The effect of facet joint injection on lumbar spinal stenosis with radiculopathy.

OBJECTIVES: Facet Joint Injection (FJI) is known to be effective in axial back pain, but the purpose of this study was to assess the effects of FJI on patients treated with it among those with Lumbar Spinal Stenosis (LSS). METHODS: We conducted a retrospective database analysis and investigated electronic medical records of 125 LSS patients treated with FJI in the pain clinic of Chungbuk National University Hospital from November 2, 2016 to July 31, 2017. Sex, age, histories of low back surgery, complaining of neurogenic claudication, symptomatic sites of patients, FJI sites, number of sites of FJI, triamcinolone dosage, Numeric Rating Scale (NRS) before and after treatment, facet joint capsule rupture during treatment, and improvement of neurogenic claudication after treatment, were examined. RESULTS: Among 125 patients, we investigated 91 patients who met the criteria. There was significant difference in NRS before and after treatment (p<0.000). Forty one patients with reduction of NRS more than 30% after FJI were allocated to effect group. FJI was more effective in patients who did not have the surgery (p=0.044), as well as those who showed an improved neurogenic claudication after treatment (p=0.001). Other measured values did not show statistical significances. CONCLUSIONS: FJI has relatively a lower risk and is simpler in terms of techniques than other interventional treatments performed within the spinal canal. Therefore, FJI may be another interventional treatment option in patients with pain by LSS. In the future, studies for FJI indication in LSS patients should be additionally required.

Myometrial relaxation of mice via expression of two pore domain acid sensitive K(+) (TASK-2) channels.

Myometrial relaxation of mouse via expression of two-pore domain acid sensitive (TASK) channels was studied. In our previous report, we suggested that two-pore domain acid-sensing K(+) channels (TASK-2) might be one of the candidates for the regulation of uterine circular smooth muscles in mice. In this study, we tried to show the mechanisms of relaxation via TASK-2 channels in marine myometrium. Isometric contraction measurements and patch clamp technique were used to verify TASK conductance in murine myometrium. Western blot and immunehistochemical study under confocal microscopy were used to investigate molecular identity of TASK channel. In this study, we showed that TEA and 4-AP insensitive non-inactivating outward K(+) current (NIOK) may be responsible for the quiescence of murine pregnant longitudinal myometrium. The characteristics of NIOK coincided with two-pore domain acid-sensing K(+) channels (TASK-2). NIOK in the presence of K(+) channel blockers was inhibited further by TASK inhibitors such as quinidine, bupivacaine, lidocaine, and extracellular acidosis. Furthermore, oxytocin and estrogen inhibited NIOK in pregnant myometrium. When compared to non-pregnant myometrium, pregnant myometrium showed stronger inhibition of NIOK by quinidine and increased immunohistochemical expression of TASK-2. Finally, TASK-2 inhibitors induced strong myometrial contraction even in the presence of L-methionine, a known inhibitor of stretch-activated channels in the longitudinal myometrium of mouse. Activation of TASK-2 channels seems to play an essential role for relaxing uterus during pregnancy and it might be one of the alternatives for preventing preterm delivery.

Mechanism of Relaxation Via TASK-2 Channels in Uterine Circular Muscle of Mouse.

Plasma pH can be altered during pregnancy and at labor. Membrane excitability of smooth muscle including uterine muscle is suppressed by the activation of K(+) channels. Because contractility of uterine muscle is regulated by extracellular pH and humoral factors, K(+) conductance could be connected to factors regulating uterine contractility during pregnancy. Here, we showed that TASK-2 inhibitors such as quinidine, lidocaine, and extracellular acidosis produced contraction in uterine circular muscle of mouse. Furthermore, contractility was significantly increased in pregnant uterine circular muscle than that of non-pregnant muscle. These patterns were not changed even in the presence of tetraetylammonium (TEA) and 4-aminopyridine (4-AP). Finally, TASK-2 inhibitors induced strong myometrial contraction even in the presence of L-methionine, a known inhibitor of stretchactivated channels in myometrium. When compared to non-pregnant myometrium, pregnant myometrium showed increased immunohistochemical expression of TASK-2. Therefore, TASK-2, seems to play a key role during regulation of myometrial contractility in the pregnancy and provides new insight into preventing preterm delivery.

