Activated human mesenchymal stem/stromal cells suppress metastatic features of MDA-MB-231 cells by secreting IFN-ß.

Our recent study showed that human mesenchymal stem/stromal cells (hMSCs) are activated to express tumor necrosis factor (TNF)-α-related apoptosis-inducing ligand (TRAIL) by exposure to TNF-α and these activated hMSCs effectively induce apoptosis in triple-negative breast cancer MDA-MB-231 (MDA) cells in vitro and in vivo. Here, we further demonstrated that activated hMSCs not only induced apoptosis of MDA cells but also reduced metastatic features in MDA cells. These activated hMSC-exposed MDA cells showed reduced tumorigenicity and suppressed formation of lung metastasis when implanted in the mammary fat pad. Surprisingly, the activated hMSC-exposed MDA cells increased TRAIL expression, resulting in apoptosis in MDA cells. Interestingly, upregulation of TRAIL in MDA cells was mediated by interferon-beta (IFN-ß) secreted from activated hMSCs. Furthermore, IFN-ß in activated hMSCs was induced by RNA and DNA released from apoptotic MDA cells in absent in melanoma 2 (AIM2) and IFN induced with helicase C domain 1 (IFIH1)-dependent manners. These observations were only seen in the TRAIL-sensitive breast cancer cell lines but not in the TRAIL-resistant breast cancer cell lines. Consistent with these results, Kaplan-Meier survival analysis also showed that lack of innate sensors detecting DNA or RNA is strongly associated with poor survival in estrogen receptor-negative breast cancer patients. In addition, cancer-associated fibroblasts (CAF) isolated from a breast cancer patient were also able to express TRAIL and IFN-ß upon DNA and RNA stimulation. Therefore, our results suggest that the crosstalk between TRAIL-sensitive cancer cells and stromal cells creates a tumor-suppressive microenvironment and further provide a novel therapeutic approach to target stromal cells within cancer microenvironment for TRAIL sensitive cancer treatment.

Spike-monitoring of anaesthesia for corpus callosotomy using bilateral bispectral index.

During corpus callosotomy for intractable epilepsy, the electrocorticogram is commonly recorded from electrodes placed on the brain surface to monitor of epileptic activity and assess the synchronisation of epileptic signals between the left and the right hemispheres. We evaluated the usefulness of bilateral bispectral index monitoring using two monitors and two sensors placed above the frontal region. Spikes were readily detected on the electroencephalogram on the bispectral index monitor, and the frequency of their occurrence increased or decreased in response to adjustment of the sevoflurane concentration. The disappearance of synchronisation between the left and the right hemispheres was observed with use of the bispectral index - in concordance with the electrocorticogram. Thus, 'spike-monitoring anaesthesia' using bilateral bispectral index was useful in assessing both the effect of anaesthetics on the electroencephalogram signals and the surgical therapeutic effect.

[Studies on surfactant replacement therapy in pediatric measles pneumonitis].

Measles pneumonitis, as well as encephalitis, is the most important complication associated with mortality in measles. Many medications including steroids and vitamin A have been applied to pediatric measles pneumonitis. However, the efficacy of such medication has not yet been established. This study is aimed at evaluating the effectiveness of surfactant replacement therapy in pediatric measles pneumonitis. Five patients (aged 1-2 years) with measles pneumonitis were transferred to our emergency center. On the transferred day, Surfactant-TA was administered by intratracheal method. After administration of surfactant, PaO2/FIO2 increased from 63.6 +/- 11.0 (mean +/- SE) to 206.2 +/- 54.1 in an hour and to 163.8 +/- 34.8 in 24. At the same time, the CO2 elimination and the dynamic compliance were improved. Because of these effects, the peak inspiratory pressure employed in mechanical ventilation could be reduced. It is concluded that surfactant replacement therapy can prevent the patients with measles pneumonitis from hypoxemia and ventilation-induced lung injury. However, further study is needed to maintain the improved oxygenation. Recently, it is reported that the effect of exogenous surfactant on oxygenation and activity of pulmonary neutrophils is regulated by the amount and/or concentration of administered surfactant. Therefore, it is an urgent issue to find out the optimum amount and concentration of exogenous surfactant used clinically.

Fibronectin induces pseudopod formation and cell migration by mobilizing internal Ca(2+) in blastoderm cells from medaka embryos.

