Desflurane inhibits endothelium-dependent vasodilation more than sevoflurane with inhibition of endothelial nitric oxide synthase by different mechanisms.

The effects of desflurane on endothelium-dependent vasodilation remain uncertain, whereas sevoflurane is known to inhibit it. Endothelium-dependent vasodilation is mainly mediated by endothelial nitric oxide synthase. The effects of desflurane on endothelium-dependent vasodilation were compared with those of sevoflurane, and inhibition mechanisms, including phosphorylation of endothelial nitric oxide synthase and the calcium pathway, were evaluated for the two anesthetics. We hypothesized that desflurane would inhibit endothelium-dependent vasodilation in a concentration-dependent manner more than sevoflurane, with inhibition of a calcium pathway. Isolated rat aortic rings were randomly assigned to treatment with desflurane or sevoflurane for measurements of the vasodilation ratio. To determine NO production with desflurane and sevoflurane, an in vitro assay was performed with cultured bovine aortic endothelial cells. These cells were also used for measurement of intracellular calcium or Western blotting. For endothelium-dependent vasodilation, the ratio of vasodilation was more significantly inhibited by 11.4% desflurane than by 4.8% sevoflurane. Inhibition did not between 5.7% desflurane and 2.4% sevoflurane. No inhibitory effect of desflurane or sevoflurane was observed in endothelium-denuded aorta. Desflurane inhibited nitric oxide production caused by stimulation of bradykinin significantly more than sevoflurane. Desflurane had a greater suppressive effect on the bradykinin-induced increase in intracellular calcium concentration than did sevoflurane. Sevoflurane, but not desflurane, inhibited phosphorylation of the serine 1177 residue by bradykinin stimulation. Desflurane inhibited endothelium-dependent vasodilation more than sevoflurane through inhibition of a calcium pathway. Sevoflurane inhibited endothelium-dependent vasodilation by inhibition of phosphorylation of the serine 1177 residue of endothelial nitric oxide synthase.

[A Patient with Klippel-Feil Syndrome Having Difficulties in Inserting and Placing an Endotracheal Tube under General Anesthesia].

A patient with Klippel-Feil syndrome had difficulties in inserting and placing an endotracheal tube under general anesthesia. Klippel-Feil syndrome, characterized by cervical vertebral fusion, scoliosis and endocardiosis, is a rare disease. Anesthesiologists should pay attention to management of anesthesia in airway troubles. A 53-year-old woman diagnosed with Klippel-Feil syndrome was scheduled for general anesthesia with intubation. We tried to insert an endotracheal tube using McGRATH MAC, but it was difficult to insert and place the tube. Finally, we managed to insert a 5.5 mm endotracheal tube. The three-dimensional computed tomography (3D-CT) images after the operation, showed tracheal stenosis at the level of the fourth and fifth cervical vertebrae. In cases where airway difficulties are expected, evaluating 3D-CT images might be useful in airway management.

Severity of Myasthenia Gravis Influences the Relationship between Train-of-four Ratio and Twitch Tension and Run-down of Rat Endplate Potentials.

BACKGROUND: Train-of-four ratio (TOFR) is often used to evaluate muscle relaxation caused by neuromuscular-blocking agents (NMBAs). However, it is unknown whether TOFR reliably correlates with the first twitch tension (T1) in patients with myasthenia gravis (MG). By using rat models of experimental autoimmune MG (EAMG), the authors verified the hypothesis that the severity of MG influences the relationship between TOFR and T1. METHODS: EAMG rats were divided into sham, moderate MG, and severe MG groups. Isometric twitch tension of the hemidiaphragm was elicited by phrenic nerve stimulation with and without use of the NMBA rocuronium to measure TOFR and T1, and run-down of endplate potentials was estimated in the three groups. Changes around the neuromuscular junction in EAMG rats were investigated by observation of electron micrographs. RESULTS: With similar attenuation of T1, TOFR was significantly (n = 6) different among the three groups in the presence of 50% inhibitory concentrations of rocuronium (IC50). Run-down in the sham group was significantly (n = 8) greater with exposure to IC50, whereas that in the severe MG group was statistically insignificant. Width of the primary synaptic cleft in the severe MG group was significantly (n = 80) greater than that in the other groups. CONCLUSIONS: Severity of MG influences the relationship between TOFR and T1, together with changes in run-down of endplate potentials and those around the neuromuscular junction in rats. TOFR may, therefore, not be an accurate indicator of recovery from NMBAs in MG patients.

[Anesthetic management of an adult patient with Ebstein's anomaly].