Wire-reinforced endotracheal tube fire during tracheostomy -A case report-.

Every operation could have a fire emergency, especially in the case of a tracheostomy. When a flammable gas meets a source of heat, the danger of fire is remarkable. A tracheal tube filled with a high concentration of oxygen is also a great risk factor for fire. Intra-tracheal tube fire is a rare, yet critical emergency with catastrophic consequences. Thus, numerous precautions are taken during a tracheostomy like, use of a special tube to prevent laser damage, ballooning of the tube with normal saline instead of air, and dilution of FiO(2) with helium or nitrogen. Since the first recorded cases on tube fires, most of the fires were initiated in the balloon and the tip. In the present case report, however, we came across a fire incidence, which originated from the wire.

Transient cortical blindness after heart surgery in a child patient -A case report-.

Visual loss occurring after pediatric cardiac surgery employing cardiopulmonary bypass (CPB) is relatively rare but the risk is substantial. Compromised cerebral perfusion due to a CPB related micro-embolization and inflammatory vascular changes as well as reduced oxygen carrying capacity in hemodilution and hypothermia during CPB might be major contributing factors to the development of postoperative visual loss after cardiac surgery with CPB. A case of immediate but transient postoperative visual loss was encountered in a 21-month-old male who underwent tricuspid valve surgery. Despite routine intraoperative measures to maintain an adequate perfusion pressure throughout the procedure, postoperative computed tomography revealed a subacute infarct in his occipital lobe. Recovery began on postoperative day 28, and the patient's vision was restored by 31 days.

Protective effects of gabapentin on allodynia and alpha 2 delta 1-subunit of voltage-dependent calcium channel in spinal nerve-ligated rats.

This study was designed to determine whether early gabapentin treatment has a protective analgesic effect on neuropathic pain and compared its effect to the late treatment in a rat neuropathic model, and as the potential mechanism of protective action, the alpha(2)delta(1)-subunit of the voltage-dependent calcium channel (alpha(2)delta(1)-subunit) was evaluated in both sides of the L5 dorsal root ganglia (DRG). Neuropathic pain was induced in male Sprague-Dawley rats by a surgical ligation of left L5 nerve. For the early treatment group, rats were injected with gabapentin (100 mg/kg) intraperitoneally 15 min prior to surgery and then every 24 hr during postoperative day (POD) 1-4. For the late treatment group, the same dose of gabapentin was injected every 24 hr during POD 8-12. For the control group, L5 nerve was ligated but no gabapentin was administered. In the early treatment group, the development of allodynia was delayed up to POD 10, whereas allodynia was developed on POD 2 in the control and the late treatment group (p<0.05). The alpha(2)delta(1)-subunit was up-regulated in all groups, however, there was no difference in the level of the alpha(2)delta(1)-subunit among the three groups. These results suggest that early treatment with gabapentin offers some protection against neuropathic pain but it is unlikely that this action is mediated through modulation of the alpha(2)delta(1)-subunit in DRG.

Regulation of membrane excitability by intracellular pH (pHi) changers through Ca2+-activated K+ current (BK channel) in single smooth muscle cells from rabbit basilar artery.

Employing microfluorometric system and patch clamp technique in rabbit basilar arterial myocytes, regulation mechanisms of vascular excitability were investigated by applying intracellular pH (pH(i)) changers such as sodium acetate (SA) and NH(4)Cl. Applications of caffeine produced transient phasic contractions in a reversible manner. These caffeine-induced contractions were significantly enhanced by SA and suppressed by NH(4)Cl. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was monitored in a single isolated myocyte and based the ratio of fluorescence using Fura-2 AM (R (340/380)). SA (20 mM) increased and NH(4)Cl (20 mM) decreased R (340/380) by 0.2 +/- 0.03 and 0.1 +/- 0.02, respectively, in a reversible manner. Caffeine (10 mM) transiently increased R (340/380) by 0.9 +/- 0.07, and the ratio increment was significantly enhanced by SA and suppressed by NH(4)Cl, implying that SA and NH(4)Cl may affect [Ca(2+)](i) (p < 0.05). Accordingly, we studied the effects of SA and NH(4)Cl on Ca(2+)-activated K(+) current (IK(Ca)) under patch clamp technique. Caffeine produced transient outward current at holding potential (V (h)) of 0 mV, caffeine induced transient outward K(+) current, and the spontaneous transient outward currents were significantly enhanced by SA and suppressed by NH(4)Cl. In addition, IK(Ca) was significantly increased by acidotic condition when pH(i) was lowered by altering the NH(4)Cl gradient across the cell membrane. Finally, the effects of SA and NH(4)Cl on the membrane excitability and basal tension were studied: Under current clamp mode, resting membrane potential (RMP) was -28 +/- 2.3 mV in a single cell level and was depolarized by 13 +/- 2.4 mV with 2 mM tetraethylammonium (TEA). SA hyperpolarized and NH(4)Cl depolarized RMP by 10 +/- 1.9 and 16 +/- 4.7 mV, respectively. SA-induced hyperpolarization and relaxation of basal tension was significantly inhibited by TEA. These results suggest that SA and NH(4)Cl might regulate vascular tone by altering membrane excitability through modulation of [Ca(2+)](i) and Ca(2+)-activated K channels in rabbit basilar artery.

