Tracheal Bronchus Detected During General Anesthesia: A Case Report.

A tracheal bronchus is a congenital abnormality of the tracheobronchial tree in which a displaced or accessory bronchus arises from the trachea superior to its bifurcation. We herein report a case in which a tracheal bronchus was incidentally found after induction of general anesthesia, and we discuss the potential airway management problems that may have ensued. An 80-year-old man was scheduled for buccal mucosa resection and abdominal skin grafting for treatment of squamous cell carcinoma of the left buccal mucosa. Because of trismus and anticipated airway difficulty, an awake intubation was performed under sedation. A 3-branched structure was incidentally observed at the first branching site that was supposed to be the carina. The tip of the endotracheal tube was repositioned 3 cm above the tracheal trifurcation, and the rest of the procedure proceeded uneventfully. A flexible fiberoptic scope is not used in many anesthesia cases, making the identification of such tracheal or bronchial abnormalities more difficult. Therefore, it is important to carefully check the bronchial morphology on any available chest radiographs before surgery, listen to lung sounds after intubation, and assess thoracic lung compliance without neglecting routine safety checks.

Unexpected Anesthetic Circuit Leak Attributed to Improper Use of a Tube Holder: A Case Report.

Leaks involving the anesthesia circuit can cause significant complications including hypoxia and hypoventilation. We present a case of a circuit leak caused by damage to the corrugated tubing attributed to improper use of the tube holder. A 58-year-old male was scheduled for resection of a palatal tumor under an intubated general anesthetic. After successful nasotracheal intubation, the anesthesiologist inserted the corrugated tubing of the anesthetic circuit into the tube holder. A leaking sound was heard and a tear in the corrugated tubing was promptly discovered. The corrugated tubing of the anesthetic circuit presumably tore because it was inserted into the groove of the tube holder at an inappropriate angle with excessive force. Anesthesiologists should be aware of potential leaks if the anesthesia circuit is damaged, which may be caused by improper use of tube holders.

Rapid elevation of brain-derived neurotrophic factor production in the bilateral trigeminal ganglia by unilateral transection of the mental nerve in mice.

OBJECTIVES: Previous spinal nerve injury studies have reported brain-derived neurotrophic factor (BDNF) mRNA upregulation in either the ipsilateral dorsal root ganglion (DRG) neurons or both the contralateral and ipsilateral DRG neurons from early period after peripheral nerve injury. This BDNF elevation induces hyperalgesia in the injured and/or uninjured sites, but this detailed mechanism remains unknown. This study aimed to investigate the BDNF mRNA expression in bilateral DRG neurons caused by unilateral nerve injury and to explore the possible mechanisms by which nitric oxide (NO) mediates BDNF production in the DRG, resulting in contralateral hyperalgesia. METHODS: Early changes in BDNF mRNA expression in the bilateral trigeminal ganglia, within 1 day after mental nerve transection, were examined. Additionally, the effects on BDNF production of the NO synthase inhibitor N(ω)-nitro-l-arginine methyl ester (L-NAME) were investigated in the bilateral trigeminal ganglia. The relationship between injured neurons and BDNF production in the trigeminal ganglia was then assessed using immunohistochemical and retrograde tracing methods. RESULTS: Reverse transcription-PCR analysis demonstrated that unilateral transection of the mental nerve induced a rapid elevation of BDNF mRNA expression, which was inhibited by the intracerebroventricular administration of L-NAME prior to nerve transection. This effect was observed in both the ipsilateral and contralateral sides to the nerve transection. BDNF immunostaining combined with FluoroGold retrograde tracing revealed two types of BDNF-reactive neurons, FluoroGold-labelled and non-FluoroGold-labelled neurons, in the ipsilateral and contralateral sides of the trigeminal ganglia. BDNF-positive cells were also observed in the trigeminal ganglia of other trigeminal nerve branches. CONCLUSIONS: Unilateral nerve injury upregulates BDNF production in the bilateral trigeminal ganglia by NO-mediated and/or indirect activation of afferent neurons, resulting in contralateral hyperalgesia.

Endotracheal Intubation Complicated by a Palatal Tooth in a Patient With Treacher Collins Syndrome.

We report a case of difficult endotracheal intubation in a patient with Treacher Collins syndrome. A sixteen-year-old female patient scheduled for general anesthesia had a displaced palatal tooth that interfered with laryngoscope insertion into the pharyngeal space. To address this problem, we successfully performed endotracheal intubation using a fiberscope while elevating the epiglottic vallecula using a King Vision™ video laryngoscope. A later operation was performed after tooth extraction without difficult laryngoscopy. Our experience stresses the importance of removing obstructions to laryngoscopic inspection prior to general anesthesia.

Protracted delay in taste sensation recovery after surgical lingual nerve repair: a case report.