During vertebrate embryogenesis, blastoderm cells at the gastrula stage migrate to new locations for subsequent development. The cellular mechanism of migration was studied in medaka (Oryzias latipes) embryos at the early gastrula stage. When fibronectin was applied iontophoretically or by the puff method, cell surface protrusion known as pseudopods and a local [Ca(2+)](i) rise at the site of application were observed in approximately half of the isolated blastoderm cells. When the pseudopod adhered to the substrate, the cell body moved toward the direction of the pseudopod as [Ca(2+)](i) declined and the pseudopod was withdrawn. Local puff application of ionomycin, a Ca(2+) ionophore, in the presence of external Ca(2+) induced protrusions of the plasma membrane similar to pseudopods, suggesting that the [Ca(2+)](i) rise itself is causing pseudopod formation. On the other hand, fibronectin induced pseudopods even in the absence of external Ca(2+), suggesting the mobilization of Ca(2+) from internal stores. In accordance with this interpretation, fibronectin failed to induce [Ca(2+)](i) rises after pretreatment with thapsigargin, a blocker of Ca(2+)-ATPase in the endoplasmic reticulum. Furthermore, chelating internal Ca(2+) with BAPTA prevented fibronectin from inducing pseudopods. U-73122, a blocker of phospholipase C, completely suppressed both the [Ca(2+)](i) rise and morphological changes accompanied with fibronectin application, suggesting involvement of the inositol phosphate pathway. On the other hand, caffeine evoked a [Ca(2+)](i) rise in a great majority of the fibronectin-responsive cells and the percentage of fibronectin-responsive cells was greatly reduced by a blocking dose of ryanodine. These results suggest that fibronectin activates phospholipase C and the initial [Ca(2+)](i) rise through IP(3) receptors further activates ryanodine receptors, achieving the local [Ca(2+)](i) rise. The decay time course of [Ca(2+)](i) after fibronectin application was prolonged in the absence of external Na(+). DCB, an inhibitor of Na(+)/Ca(2+) exchangers, also prolonged the time course of the [Ca(2+)](i) decay, suggesting the contribution of Na(+)/Ca(2+) exchangers. Cytochalasin D, an inhibitor of actin polymerization by binding to the barbed end of F-actin, induced swelling in fibronectin-responsive cells and prevented fibronectin from inducing pseudopod formation without suppressing the [Ca(2+)](i) rise. These results support the hypothesis that fibronectin facilitates cell migration via pseudopod formation during gastrulation.

Marked regional heterogeneity in venous oxygen saturation in severe head injury studied by superselective intracranial venous sampling: case report.

OBJECTIVE: Continuous monitoring of jugular venous oxygen saturation (SjvO2) is useful in the management of severe head injury. Abnormally high SjvO2 values can be caused by increased cerebral blood flow, decreased cerebral metabolism, brain death, contamination from extracerebral venous blood, or traumatic arteriovenous fistula. CLINICAL PRESENTATION: A 20-year-old man with severe head injury was diagnosed to have a traumatic dural carotid-cavernous sinus fistula on the day of trauma. Continuous left SjvO2 monitoring from Days 4 to 12 revealed oxygen saturation ranging between 85 and 98%. INTERVENTION: Superselective intracranial and extracranial venous sampling on Day 5 demonstrated marked regional heterogeneity in venous oxygen saturation as follows: superior sagittal sinus, 95 to 97%; straight sinus, 88%; right transverse sinus, 94%; left transverse sinus, 74%; right SjvO2, 95%; left SjvO2, 89%; the basilar plexus, 99%; right internal jugular vein, 98%; the left internal jugular vein, 94%. Extremely high oxygen saturation in the superior sagittal sinus and basilar plexus was attributed to severe brain damage and carotid-cavernous sinus fistula, respectively. CONCLUSION: Although jugular bulb oximetry is useful in the management of severe head injury, high oxygen saturation values should be interpreted with caution because they cannot show the intracranial heterogeneity of venous oxygen saturation.

Two types of external Cl(-)-dependent Cl(-) channels and one type of stretch receptor cation channel contribute to the formation of isotonic blastocoel fluid in early medaka fish embryo.

