Health Worlds

1, intravenous anesthetics and memory dysfunction caused by? Mechanism? Duration?
Postoperative cognitive dysfunction (post-operative cognitive dysfunction, POCD) after anesthesia is learning (learning) and memory function, executive function, attention and language dysfunction, disorders and other mental performance. Common in older patients. Data show that 60 patients over the age of 1 week after non-cardiac major surgery, POCD incidence of 25.8%, 3 months, 9.9%; aortic aneurysm surgery was 46%, open heart surgery 7 % to 77%, 50% of liver and lung transplant, orthopedic surgery up to 13% to 41%, upper abdominal surgery was 7% to 17% [6]. The etiology and pathogenesis of POCD is not clear. Previous studies suggest a number of possible factors associated with POCD, including age, preoperative complications, and brain function, and perioperative medication (benzodiazepine class of anticholinergic drugs), intraoperative events, postoperative complications and so on. Because the content of cognitive function included a wide, is only in respect of which the most important learning and memory to do one described.
Common intravenous anesthetics such as propofol anesthesia can harm learning and memory. At present, the production of narcotic drugs inhibit brain function would have been an indisputable fact. Learning and memory (memory and learning) is one of the advanced features of the brain, has been one of the hot spots. The field of anesthesia considerable experimental


and clinical studies, narcotic drugs such as intravenous anesthetics ketamine (Ketamine), midazolam, etomidate (Etomidate), inhaled anesthetics propofol and NO2, isoflurane (Isoflurane) , sevoflurane (Sevoflurane), desflurane (Desflurane) Dengjun can cause memory impairment, the mechanism through various means (including receptors, proteins, signal transduction, etc.) is finally shown inhibition of hippocampal (Hippocampus) long slices LTP (Long-term potentiation, LTP) formation. Which midazolam hippocampus, mainly through increased energy -aminobutyric acid (GABAA receptor-mediated) neuronal function, thereby inhibiting the formation of LTP [7,8]; Spahr so that propofol can reduce the cultured nerve cells of GABA neurons, long-term use also contribute to glial cell death, low-dose propofol can destroy the coordination of synaptic transmission, inhibition of LTP maintenance. Memory of information maintained by the length of time can be divided into transient memory (0.25 ~ 2s), short-term memory (number min), long-term memory (number of min ~ number of h) and permanent memory (lifetime). Forgetting (loss of memory) is the partial or complete loss of the ability to recall and recognition, short-term memory and its essence is the transition to the long-term memory disorder. Clinically, the forgotten into anterograde amnesia (anterograde amnesia) and retrograde amnesia (retrograde amnesia). A number of important degenerative brain diseases such as Alzheimer disease on the performance of short-term memory is not impaired, but long-term memory disorder. Therefore, the research on the long-term memory is more important. In certain doses, midazolam and propofol could produce anterograde amnesia, both short-term memory is no effect on the expense of long-term memory of the drug.
Anesthetic dose relationship with learning and memory is complex, not generally believed that the greater the dose, the longer the administration of learning and memory to large. Studies have shown that different anesthetic drugs (including barbiturates, benzodiazepines class, caffeine, cocaine, etc.), different doses (low, medium, high) and duration (eg, long-term tolerance of repeated drug use (long- term tolerance) and single-dose lead to short-term discomfort (short-term tolerance)), can cause memory impairment or enhancing memory. Anesthetics on learning and memory with its depth of anesthesia or sedation is not proportional to the benzodiazepines, such as drugs, in the light level of sedation can cause learning and memory; Some studies suggest that propofol sedation has nothing to do with the forgotten role of ; also found that different drugs produce the same level of sedation, memory impairment caused by the extent of it is different.
2: cerebral hypoxia caused by metabolic dysfunction, cognitive dysfunction after? Pathophysiology?
Hypoxia did not cause any cognitive impairment studies conducted, but according to neurological data, which may directly damage the central neurons. Hypoxia causes inhibition of neuronal function may be the cause of cognitive impairment produced. Recently, cognitive dysfunction after subarachnoid hemorrhage in the study, but also Alzheimer's disease-related cognitive impairment on the pathogenesis of amyloid toxic effect on the central nervous system is one of the metabolism of nerve cells caused by This push and, hypoxia may also cause problems with metabolism of the neurons, but reversible and irreversible problems.
3: general , as the patient oxygen is not long, after 2 days there have been improvement in symptoms, it is estimated that the problem is not big! To talk about their point of
In this connection, children, analyzed in two major areas: First, intravenous anesthetics on memory; the second is caused by cerebral hypoxia cerebral metabolic disorders; may be the cause of a certain kind of interaction of two reasons or results.
1, the role of general anesthesia:
