Sevoflurane and isoflurane protect the reperfused guinea pig heart by reducing postischemic adhesion of polymorphonuclear neutrophils.
(17/1149)
BACKGROUND: Polymorphonuclear neutrophils (PMNs) contribute to reperfusion injury. Because volatile anesthetics can reduce PMN adhesion in the reperfused, nonworking heart, the authors analyzed whether this action of volatile anesthetics affects cardiac performance after ischemia and reperfusion and further clarified the underlying mechanism. METHODS: Isolated guinea pig hearts perfused with crystalloid buffer and performing pressure-volume work were used. Hearts were subjected to 15 min global ischemia and 20 min reperfusion. In the intervention groups an intracoronary bolus of 3 x 10(6) PMNs was applied in the second min of reperfusion, either in the absence or presence of 0.5 or 1 minimum alveolar concentration sevoflurane or isoflurane. The number of sequestered PMNs was calculated from the difference between coronary input and output (coronary effluent) of PMNs. Performance of external heart work, determined pre- and postischemically, served as criterion for recovery of myocardial function. Additionally, the expression of the integrin CD11b on the cell surface of PMN was measured before and after coronary passage. RESULTS: Injection of PMN in the reperfusion phase, but not under nonischemic conditions, reduced recovery of external heart work significantly (from 55+/-7% to 19+/-11%). Addition of sevoflurane or isoflurane in concentrations of 0.5 and 1 minimum alveolar concentration to the perfusate reduced postischemic PMN adhesion from 36+/-8% to basal values (20+/-7%) and prevented decline of cardiac function. CD11b expression on PMNs increased significantly during postischemic coronary passage under control conditions. Again, both anesthetics in both concentrations inhibited that activation. CONCLUSIONS: Volatile anesthetics reduce PMN adhesion in the reperfused coronary system and thereby preserve cardiac function. Reduced expression of the adhesion molecule CD11b on PMNs in the presence of sevoflurane or isoflurane is, at least in part, responsible for the cardioprotective effect. (+info)
Nasal sensory receptors responding to capsaicin, water and tactile stimuli in sevoflurane-anesthetized dogs.
(18/1149)
Responses of nasal receptors to capsaicin and water were studied from afferent recordings of the posterior nasal nerve (PNN) in 12 anesthetized dogs. Out of 12 non-respiration-modulated nasal receptors, 7 responded only to capsaicin, 3 responded to both water and capsaicin, and 2 to neither of them. All the fibers showed a rapid adaptation to mechanical probing of the nasal mucosa. These results indicate that the presence of sensory receptors responding to capsaicin and water are involved in PNN afferents of the dog. (+info)
Sevoflurane anaesthesia with an Oxford Miniature Vaporizer in vaporizer inside circle mode.
(19/1149)
Anaesthesia was induced and maintained successfully with sevoflurane using an Oxford Miniature Vaporizer (OMV) in vaporizer inside circle (VIC) mode. With continuous monitoring using the Drager Narkomed 4 machine agent analyser, the expired sevoflurane concentration was monitored and controlled easily. During induction, there was no cardiovascular depression, apnoea or coughing, but involuntary movements and breath-holding were common. (+info)
Sevoflurane requirements for tracheal intubation with and without fentanyl.
(20/1149)
We studied 80 healthy ASA 1 patients (aged 20-52 yr) to determine if fentanyl affects sevoflurane requirements for achieving 50% probability of no movement in response to laryngoscopy and tracheal intubation (MAC-TI). Patients were allocated randomly to one of four fentanyl dose groups (0, 1, 2 and 4 micrograms kg-1). Patients in each group received sevoflurane at a pre-selected end-tidal concentration according to an 'up-down' technique. After steady state sevoflurane concentration had been maintained for at least 10 min, fentanyl was administered i.v. Tracheal intubation was performed 4 min after administration of fentanyl, and patients were assessed as moving or not moving. Heart rate (HR) and mean arterial pressure (MAP) were recorded before induction of anaesthesia, just before administration of fentanyl, just before laryngoscopy for intubation, and after intubation. The MAC-TI of sevoflurane was 3.55% (95% confidence intervals 3.32-3.78%), and this was reduced markedly to 2.07%, 1.45% and 1.37% by addition of fentanyl 1, 2 and 4 micrograms kg-1, with no significant difference in the reduction between 2 and 4 micrograms kg-1, showing a ceiling effect. Fentanyl attenuated haemodynamic responses (HR and MAP) to tracheal intubation in a dose-dependent manner, even with decreasing concomitant sevoflurane concentration. Fentanyl 4 micrograms kg-1 suppressed the changes in HR and MAP more effectively than fentanyl 1 or 2 micrograms kg-1 at sevoflurane concentrations close to MAC-TI. (+info)
Huntington's disease: review and anesthetic case management.
(21/1149)
Huntington's disease is a dominantly inherited progressive autosomal disease that affects the basal ganglia. Symptoms appear later in life and manifest as progressive mental deterioration and involuntary choreiform movements. Patients with Huntington's disease develop a progressive but variable dementia. Dysphagia, the most significant related motor symptom, hinders nutrition intake and places the patient at risk for aspiration. The combination of involuntary choreoathetoid movements, depression, and apathy leads to cachexia. Factors of considerable concern to the anesthesiologist who treats patients with Huntington's disease may include how to treat frail elderly people incapable of cooperation, how to treat patients suffering from malnourishment, and how to treat patients with an increased risk for aspiration or exaggerated responses to sodium thiopental and succinylcholine. The successful anesthetic management of a 65-yr-old woman with Huntington's disease who presented for full-mouth extractions is described. (+info)
Additive contribution of nitrous oxide to sevoflurane minimum alveolar concentration for tracheal intubation in children.