Ionic channels in blastoderm cells dissociated from medaka fish embryos at the late blastula stage were studied by the patch-clamp technique in whole-cell, inside-out and cell-attached patch configurations. These cells were mechanically dissociated without using proteo-lytic enzymes. I have reported previously an external anion-dependent type I Cl(-) channel, which was observed at the early blastula stage, and its voltage dependency shifted toward the positive direction with a reduction in [Cl(-)](o). The type I Cl(-) channel was observed in about half of the blastoderm cells at the late blastula stage. I also observed another external anion-dependent Cl(-) channel (type II) whose voltage dependency shifted toward the negative direction with a reduction in [Cl(-)](o) and a cation selective stretchactivated channel. The$coexistence of the type II Cl(-) channel and stretch-activated cation channel would produce the efflux of both cations and anions in response to low ionic strength fluid. Further, the initial rise of blastocoel [Cl(-)] by this mechanism would trigger positive feedback between the type I Cl(-) channel conductance and blastocoel [Cl(-)]. At the early blastula stage, the blastocoel cavity fluid has a low ionic strength similar to that of pond water. I proposed that the cooperation of three types of ion channels at the late blastula stage generates isotonic blastocoel cavity fluid.

[A case of Salmonella subdural empyema developed in chronic subdural hematoma].

A case of Salmonella subdural empyema developed in chronic subdural hematoma (Infected Subdural Hematoma; ISH) was reported. A 64-year-old man had been in a nearby hospital due to myelodysplastic syndrome with cerebral infarction for two months. His condition there had been almost uneventful. But spike fever occurred and the patient became drowsy two days before his transfer to our medical center. His consciousness level deteriorated progressively and CT scan showed a right chronic subdural hematoma. He had had no history of head trauma in the previous two months. On admission to our center, his consciousness level was semicoma with anisocoria. An emergency operation was performed via a single burr hole initially. From the burr hole, old bloody fluid accompanied by yellowish pus was obtained. Thus so-called ISH was diagnosed and the craniotomy was carried out. Gram stain of the specimen revealed gram negative rods. Although an epileptic state developed after the operation, it was controlled by barbiturate coma therapy for 3 days, followed by phenytoin administration. Fever subsided gradually with antibiotics sensitive to the bacteria and his anisocoria disappeared on the 4th postoperative day. In this case, Salmonella enteritidis was detected from bacterial culture both of the specimen and of the arterial blood. Salmonella enteritidis might have been implanted on the capsule of the chronic subdural hematoma by bacteremia derived from immunological dysfunction due to myelodysplastic syndrome. In conclusion, the possibility of ISH should be considered in chronic subdural hematoma patients with immunological dysfunction.

Endovascular treatment of intractable oronasal bleeding associated with severe craniofacial injury.

BACKGROUND: Severe craniofacial injury may cause intractable oronasal bleeding, which is refractory to conventional treatments. This study will evaluate the efficacy of endovascular treatment for such oronasal bleeding. METHODS: Nine males between the ages of 19 and 62 years who had intractable oronasal bleeding resulting from severe craniofacial injuries received treatments of transarterial embolization using Gelfoam pledgets, polyvinyl alcohol particles, or platinum coils. We then reviewed their clinical and neuroradiologic characteristics retrospectively. RESULTS: In all but one case, angiography demonstrated bleeding points as extravasation. These bleeding points were multiple in seven cases. Except for bleeding from ethmoidal arteries, selective embolization was successful. In all cases, intractable oronasal bleeding was controlled. Patient survival was not directly related to oronasal bleeding, but rather was strongly correlated with associated brain injuries. CONCLUSION: Endovascular treatment is an acceptable treatment for intractable oronasal bleeding associated with severe craniofacial injuries when conventional treatments have failed.

Blood purification for crush syndrome.

At least 372 people developed crush syndrome after they were injured by the Great Hanshin-Awaji Earthquake. Of these, 23 were transferred to Osaka City General Hospital from the disaster area. The serum creatinine kinase (CK) of each of the 23 patients exceeded 10,000 IU/L. Sixteen of these patients were treated with various methods of blood purification including hemodialysis (HD), plasma exchange (PE), and continuous hemodiafiltration (CHDF). The effectiveness on each method of blood purification was evaluated in this study based on the clearance of myoglobin and the length of time until recovery from acute renal failure (ARF). None of the patients died, and none suffered from ARF longer than 2 months. The length of time required for blood purification was significantly correlated with the serum CK and myoglobin levels on admission. The serum myoglobin levels decreased linearly regardless of the method of blood purification used. Our findings showed that the severity of ARF that occurred in association with crush injury was proportional to the amount of crushed muscle and that once ARF had developed, the clearance of myoglobin was not affected by any of the blood purification methods tested including HD, PE, and CHDF. Therefore, the method of blood purification employed for crush syndrome should be selected for its effectiveness in treating ARF, rather than the elimination of myoglobin.

