Anesthesia and analgesia
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Anesthesia and analgesia · Oct 2002
A neurosteroid anesthetic, alphaxalone, inhibits nicotinic acetylcholine receptors in cultured bovine adrenal chromaffin cells.
Several lines of evidence suggest that nicotinic acetylcholine receptors (nAChRs) are a target of general anesthetics. Alphaxalone (5alpha-pregnan-3alpha-ol-11, 20-dion) is a neurosteroid, which was used clinically for anesthesia, but its effects on the function of nAChRs have not been well investigated. We examined the effects of alphaxalone on nAChRs in cultured bovine adrenal chromaffin cells. We studied the effects of alphaxalone on nicotine-induced increases in the cytosolic Ca(2+) concentration ([Ca(2+)](i)) and on membrane currents using Ca(2+)-imaging and whole-cell patch-clamp techniques, respectively, in these cells. We also examined the effects of alphaxalone on gamma-aminobutyric acid A receptors in the same cells and compared them with the effects on nAChRs. Alphaxalone (0.1-100 micro M) inhibited nicotine-induced [Ca(2+)](i) increases in a concentration-dependent manner. Alphaxalone inhibited high K(+)-induced [Ca(2+)](i) increases, but the inhibition was observed only at 100 micro M. In voltage-clamp experiments using negative holding potentials, alphaxalone (0.1-100 micro M) itself induced inward currents, which were abolished by the gamma-aminobutyric acid A receptor antagonist picrotoxin. Alphaxalone also inhibited nicotine-induced inward currents, and the inhibition was unaffected by picrotoxin. We conclude that alphaxalone, at anesthetic concentrations, inhibits nAChRs in adrenal chromaffin cells. Alphaxalone may affect the sympathetic and other nervous systems via inhibition of nAChRs. ⋯ Alphaxalone inhibits the function of nAChRs at clinically relevant concentrations in adrenal chromaffin cells. Thus, the present findings may provide some information for understanding the anesthetic mechanism of alphaxalone.
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Anesthesia and analgesia · Oct 2002
Flumazenil recovers diaphragm muscle dysfunction caused by midazolam in dogs.
We studied the effects of flumazenil on diaphragm muscle dysfunction caused by midazolam in dogs. Animals were divided into three groups of eight each. In each group, anesthetic doses (0.1 mg/kg initial dose plus 0.5 mg. kg(-1). h(-1) maintenance dose) of midazolam were administered for 60 min. Immediately after the end of midazolam administration, Group 1 received no study drug; Group 2 was infused small-dose (0.004 mg. kg(-1). h(-1)) flumazenil; Group 3 was infused with large-dose (0.02 mg. kg(-1). h(-1)) flumazenil. We assessed diaphragm muscle function (contractility and electrical activity) by transdiaphragmatic pressure (Pdi) and integrated electrical activity of the diaphragm (Edi). After midazolam was administered in each group, Pdi at low-frequency (20-Hz) and high-frequency (100-Hz) stimulation decreased from baseline values (P < 0.05), and values of Edi at 100-Hz stimulation were less than those obtained during baseline (P < 0.05). In Group 1, Pdi and Edi to each stimulus did not change from midazolam-induced values. In Groups 2 and 3, with an infusion of flumazenil, Pdi at both stimuli and Edi at 100-Hz stimulation increased from midazolam-induced values (P < 0.05). The increase in Pdi and Edi was more in Group 3 than in Group 2 (P < 0.05). We conclude that flumazenil recovers the diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by anesthetic doses of midazolam in dogs. ⋯ In dogs, flumazenil recovers diaphragm muscle dysfunction (reduced contractility and inhibited electrical activity) caused by midazolam in a dose-related manner.
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Anesthesia and analgesia · Oct 2002
Case ReportsLaryngeal trauma during awake fiberoptic intubation.
We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients' windpipes. Airway injury occurred during the use of this technique. Although largely a safe technique, care should be exercised when anesthesiologists choose equipment and when they perform this technique.
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Anesthesia and analgesia · Oct 2002
Difficult endotracheal intubation in patients with sleep apnea syndrome.
Although sleep apnea syndrome (SAS) is common, studies assessing the anesthetic management of these patients are rare and consist mainly of case studies. We performed a retrospective case-control study to determine the incidence of difficult intubation in SAS patients and to determine the relationship between the severity of SAS and the occurrence of difficult intubation. Among 113 patients included (36 and 77 in the SAS and control groups, respectively), difficult intubation occurred more often in SAS patients than in controls (21.9% versus 2.6%, respectively; P < 0.05). No relationship was found between the severity of SAS and the occurrence of difficult intubation. Disappointingly, no single factor was associated with the occurrence of difficult intubation in SAS patients. We conclude that SAS is a risk factor for difficult intubation. ⋯ Because patients with sleep apnea syndrome have an increased risk of difficult endotracheal intubation and may present with cardiovascular disease, preoperative preventive measures should be undertaken to avoid untoward events.
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Anesthesia and analgesia · Oct 2002
Hypertonic-hyperoncotic solutions reduce the release of cardiac troponin I and s-100 after successful cardiopulmonary resuscitation in pigs.
In some patients, cardiopulmonary resuscitation (CPR) can revive spontaneous circulation (ROSC). However, neurological outcome often remains poor. Hypertonic-hyperoncotic solutions (HHS) have been shown to improve microvascular conductivity after regional and global ischemia. We investigated the effect of infusion of HHS in a porcine CPR model. Cardiac arrest was induced by ventricular fibrillation. Advanced cardiac life support was begun after 4 min of nonintervention and 1 min of basic life support. Upon ROSC, the animals randomly received 125 mL of either normal saline (placebo, n = 8) or 7.2% NaCl and 10% hydroxyethyl starch 200,000/0.5 (HHS, n = 7). Myocardial and cerebral damage were assessed by serum concentrations of cardiac troponin I and astroglial protein S-100, respectively, up to 240 min after ROSC. In all animals, the levels of cardiac troponin I and S-100 increased after ROSC (P < 0.01). This increase was significantly blunted in animals that received HHS instead of placebo. The use of HHS in the setting of CPR may provide a new option in reducing cell damage in postischemic myocardial and cerebral tissues. ⋯ Infusion of hypertonic-hyperoncotic solutions (HHS) after successful cardiopulmonary resuscitation in pigs significantly reduced the release of cardiac troponin I and cerebral protein S-100, which are sensitive and specific markers of cell damage. Treatment with HHS may provide a new option to improve the outcome of cardiopulmonary resuscitation.