INTRODUCTION: Lingual nerve injury is sometimes caused by dental treatment. Many kinds of treatment have been reported, but many have exhibited poor recovery. Here the authors report changes in somatosensory and chemosensory impairments during a long-term observation after lingual nerve repair. CASE PRESENTATION: A 30-year-old Japanese woman claimed dysesthesia and difficulty eating. Quantitative sensory test results indicated complete loss of sensation in the right side of her tongue. She underwent a repair surgery involving complete resection of her lingual nerve using a polyglycolic acid tube containing collagen 9 months after the injury. A year after the operation, her mechanical touch threshold recovered, but no other sensations recovered. Long-term observation of her somatosensory and chemosensory function after the nerve repair suggested that recovery of taste sensation was greatly delayed compared with that of somatosensory function. CONCLUSION: This case shows characteristic changes in somatosensory and chemosensory recoveries during 7 postoperative years and suggests that taste and thermal sensations require a very long time to recover after repair surgery.

Functional serotonin and histamine receptor subtypes in porcine ciliary artery in comparison with middle cerebral artery.

Functional serotonin (5-HT) and histamine receptor subtypes were investigated in porcine middle cerebral and ciliary arteries. An H(1) antagonist, mepyramine, antagonized histamine-induced responses with pK(B) values of 8.91-9.10. In the presence of 1 muM mepyramine, however, histamine caused dilation through H(2) receptors in the middle cerebral but not in the ciliary artery. A 5-HT(2A) antagonist, ketanserin, antagonized 5-HT-induced responses, causing rightward shifts in the concentration-response curves with pK(B) values of 8.52-8.71. A 5-HT(1B) antagonist, SB224289, produced rightward shifts of the concentration-response curves to sumatriptan with pK(B) values (6.66) only in the middle cerebral artery. In contrast, a 5-HT(1D) antagonist, BRL15572, had no effect in either artery. An RT-PCR study demonstrated the gene expression of the mRNAs of all three receptors (5HT(1B), 5HT(1D) and 5HT(2A)) in both arteries. These results suggest that histamine-induced contraction is mediated only through functional H(1) receptor in these arteries. Interestingly, there are functional 5-HT(2A) and 5-HT(1B) receptor subtypes in the middle cerebral artery, whereas the only functional receptor is 5-HT(2A) in the ciliary artery. The difference may be important for treatment with 5-HT(1B/1D) agonists (e.g. for migraine) without ocular side effect.

Potentiation by neuropeptide Y of histamine H1 receptor-mediated contraction in rat blood vessels.

Histamine-induced contraction and its potentiation by neuropeptide Y were investigated in rat blood vessels. Rat arteries and veins constricted with single concentrations of histamine dose-dependently (0.1-100 microM). This histamine-induced contraction immediately desensitized. Histamine H1 receptor antagonists, 1 microM mepyramine and 1 microM diphenhydramine, abolished this transient contraction completely, whereas cimetidine, phentolamine, reserpine and tetrodotoxin failed to inhibit the contraction. Histamine H1 receptor mRNA level by reverse transcription-polymerase chain reaction was quite parallel to histamine H1 receptor-mediated contraction, indicating that the contraction is mediated through histamine H1 receptors in the smooth muscle. Neuropeptide Y (10 nM in arteries and 3 nM in veins, respectively) significantly potentiated histamine H1 receptor-mediated contraction via neuropeptide Y1 receptors in most of rat blood vessels. Since the phospholipase C inhibitors, neomycin (1 mM) and 2-nitro-4-carboxyphenyl-N, N-diphenylcarbamate (NCDC, 10 microM), respectively, specifically abolished the potentiation, the potentiation by neuropeptide Y may depend on activation of phospholipase C.

Potentiation by neuropeptide Y of 5HT2A receptor-mediated contraction in porcine coronary artery.

Potentiation by neuropeptide Y of serotonin (5-HT)-induced vasoconstriction was investigated in porcine coronary artery. 5-HT caused concentration-dependent contraction through 5-HT2A receptors. Neuropeptide Y (30 nM) significantly increased the 5HT-induced contraction by 16+/-5% in arteries with intact endothelium. Removal of the endothelium abolished the potentiation. A neuropeptide Y1 antagonist, BIBP3226, blocked this neuropeptide Y-induced potentiation. In vessels with intact endothelium, the potentiation by neuropeptide Y was inhibited by in the presence of a cyclo-oxygenase inhibitor, indomethacin (30 microM), but not by the presence of ETA or ETB endothelin receptor antagonists or an NO synthase inhibitor, NG-nitro-L-arginine (L-NNA) (1 mM) at all. A thromboxane A2 (TXA2) synthase inhibitor, ozagrel, and prostanoid TP receptor antagonists, seratrodast and ONO-3708, also inhibited the neuropeptide Y-induced potentiation. In the endothelium-denuded arteries, a prostanoid TP receptor agonist, U-46619 (0.01-0.1 nM), potentiated 5-HT-induced contraction. These results indicate that neuropeptide Y potentiates the 5-HT-induced contraction, due to release of TXA2 from the endothelium via neuropeptide Y1 receptors, in porcine coronary artery.