External-anion-dependent anionic current in blastoderm cells of early medaka fish embryos.

1. Anionic current was studied by a whole-cell variation of the patch-clamp technique in blastoderm cells dissociated from medaka (Oryzias latipes) embryos at the early blastula stage. The blastoderm cells were mechanically dissociated without using proteolytic enzymes. 2. The anionic current was deactivated by hyperpolarizing steps. The steady-state current-voltage (I-V) relationship of the anion current was accurately represented by the Boltzmann relation with z = 1.01 +/- 0.02 (+/- S.E.M., n = 4) for voltage-dependent activation when internal calcium ions were buffered at 100 nM by BAPTA-Ca2+ buffer. 3. When the internal calcium concentration was reduced to 10 nM, this anionic current became an external-calcium-dependent current and was remarkably decreased by removal of external calcium ions. Furthermore, this anionic current was almost abolished when the internal calcium concentration was greatly reduced by chelating Ca2+ ions with 10 mM BAPTA. 4. This current was not affected by replacing external Na+ with TEA+ or N-methyl-D-glucamine. The reversal potentials shifted by +58.6 mV for a 10-fold decrease in the external Cl-concentration. External Cl-ions were substituted with various anions and respective current-reversal potentials were measured. The order of permeability was I- > Br- > Cl- > F-. Both the outward and inward currents almost disappeared in external Cl(-)-free solutions. 5. The voltage dependency of the anionic current shifted in a positive direction with the reduction in the external Cl- concentration, the potentials at which half the channels were activated (V 1/2) being -59.8 +/- 1.2 mV (n = 4), -40.7 +/- 0.8 mV (n = 4), -14.9 +/- 0.7 mV (n = 4), and -0.7 +/- 0.6 mV (n = 4) for 135, 90, 67, and 45 mM Cl-, respectively. This implies that the inward current, brought by efflux of internal anions, decreases with reductions in the external Cl- concentration. In the presence of external 135 mM Br-, the voltage dependency of the anionic current shifted in the negative direction (V 1/2 = -84.5 +/- 1.0 mV and z = 0.91 +/- 0.02 (n = 3)) in comparison with that in the external Cl- medium. It further shifted in the negative direction in the presence of 135 mM I- (V 1/2 = -93.8 +/- 1.5 mV and z = 0.85 +/- 0.03 (n = 3)). The inward current of the anion channel is considered to be affected by both the type and the concentration of external halide ions. 6. At the beginning of the blastula stage, the blastocoel cavity is formed for the first time. A mechanism is necessary to transport ions to the cavity without losing them to pond water outside the embryos. Since this anion channel is external-anion dependent, the current cannot be activated in the membrane facing the pond water, where concentrations of anions are much lower than those of the intracavernous solution. Only after blastocoel formation are blastoderm cells first exposed to the extracellular fluid with high ionic concentrations. Then, the anion channel would become effective for maintaining the Cl- equilibrium potential.

The release of glutamate and accumulation of intracellular calcium in the guinea pig hippocampal slices during glucose deprivation.

Simultaneous recordings of the time course of change in the extracellular glutamate concentration ([Glu]O) and intracellular Ca2+ level [Ca2+]i during glucose deprivation were performed in the CA3 area of hippocampal slices from guinea pig. Direct measurement of [Glu]O with a glutamate sensitive sensor revealed that [Glu]0 showed a biphasic increase during glucose deprivation and decreased rapidly after re-introduction of glucose in the perfusing medium. The initial increase of [Glu]O preceded [Ca2+]i increase and thereafter a sustained increase of [Glu]O was observed concomitant with massive [Ca2+]i accumulation. Replacement of Na with Li markedly attenuated the rapid reduction of [Glu]O, suggesting that the reduction of [Glu]O was due to Na-dependent glutamate uptake system, which worked immediately after energy recovery.

The role of inositol trisphosphate on ACh-induced outward currents in bullfrog saccular hair cells.