Cerebral cortex, hypothalamus, and the network of brain structures involved in forebrain structures including the formation of consciousness. Speculated that general anesthetics may be the first selective integration of the brain (such as EEG synchronization system, a special neural network, etc.) lost and then interference cortex - hypothalamic system, namely the anesthesia drug-induced loss of consciousness may ultimately through inhibition of the hypothalamus and midbrain functions can be realized. Of course, other parts of the spinal cord to the brain, such as support for upstream traffic is also involved in the regulation of general anesthesia drugs on the impact of the state of consciousness. But there are also that the state of consciousness and the entire central nervous system signal transduction network integration activities, such as synchronization between neurons activity, neural oscillations, adaptive resonance, awareness of the disappearance of anesthesia drugs on the inhibition of such integration activities or blocking of the results, with a particular group of nerve cells, or anatomical structure has nothing to do.
General anesthetics on memory mainly as anterograde amnesia (of transient or short-term memory and declarative memory), in which the prefrontal cortex, the top of the cortex and other regions may produce sedation and amnesia are the important parts, but contains the complex mechanisms of memory disturbances, including: (1) improve the perception threshold intensity decreased to input information; (2) interfere with nerve conduction and reduce the amount of information to reach the central cortex; (3) curing interference information so that short-term memory can not be converted to long-term memory , which was quickly forgotten; (4) interfere with memories of leaving the existing mechanisms of information can not be output. A variety of general anesthetics on memory there are also significant differences in explicit memory of the anesthesia drug sensitivity than implicit memory, suggesting that anesthesia drugs on the mechanism and the two sites are not the same.
Propofol
The suppression of hypoxia induced intracellular (Na Ca) increased, on hypoxic injury of hippocampal CA1 neurons has a protective effect.
The neuroprotective effect of propofol to a large extent through the GABA receptor. Direct activation of GABA receptors, strengthening the role of GABA, directly activate the receptor in a site, the enhancement occurred at different sites. At the same time, propofol has antioxidant, inhibiting lipid peroxidation. Propofol by protecting the NHE1 (Na-H exchanger) in order to maintain the activity of oxidative stress in glial cells during glutamate uptake capacity.
Ketamine
Ketamine is a NMDA receptor antagonist. Acting on NMDA receptors linked to ion channels, inhibition of Na and Ca influx, so non-competitive NMDA antagonist, such as glutamate receptor agonists. Chlorine
NMDA receptor ammonia and ketones. Glutamate after cerebral ischemia-mediated nerve injury may provide therapeutic effects. And other anesthetics on the inhibitory effect of different central nervous system, ketamine increased cerebral metabolic rate, followed by increase in local glucose utilization, cerebral blood volume and CSF pressure.
Intravenous anesthetic ketamine and propofol can inhibit glutamate-induced neuronal apoptosis in PC12 cells and thus play a neuroprotective role. PC12 cells play a neuroprotective role. the event of disruption of blood flow in brain tissue, in the 6 ~ 7s oxygen that can be used within the depletion;
PaO2 fell 4kPa (30mmHg) below the threshold in the power failure that caused loss of consciousness, EEG slow wave converted from the flat line.
cells required for active transport and biological synthesis of creatine phosphate (PCr) and adenosine triphosphate (ATP) of the storage time at 1min and 2min exhausted.
energy reaction to a complete standstill when about 5min.
ion transfer:
Phase 1: initial cerebral ischemia 1. 5 ~ 2. 0min. Extracellular K slowly increased to 10 ~ 15mmol / L, Na, Ca2, Cl-constant or rose slightly.
Phase 2: (reserve equivalent to PCr and ATP depletion). Extracellular fluid (ECF) of K rapidly increased to 60mmol / L, Na, Ca2, Cl-enter the cell, its concentration decreased quickly, with the ion transfer due to H2O, resulting in extracellular fluid volume reduction of 50% to result in control cells the edema.
The above is due to membrane Na-K-ATP pump failure enzymes, ion channels open door and a sudden increase in membrane permeability consequent results.
acid-base imbalance:
Ischemia due to hypoxia induced an increase in anaerobic glycolysis and lactic acid formation, 5s intracellular lactate concentration began to increase, 60s straight up inside, 90s when you can reach 8umol / g, so not only the cell [H] increased also increased cell swelling. Cerebral blood flow because of no retreat in the state, H is in full bloom HCO3-buffered CO2 retention in the cell Erzhi PCO2 increased significantly lower intracellular pH. Therefore, cerebral ischemia is the essence of metabolic acidosis, CPR was buffered when the performance of respiratory acidosis.

Individuals tend to narcotic drugs on inhibition of brain function, and then hypoxic brain metabolic disorders lead to prolonged recovery time in brain functions.
Personally think that there is no secondary injury in children (known as reperfusion injury or re-oxygenation injury): because there is no stop cycle.
Cerebral edema: cytotoxic and vasogenic including two mechanisms. The former aly started during the ischemia, an intracellular edema in the reperfusion period may continue to increase; the latter secondary to reperfusion, the main phase with a number of blood damage and endogenous factors (including the transmitter and the media, etc.) vascular endothelial cell injury. So I ask you:
(1), did not stop the cycle if the patient is not brain edema should not it?
(2), in the event of short-term hypoxia, as usual there will be brain metabolic disorders, but in general anesthesia, the intravenous anesthetics have a protective role of the brain, the cerebral metabolism will slow down in disturbance of the time?


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