(22/1149)
BACKGROUND: To study the interaction between nitrous oxide and sevoflurane during trachea intubation, the authors determined the minimum alveolar concentration of sevoflurane for tracheal intubation (MAC(TI)) with and without nitrous oxide in children. METHODS: Seventy-two children aged 1-7 yr were assigned randomly to receive one of three end-tidal concentrations of nitrous oxide and one of four end-tidal concentrations of sevoflurane: 0% nitrous oxide with 2.0, 2.5, 3.0, or 3.5% sevoflurane: 33% nitrous oxide with 1.5, 2.0, 2.5, or 3.0% sevoflurane; or 66% nitrous oxide with 1.0, 1.5, 2.0, or 2.5% sevoflurane. After steady state end-tidal anesthetic concentrations were maintained for at least 10 min, laryngoscopy and intubation were attempted using a straight-blade laryngoscope and an uncuffed tracheal tube. The interaction between nitrous oxide and sevoflurane was investigated using logistic regression analysis of the responses to intubation. RESULTS: Logistic regression curves of the probability of no movement in response to intubation in the presence of sevoflurane and 0, 33, and 66% nitrous oxide were parallel. The interaction coefficient between nitrous oxide and sevoflurane did not differ significantly from zero (P = 0.89) and was removed from the logistic model. The MAC(TI) (+/- SE) of sevoflurane was 2.66+/-0.16%, and the concentration of sevoflurane required to prevent movement in 95% of children was 3.54+/-0.25%. Thirty-three percent and 66% nitrous oxide decreased the MAC(TI) of sevoflurane by 18% and 40% (P<0.001), respectively. CONCLUSIONS: We conclude that nitrous oxide and sevoflurane suppress the responses to tracheal intubation in a linear and additive fashion in children. (+info)
Direct cerebral vasodilatory effects of sevoflurane and isoflurane.
(23/1149)
BACKGROUND: The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. METHODS: Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. RESULTS: Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. CONCLUSIONS: In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane. (+info)
Sevoflurane mimics ischemic preconditioning effects on coronary flow and nitric oxide release in isolated hearts.
(24/1149)
BACKGROUND: Like ischemic preconditioning, certain volatile anesthetics have been shown to reduce the magnitude of ischemia/ reperfusion injury via activation of K+ adenosine triphosphate (ATP)-sensitive (K(ATP)) channels. The purpose of this study was (1) to determine if ischemic preconditioning (IPC) and sevoflurane preconditioning (SPC) increase nitric oxide release and improve coronary vascular function, as well as mechanical and electrical function, if given for only brief intervals before global ischemia of isolated hearts; and (2) to determine if K(ATP) channel antagonism by glibenclamide (GLB) blunts the cardioprotective effects of IPC and SPC. METHODS: Guinea pig hearts were isolated and perfused with Krebs-Ringer's solution at 55 mm Hg and randomly assigned to one of seven groups: (1) two 2-min total coronary occlusions (preconditioning, IPC) interspersed with 5 min of normal perfusion; (2) two 2-min occlusions interspersed with 5 min of perfusion while perfusing with GLB (IPC+GLB); (3) SPC (3.5%) for two 2-min periods; (4) SPC+GLB for two 2-min periods; (5) no treatment before ischemia (control [CON]); (6) CON+GLB; and (7) no ischemia (time control). Six minutes after ending IPC or SPC, hearts of ischemic groups were subjected to 30 min of global ischemia and 75 min of reperfusion. Left-ventricular pressure, coronary flow, and effluent NO concentration ([NO]) were measured. Flow and NO responses to bradykinin, and nitroprusside were tested 20-30 min before ischemia or drug treatment and 30-40 min after reperfusion. RESULTS: After ischemia, compared with before (percentage change), left-ventricular pressure and coronary flow, respectively, recovered to a greater extent (P<0.05) after IPC (42%, 77%), and treatment with SPC (45%, 76%) than after CON (30%, 65%), IPC+GLB (24%, 64%), SPC+GLB (20%, 65%), and CON+GLB (28%, 64%). Bradykinin and nitroprusside increased [NO] by 30+/-5 (means +/- SEM) and 29+/-4 nM, respectively, averaged for all groups before ischemia. [NO] increased by 26+/-6 and 27+/-7 nM, respectively, in SPC and IPC groups after ischemia, compared with an average [NO] increase of 8+/-5 nM (P<0.01) after ischemia in CON and each of the three GLB groups. Flow increases to bradykinin and nitroprusside were also greater after SPC and IPC. CONCLUSIONS: Preconditioning with sevoflurane, like IPC, improves not only postischemic contractility, but also basal flow, bradykinin and nitroprusside-induced increases in flow, and effluent [NO] in isolated hearts. The protective effects of both SPC and IPC are reversed by K(ATP) channel antagonism. (+info)