Acetylcholine (ACh) is considered as the most likely candidate for a neurotransmitter of the efferent synapse onto hair cell. In this paper, the nature of this cholinergic receptor mechanism on dissociated bullfrog saccular hair cell was examined by using whole cell recording and Ca2+ sensitive fluorophotometric technique. Both the ACh-induced current and the increase of [Ca2+]i were observed in an oscillatory manner, and were the largest around the basal part of the cell where the efferent synapse is thought to make a contact with the membrane. The reversal potential of ACh-induced current indicated that ACh activated a K+ conductance. The ACh-induced current was reversibly blocked by atropine, d-tubocurarine (dTC), apamin, tetraethylammonium (TEA) and quinine. Neither muscarine nor nicotine mimicked the ACh-induced current. When GTP gamma S was injected into a hair cell, the first ACh application induced an outward current of transient kinetics, but in subsequent trials ACh-induced current lost its decay phase. Intracellularly injected D-myo-inositol 1,4,5-trisphosphate (InsP3) generated outward currents. Intracellularly injected heparin suppressed ACh-induced currents, and lithium (Li+) increased ACh-induced currents. These results indicate that ACh activates a receptor coupled with a guanine nucleotide binding protein (G-protein) which triggers metabolic cascades of InsP3 and Ca2+ leading to the activation of the Ca(2+)-activated K+ channel.

Muscarinic receptor hyperpolarizes cochlear hair cells of chick by activating Ca(2+)-activated K+ channels.

1. Electrical responses to extracellularly applied acetylcholine (ACh) and to intracellularly introduced substances were studied in isolated short and tall hair cells from the chick cochlear organ by a whole-cell voltage clamp technique using a patch electrode. These cells were isolated without using proteolytic enzymes. 2. Short hair cells generated a transient outward current at -50 mV in normal saline in response to puff-applied 100 microM-ACh, when the patch electrode was filled with a 160 mM-K+ and 100 microM-EGTA-based intracellular medium. The amplitude was 317.1 +/- 97.1 pA (n = 32). When ACh was applied ionophoretically, the outward current was generated with a delay of about 10 ms. 3. The amplitude of ACh-induced current was dose dependent with a KD of 19 microM and a Hill coefficient of 1.6 when measured at -50 mV. 4. The ACh (100 microM)-induced current was suppressed by 1 microM-atropine. ACh-induced current was generated in a Ca(2+)-free extracellular medium; however, the second ACh puff in the Ca(2+)-free medium generated a much reduced response. ACh-induced current was suppressed reversibly by 100 microM-quinine. 5. Intracellular injections of guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S), inositol 1,4,5-trisphosphate (IP3) or Ca2+ (1 microM) via the patch pipette activated outward currents at -50 mV. 6. When the internal medium with strong Ca(2+)-buffering capacity (5 mM-EGTA) was used, the ACh-induced current was reduced to 39.3 +/- 6.8 pA (n = 4) at -50 mV (12.3% of the response in the low-EGTA medium). 7. The reversal potential of the ACh-induced current was -85.7 +/- 4.2 mV (n = 3) in normal saline containing 5 mM-K+. The reversal potential was dependent on the extracellular K+ concentration ([K+]o) and was shifted 57 mV by a 10-fold increase in [K+]o at room temperature (20-25 degrees C). 8. These results (points 4-7) indicate that ACh induces a K+ conductance by releasing Ca2+ intracellularly, probably by activating the pathway of muscarine receptor, G-protein and IP3. 9. Channel activities were recorded using cell-attached patch electrodes. Channel activities were rarely observed when ACh was applied to the extra-patch membrane, while robust channel activities were observed when ACh was included in the patch pipette medium. It is therefore suggested that Ca(2+)-activated K+ channels exist in the membrane in close vicinity to muscarinic receptor molecules and intracellular Ca2+ release sites.(ABSTRACT TRUNCATED AT 400 WORDS)

Mobilization of intracellular Ca2+ and suppression of inward currents in a neuronal hybrid cell line triggered by bradykinin.

Bradykinin triggered intracellular Ca mobilizations and ionic conductance changes were studied in the neuroblastoma x glioma hybrid cell line NG108-15 using Ca-sensitive fluorescent indicator fura-2 under patch pipette whole cell voltage clamp condition. The time course of outward current induced by bradykinin was closely related to the time-course of [Ca2+]i change. Following application of bradykinin, [Ca2+]i increased transiently and then decreased below the basal level before bradykinin application. The inward currents activated by step-depolarization were suppressed after bradykinin application, but the time-course of the suppression did not go in parallel with the [Ca2+]i changes: the suppression started before the [Ca2+]i change emerged and outlasted the phase of [Ca2+]i increase. Both transient type and long-lasting type Ca current were suppressed by bradykinin. [Ca2+]i increase induced by high potassium depolarization was suppressed by bradykinin. Pertussis toxin did not affect the Ca transient nor the suppression of Ca channel induced by bradykinin. Our results suggest that the modifications of ionic channels by bradykinin could be through the other mechanisms than the well established activation of the G-protein leading to the IP3 mechanisms and that the bradykinin receptor might couple with the pertussis toxin-insensitive G protein which regulates the calcium channels.

