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General anesthetics profoundly alter brain function and consciousness, yet the mechanisms underlying these effects remain incompletely understood. Although traditional studies have primarily focused on neuronal targets, accumulating evidence suggests that microglia dynamically respond to anesthetic exposure and may participate in anesthesia-associated neurophysiological changes. Beyond their established immune functions, microglia are increasingly implicated in synaptic remodeling, metabolic regulation, neuronal activity surveillance, and neuron-glia communication. Recent studies indicate that different classes of anesthetic agents modulate microglial activity through diverse and context-dependent mechanisms involving inflammatory signaling, purinergic pathways, calcium dynamics, mitochondrial metabolism, and neural circuit interactions. These responses are associated with postoperative neurocognitive disorders, altered synaptic plasticity, and anesthesia-related changes in brain states. In this review, we summarize current evidence regarding the effects of volatile anesthetics, intravenous anesthetics, and analgesics on microglial function and discuss the molecular, functional, and circuit-level mechanisms underlying anesthesia-associated neuron-microglia interactions. We further highlight the dynamic and heterogeneous nature of microglial responses during anesthesia and discuss current limitations in the field, including the lack of temporally resolved and cell-specific approaches. Understanding these processes may provide insights into anesthesia-associated neurocognitive dysfunction and support the development of neuroimmune-targeted strategies in anesthesiology.
During general anesthesia for bronchoscopy, hypoxemia is a major risk, especially in patients with a severe intrapulmonary shunt. With the technique of apnea in pure oxygen, after one hour denitrogentation, and with an intake of 50 liters of oxygen per minute through the bronchoscope, the PaO2 was greater than 400 mm of Hg, but hypercapnia and acidosis occurred. To compensate the latter, five minute sessions of apnea, alternating with two minutes of jet hyperventilation, nevertheless, have the disadvantage of producing a Ventrui phenomena at the proximal end of the bronchoscope, hence a fall in FiO2 which was dangerous in these high risk patients. The authors propose a method so that the Venturi phenomenon, which cannot be prevented, occurs in pure oxygen.
OBJECTIVES: To evaluate the effects of spinal and general anesthesia on the intraocular pressure (IOP) in patients, who had lumbar spine and lower extremity orthopedic surgeries. METHODS: Sixty adult were randomly classified into Group spinal anesthesia (SA) and Group general anesthesia (GA). The IOP, mean systemic arterial pressure, and heart rhythm were measured at 6 pre-determined timepoints (T0: Baseline, T1: Before spinal procedure or anesthesia induction, T2: After injection with intrathecal or anesthesia induction, T3: 5th minutes (min) after spinal procedure or tracheal intubation, T4: 30th min intraoperative, T5: At the end of surgery, T6: 5th min after surgery or tracheal extubation in the operation room. RESULTS: The baseline IOP and IOP1 measurements during were not significantly different between the groups (SA = 14.28 ± 0.8 mmHg; GA = 14.62 ± 0.9 mmHg, p = 0.923; and IOP1: SA = 15.83 ± 0.9 mmHg; GA = 15.88 ± 0.9 mmHg, p = 0.929). The most significant decrease in IOP in both groups was recorded at T2 (SA: 12.37 ± 0.6. GA: 12.24 ± 0.4, p < 0.001). The decrease in IOP2 was more significant in the GA group. The IOP3 was significantly higher in GA group after intubation (GA: 19.82 ± 1.2, SA: 12.86 ± 1.0)(p < 0.05). The IOP4 and IOP5 in the SA group were lower than those in the GA group. The IOP6 in both groups was higher (SA: 15.20 ± 0.8, GA: 16.50 ± 1.0) than the baseline IOP values, albeit not significant (p > 0.05). In prone position, IOP at the T4 and T5 timepoints were significantly higher than the initial values in both the SA and the GA groups; however, the increase in the GA group was more higher than that of the SA group. CONCLUSION: In intraoperative period, intraocular pressure may increase in both management of anesthesia, but this increase is higher in the general anesthesia group.
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Central and peripheral pulmonary mucociliary clearance was assessed by tantalum bronchography and serial chest roentgenograms in dogs. Thiopental, 25 mg/kg, did not change clearance from awake values. Halothane 1.2 MAC, for six hours, delayed both central and peripheral clearance by at least three hours. After halothane or diethyl ether, 1.2 MAC, for two hours, recovery of mucociliary clearance was delayed for approximately three and a half hours
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The cardiovascular responses of aortic cross-clamping and declamping with normal and high ventricular filling pressures were compared during epidural and nitrous oxide-morphine anesthesia in 32 male patients undergoing reconstructive aortic surgery. The patients were divided into four groups. Groups I and II had lumbar epidural blocks with bupivacaine and received nitrous oxide in oxygen to breathe; groups III and IV were anesthetized with morphine (2 mg/kg) and nitrous oxide. During aortic occlusion groups I and III received Ringer's lactate at a rate which maintained mean pulmonary capillary wedge pressure (PCWP) 3 to 4 torr above pre-anesthetic values whereas groups II and IV were given Ringer's lactate rates which kept PCWP similar to pre-anesthetic values. Prior to cross-clamping mean arterial blood pressure and systemic vascular resistance were lower in groups I and II than in groups III and IV but cardiac output, PCWP, and pulmonary vascular resistance were similar in the four gropus. Cross-clamping of the aorta produced no significant change in any cardiovascular variable measured in any group. Declamping did not significantly alter any variable in groups I and III but produced moderate hypotension in group IV and severe hypotension in group II as well as significant decreases in PCWP in both groups. Our data demonstrate that aortic cross-clamping and release result in little change in cardiovascular dynamics in patients anesthetized with epidural or morphine-nitrous oxide and given balanced salt solutions intravenously in amounts adequate to increase left ventricular filling pressures prior to release of the aortic cross-clamp. Our findings also indicate that hypotension can occur in patients in whom left ventricular filling pressures are maintained at normal levels prior to cross-clamp release, especially in patients given epidural anesthesia.
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