Isoflurane preconditioning protects motor neurons from spinal cord ischemia: its dose-response effects and activation of mitochondrial adenosine triphosphate-dependent potassium channel.

We examined in a rabbit model of transient spinal cord ischemia (SCI) whether isoflurane (Iso) preconditioning induces ischemic tolerance to SCI in a dose-response manner, and whether this effect is dependent on mitochondrial adenosine triphosphate-dependent potassium (K(ATP)) channel. Eighty-six rabbits were randomly assigned to 10 groups: Control group (n=8) received no pretreatment. Ischemic preconditioning (IPC) group (n=8) received 5 min of IPC 30 min before SCI. The Iso 1, Iso 2 and Iso 3 groups (n=10, 9, 8) underwent 30 min of 1.05, 2.1 and 3.15% Iso inhalation commencing 45 min before SCI. The Iso 1HD, Iso 2HD and Iso 3HD groups (n=9, 9, 8) each received a specific mitochondrial K(ATP) channel blocker, 5-hydroxydecanoic acid (5HD, 20mg/kg), 5 min before each respective Iso inhalation. The 5HD group (n=8) received 5HD without Iso inhalation. The sham group (n=9) had no SCI. SCI was produced by infra-renal aortic occlusion via the inflated balloon of a Swan-Ganz catheter for 20 min. The Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and more viable motor nerve cells (VMNCs) in the anterior spinal cord 72 h after reperfusion than the control group (p<0.05). Iso 3 group showed a better neurologic outcome and more VMNCs than Iso 1 group (p<0.05). And, the Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and higher VMNC numbers than the corresponding Iso 1HD, Iso 2HD and Iso 3HD groups (p<0.05). This study demonstrates that Iso preconditioning protects the spinal cord against neuronal damage due to SCI in a dose-response manner via the activation of mitochondrial K(ATP) channels.

Effect of ketamine on apoptosis by energy deprivation in astroglioma cells using flow cytometry system.

Apoptosis is a programmed, physiologic mode of cell death that plays an important role in tissue homeostasis. As for the central nervous system, ischemic insults can induce pathophysiologic cascade of apoptosis in neurophils. Impairment of astrocyte functions during brain ischemia can critically influence neuron survival by neuronglia interactions. We aimed to elucidate the protective effect of ketamine on apoptosis by energy deprivation in astrocytes. Ischemic insults was induced with iodoacetate/ carbonylcyanide m-chlorophenylhydrazone (IAA/CCCP) 1.5 mM/20 microm or 150 microm/2 microm for 1 hr in the HTB-15 and CRL-1690 astrocytoma cells. Then these cells were reperfused with normal media or ketamine (0.1 mM) containing media for 1 hr or 24 hr. FITC-annexin-V staining and propidium iodide binding were determined by using flow cytometry. Cell size and granularity were measured by forward and side light scattering properties of flow cytometry system, respectively. An addition of ketamine during reperfusion increased the proportion of viable cells. Ketamine alleviated cell shrinkage and increased granularity during the early period, and ameliorated cell swelling during the late reperfusion period. Ketamine may have a valuable effect on amelioration of early and late apoptosis in the astrocytoma cells, even though the exact mechanism remains to be verified.