Muscarinic agonists and ATP increase the intracellular Ca2+ concentration in chick cochlear hair cells.

1. Cholinergic muscarinic agonists applied by the pressure puff method increased intracellular Ca2+ concentration in Fura-2-loaded hair cells. The Ca2+ response outlasted the agonist application. 2. The Ca2+ response induced by acetylcholine (ACh) was ACh dose dependent with a KD of 200 microM. Desensitization was negligible, and almost identical Ca2+ responses were observed when two ACh puffs were separated by 150 s. The response was blocked by d-tubocurarine (dTC). The KD of dTC blocking was 500 microM when 100 microM-ACh induced the Ca2+ response. 3. The amplitude of the ACh-induced Ca2+ responses were potentiated to 3 times the control by incubation with calcitonin gene-related peptide (CGRP; 0.1-1 microM). CGRP did not affect the resting Ca2+ concentration. Glycine (100 microM) potentiated the ACh response to 1.4 times the control, and also increased the resting Ca2+ concentration slightly. 4. The ACh-induced Ca2+ response was suppressed by atropine. It was induced in Ca2(+)-free extracellular medium, and in Ca2(+)-free medium desensitization to a second ACh stimulation was significant. The amplitude of the second Ca2+ response was 44% of the first when two ACh puffs were separated by 117 s in Ca2+ free medium. 5. Muscarine and carbamylcholine induced similar Ca2+ responses, with KD values of 130 microM for muscarine and 340 microM for carbamylcholine. Desensitization of Ca2+ responses was negligible in both agonists. 6. ATP co-exists with ACh in some presynaptic nerve terminals (Burnstock, 1981). Puff-applied ATP (100 microM) generated a Ca2+ response with a rapid rising phase and a following slow phase. In Ca2(+)-free medium the rapid phase disappeared and only the slow phase was observed. The rapid phase is due to the influx of Ca2+ ions and the slow phase is due to a release of Ca2+ ions from an intracellular reservoir. Under voltage clamp ATP induced a fast inward current and a following slow outward current. 7. Nicotine, adenosine, glycine, GABA, glutamate and bradykinin did not induce Ca2+ responses in the hair cell. 8. ACh induced hyperpolarization of the hair cell membrane under current clamp, most probably by the activation of Ca2+ activated K+ conductance. Therefore, a cholinergic muscarinic receptor may mediate the inhibitory effects of efferent innervation observed in hair cells.

Intracellular calcium mobilization triggered by a glutamate receptor in rat cultured hippocampal cells.

1. Intracellular free calcium ([Ca2+]i) was monitored by means of Fura-2 fluorescence measurements in hippocampal cells in primary cultures from newborn rats. 2. In external media containing 200 microM-DL-2-amino-5-phosphonovalerate and 1 mM-kynurenate, but no added Ca2+, an increase in [Ca2+]i was observed in 30-40% of cells examined in response to quisqualate or L-glutamate. 3. Under such conditions, [Ca2+]i often increased gradually with a latency of a few seconds after application of the agonists. 4. Pre-treatment of the cultured cells with pertussis toxin reduced the extent of quisqualate-stimulated [Ca2+]i increase in Ca2+-free media, but the percentage of the responsive cells was not affected appreciably. 5. It is concluded that quisqualate and L-glutamate can trigger the release of Ca2+ from intracellular Ca2+ stores, most likely by activating a glutamate receptor coupled to a pertussis toxin-sensitive G-protein.

[Hemodynamic effects of extubation of an endotracheal tube in patients following cardiac surgery--inspiratory or expiratory phase?].

The question whether an endotracheal tube should be removed in the inspiratory phase or in the expiratory phase is still controversial. Hemodynamic effects of extubation at each phase were compared in 14 patients following cardiac surgery. In the patients who were extubated in the expiratory phase, marked changes in heart rate (HR), systolic arterial pressure (SAP), mean arterial pressure (MAP), and rate pressure product (RPP) were observed at one, five and 10 minutes after the extubation. In the patients whose endotracheal tubes were removed in the inspiratory phase, only small changes in SAP, MAP and RPP were observed at one and five minutes after the extubation. Since hemodynamic changes after cardiac surgery must be prevented as much as possible, we may conclude that the endotracheal tube should be removed in the inspiratory phase.