Neuropeptide Y-induced contraction and its desensitization through the neuropeptide Y receptor subtype in several rat veins.

Exogenous neuropeptide Y produced marked contractions in rat isolated common jugular, brachial, and caudal veins, while it produced little or no contractions in common carotid, brachial, and caudal arteries. Neuropeptide Y (30 nM) produced larger contractions in these veins than did phenylephrine (1 microM), with maximal contractions through the neuropeptide Y receptor and the alpha1-adrenoceptor, respectively. In contrast, neuropeptide Y (30 nM) produced smaller contractions than did phenylephrine (1 microM) in the arteries. Pre-treatment with neuropeptide Y (30 nM) showed remarkable desensitization to neuropeptide Y (30 nM). This desensitization lasted for 1 h in the caudal vein or for 2 h in the common carotid and brachial veins. The neuropeptide Y-induced contraction and its desensitization probably occurred through the neuropeptide Y receptor subtype Y1, because only the neuropeptide Y receptor subtype Y1 was detected in the smooth muscle by the reverse transcriptase-polymerase chain reaction.

Leptin-induced transactivation of NPY gene promoter mediated by JAK1, JAK2 and STAT3 in the neural cell lines.

Neuropeptide Y (NPY) plays an important role in the central and sympathetic regulation of food intake and blood pressure. Although the NPY gene expression is regulated by a number of agents such as leptin, the mechanism responsible for leptin-induced regulation of the transcription of the NPY gene remains to be explored. In this study, the NPY gene promoter was transactivated by leptin in N18TG2, NG108-15 and PC12 cells which expressed the functional leptin receptor. The long isoform of leptin receptor (OB-Rb) could induce the transactivation, but the C-terminal truncated form (OB-Ra) could not. When dominant negative type of STAT3, JAK1 or JAK2 and was co-expressed, the leptin-induced transactivation was suppressed almost completely. The leptin-response element which confers NPY gene transactivation by leptin was determined in the 221-bp region of rat NPY gene promoter (-553/-335), where two STAT3-binding site-like elements (TCCAGTA) exist. These results indicated that activation of JAK1, JAK2 and STAT3 is necessary for leptin-induced transactivation of NPY gene through the leptin-response element in these neural cells.

Neuropeptide Y selectively potentiates alpha1-adrenoceptor-mediated contraction through Y1 receptor subtype in rat femoral artery.

The aim of this study was to investigate the synergism between neuropeptide Y and other vasoconstrictors (phenylephrine and serotonin) and which neuropeptide Y receptor subtype is responsible for the neuropeptide Y-induced potentiation. Exogenous neuropeptide Y (10 nM) potentiated alpha1-adrenoceptor-mediated (PE-induced) contraction in rat femoral artery permissively without its direct action, but not in the thoracic aorta. In contrast, neuropeptide Y produced no change in serotonin-induced contraction in both arteries. Increasing concentrations of neuropeptide Y caused dose-dependent potentiation of the phenylephrine-induced contraction in the femoral artery. This potentiation was blocked by a selective neuropeptide Y-Y1 receptor antagonist, BIBP3226 [(R)-N2-(diphenylacetyl)-N-[4-hydroxyphenyl)methyl]-argininamide] (1 microM). Semiquantitative reverse transcriptase polymerase chain reaction showed the selective expression of neuropeptide Y-Y1 receptor mRNA in the femoral artery. These findings indicated that the neuropeptide Y-induced selective potentiation of alpha1-adrenoceptor-mediated contraction is mediated through neuropeptide Y-Y1 receptor in rat femoral artery.

Marked neuropeptide Y-induced contractions via NPY-Y1 receptor and its desensitization in rat veins.

The aim of this study was to investigate neuropeptide Y (NPY)-induced vasoconstrictions in rat blood vessels and which NPY receptor subtype is involved in vasoconstrictions. NPY produced marked contractions in rat common jugular, brachial, portal, femoral and tail veins, and vena cava inferior, whereas it produced little or no contractions in rat common carotid, brachial, femoral and tail arteries, and thoracic and abdominal aortae. The maximal NPY-induced contractions were larger than maximal phenylephrine (PE)-induced contractions in the veins. These NPY-induced contractions were blocked by the Y1 antagonists, SRL-21, and BIBP3226 but not by the Y5 antagonist, L-152804. A Y2 agonist, NPY (13-36), did not produce contractions. RT-PCR showed that NPY-Y1 was the only receptor subtype in the veins indicating that NPY-induced contractions are mediated through the Y1 receptor. Pretreatment with NPY showed a rapid and long-lasting desensitization of these contractions. The marked NPY-induced contractions and its desensitization in the veins suggest the physiological relevance of NPY in the venous circulation.