Ebstein's anomaly is a rare congenital heart disease. An adult patient with Ebstein's anomaly was scheduled for Hetzer's procedure (modified tricuspid valve repair). This 36-year-old female had been diagnosed as Ebstein's anomaly and a patent foramen ovale during pregnancy, and Hetzer's repair procedure for tricuspid valve incompetence and closure of the foramen ovale were performed. The surgical techniques were chosen based on preoperative transthoracic echocardiography and intraoperative transesophageal echocardiography. During the operation, maximal attention was paid to prevent hypoxemia and paradoxical embolization. The patient's postoperative course was successful, and she was discharged from the hospital on the 14th postoperative day. Tricuspid valve regurgitation was reduced from IV to I, and New York Heart Association functional class was improved from III to I in the postoperative period. Hetzer's procedure is a useful technique for tricuspid repair of Ebstein's anomaly. Accurate morphological evaluation of the tricuspid valve by preoperative transthoracic and intraoperative transesophageal echocardiography is very important for the surgeon to plan surgery appropriately. Anesthesiologists should understand transesophageal echocardiography for congenital heart disease well.

[Three cases of ATP-induced bronchospasm during thoracic endovascular aortic repair].

We report three cases (73-year-old, 69-year-old and 76-year-old men) of bronchospasm induced by adenosine triphosphate (ATP) during thoracic endovascular aortic repair (TEVAR). Severe broncospasm occurred soon after administration of ATP to obtain transient asystole during TEVAR. All three cases were complicated with asthma or chronic obstructive pulmonary disease (COPD) before TEVAR, and airway hyper-reactivity was suspected. One case (73-year-old) required postoperative intensive care to treat bronchospasm, and the other two cases recovered during the operation. The possible mechanism of adenosine-induced bronchoconstriction is selective interaction with active mast cells with subsequent release of preformed and newly formed mediators. Careful attention should be paid when ATP is injected during TEVAR in patients with asthma or COPD.

[Ultrasound-guided subcostal and mid-axillary transverus abdominis plane block: a cadaveric study of the spread of injectate].

BACKGROUND: Mid-axillary transversus abdominis plane block (TAP-B) and subcostal TAP-B have become well-known blocks to provide considerable analgesia for abdominal surgery. However, proper approach and adequate volume of injectate have not still been clarified. In this study, a combination of mid-axillary TAP-B and subcostal TAP-B was performed in cadavers to establish the spread of injectate and segmental nerve involvement. METHODS: Ultrasound-guided dye injections (10 ml each) into the TAP were performed with mid-axillary and subcostal approaches. Injections were performed for hemiabdominal walls of 4 Thiel's embalmed human cadavers. Dye spread and nerve involvement were evaluated by dissection 10 min after the injections. RESULTS: All 7 hemiabdominal walls were successfully injected and dissected after 1 pilot study. Thoracic nerves (T7-12) and the first lumbar nerve (L1) were found. Segmental nerves T7 (14%), T8-11 (100%), T12 (71%), and L1 (43%)were involved. CONCLUSIONS: This study demonstrated that the combination of ultrasound-guided mid-axillary TAP-B and subcostal TAP-B involve T8-L1 nerves. This technique can be used not only in lower abdominal surgery but also in upper abdominal surgery.

Blockers of adenosine A1, but not muscarinic acetylcholine, receptors improve excessive extracellular glutamate-induced synaptic depression.

We investigated adenosinergic and cholinergic effects on excessive glutamate-induced depressions of central excitatory synaptic transmissions in vitro. From the CA1 region in rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) at 0.1Hz were simultaneously recorded. ANOVA was used for statistics, and p<0.05 was accepted as significant. Glutamate (10mM for 10min) completely depressed PSs and fEPSPs, which were partially recovered by the following washout for 40min (67.5±15.7% and 65.4±13.9% of the control, respectively, p<0.01, n=12). The recoveries in PSs and fEPSPs were exacerbated by edrophonium and carbamoylcholine but improved by non- and A1-selective adenosine receptor antagonists (p<0.01, n=6). The recovery in PSs, not that in fEPSPs, was exacerbated by adenosine, adenosine A1-receptor agonist and A2a-receptor antagonist (p<0.01, n=6). The effects of edrophonium were blocked by non-, M2- and M4-selective muscarinic acetylcholine receptor antagonists (p<0.01, n=6). Excessive glutamate depresses glutamatergic excitatory synaptic transmissions, which are exacerbated by muscarinic acetylcholine receptor stimulation but improved by adenosine A1 receptor block. Somatic excitability is impaired by excessive glutamate with adenosine A1 receptor stimulation.