antagonist xestospongin C on isoflurane-induced cytotoxicity and calcium release from the ER in L286V PC12 cells were also determined. The results showed that isoflurane at 1 MAC for 12 h induced cytoxicity in L286V but not WT PC12 cells, which was also associated with greater and faster elevation of peak [Ca2+]c in L286V than in the WT cells. Xestospongin C significantly amelio- rated isoflurane cytotoxicity in L286V cells, as well as inhibited the calcium release from the ER in L286V cells. Sevoflurane and desflurane at equivalent exposure to isoflurane did not induce similar cytotoxicity or elevation of peak [Ca2+]c in L286V PC12 cells. These results suggested that isoflurane induced cytoxicity by partially causing abnormal calcium release from the ER via activation of IP3 receptors in L286V PC12 cells. Sevoflurane and desflurane at equivalent exposure to isoflumne did not induce similar elevation of [Ca2+]c or neurotoxicity in PC12 cells transfected with the Alzheimer's PS1 mutation.