[A Case of Acute Pulmonary Edema after Open Abdominal Aortic Aneurysm Repair].

A 61-year-old man, who had previously undergone percutaneous coronary intervention (PCI) of the left anterior descending artery (LAD), was scheduled for open abdominal aortic aneurysm repair under general anesthesia. Although the left ventricular (LV) ejection fraction was 63%, diastolic dysfunction was identified (E/A 0.61). The patient received inhalation induction with 5% sevoflurane and an infusion of remifentanil (0.2µg · kg⁻¹ · min⁻¹). Rocuronium (0.6 mg · kg⁻¹) was administered and tracheal intubation was performed. Anesthesia was maintained with air-oxygen- sevoflurane, an infusion of remifentanil, and 700 µg fentanyl administered intravenously. An infusion of fentanyl (25 µg · hr⁻¹) in combination with rectus sheath block was administered for postoperative anal- gesia. Intraoperatively, we used arterial pressure-based cardiac output (CO), stroke volume variation (SVV), and transesophageal echocardiography as a guide for circulatory management The intraoperative net fluid in-out balance was 5,296 ml, and the duration of the procedure was 5.5 hr. The patient was extubated in the operating room because no significant findings were observed on the postoperative chest X-ray, and PaO2/FI02 (P/F) ratio was 405. At the termination of anesthesia, systolic blood pressure increased to 200 mmHg. The hypertension lasted until after extubation, following which SpO2 diminished gradually. And SpO2 was 78% and PaO2 was 56.7 Torr under 8 l of oxygen. A chest X-ray at this time showed pulmonary edema. There were no findings of ischemic heart disease on either ECG or echocardiography. Immediate vasodilator treatment for the hypertension and non-invasive posi- tive pressure ventilation for the hypoxia were commenced. The P/F ratio recovered to 240 by the night of the surgery, and a chest X-ray showed that the pul- monary edema had resolved. The patient was moved out of the ICU on the first day after the surgery. This case highlights the fact that even when LV systolic function is preserved, diastolic dysfunction may occur, leading to pulmonary congestion due to increased afterload.

[Anesthetic management of intra-aortic balloon occlusion (IABO) for seven cases of placenta accreta--a six year experience at our institute].

We studied retrospectively amount of bleeding, clamping time, and the presence or absence of ischemia-reperfusion injury in all seven cases of IABO performed for placenta accreta from 2007 to 2012 at our hospital. We also examined rSO2 change before and after clamping in four cases in which lower-limb rSO2 monitoring was performed with NIRS (near-infrared spectroscopy). There was no case suspected of ischemia-reperfusion injury during and after clamping with the amount of bleeding around 1,580-10,973 ml (mean 4,536 ml) and clamping time of 10-83 min (mean 44 min). No significant decrease was observed in lower-limb rSO2 with 73.5 ± 5.9% before clamping and 70.8 ± 5.6% (mean ± SD) after clamping.

The antinociceptive effect of intrathecal administration of glycine transporter-2 inhibitor ALX1393 in a rat acute pain model.

BACKGROUND: Glycinergic neurons in the spinal dorsal horn have been implicated in the inhibition of spinal pain processing in peripheral inflammation and chronic pain states. Neuronal isoform glycine transporter-2 (GlyT2) reuptakes presynaptically released glycine and regulates the glycinergic neurotransmission. In this study, we examined whether a selective GlyT2 inhibitor, ALX1393, elicits an antinociceptive effect in a rat acute pain model. METHODS: Male Sprague-Dawley rats were implanted with a catheter intrathecally. The effects of intrathecal administration of ALX1393 (4, 20, or 40 microg) on thermal, mechanical, and chemical nociception were evaluated by tail flick, hot plate, paw pressure, and formalin tests. Furthermore, to explore whether ALX1393 affects motor function, a rotarod test was performed. RESULTS: ALX1393 exhibited antinociceptive effects on the thermal and mechanical stimulations in a dose-dependent manner. The maximal effect of ALX1393 was observed at 15 min after administration, and a significant effect lasted for about 60 min. These antinociceptive effects were reversed completely by strychnine injected immediately after the administration of ALX1393. In the formalin test, ALX1393 inhibited pain behaviors in a dose-dependent manner, both in the early and late phases, although the influence was greater in the late phase. In contrast to antinociceptive action, ALX1393 did not affect motor function up to 40 microg. CONCLUSIONS: This study demonstrates the antinociceptive action of ALX1393 on acute pain. These findings suggest that the inhibitory neurotransmitter transporters are promising targets for the treatment of acute pain and that the selective inhibitor of GlyT2 could be a novel therapeutic drug.

Spinal astrocyte glutamate receptor 1 overexpression after ischemic insult facilitates behavioral signs of spasticity and rigidity.

Using a rat model of ischemic paraplegia, we examined the expression of spinal AMPA receptors and their role in mediating spasticity and rigidity. Spinal ischemia was induced by transient occlusion of the descending aorta combined with systemic hypotension. Spasticity/rigidity were identified by simultaneous measurements of peripheral muscle resistance (PMR) and electromyography (EMG) before and during ankle flexion. In addition, Hoffman reflex (H-reflex) and motor evoked potentials (MEPs) were recorded from the gastrocnemius muscle. Animals were implanted with intrathecal catheters for drug delivery and injected with the AMPA receptor antagonist NGX424 (tezampanel), glutamate receptor 1 (GluR1) antisense, or vehicle. Where intrathecal vehicle had no effect, intrathecal NGX424 produced a dose-dependent suppression of PMR [ED50 of 0.44 microg (0.33-0.58)], as well as tonic and ankle flexion-evoked EMG activity. Similar suppression of MEP and H-reflex were also seen. Western blot analyses of lumbar spinal cord tissue from spastic animals showed a significant increase in GluR1 but decreased GluR2 and GluR4 proteins. Confocal and electron microscopic analyses of spinal cord sections from spastic animals revealed increased GluR1 immunoreactivity in reactive astrocytes. Selective GluR1 knockdown by intrathecal antisense treatment resulted in a potent reduction of spasticiy and rigidity and concurrent downregulation of neuronal/astrocytic GluR1 in the lumbar spinal cord. Treatment of rat astrocyte cultures with AMPA led to dose-dependent glutamate release, an effect blocked by NGX424. These data suggest that an AMPA/kainate receptor antagonist can represent a novel therapy in modulating spasticity/rigidity of spinal origin and that astrocytes may be a potential target for such treatment.

[Anesthetic management for on-pump coronary arterial bypass graft in a patient with cardiac resynchronization therapy].

We experienced anesthetic management for on-pump beating coronary arterial bypass graft in a 73-year-old male patient with cardiac resynchronization therapy (CRT), a non-pharmacological therapy in chronic heart failure. Anesthesia was induced and maintained with sevoflurane and fentanyl under intraaortic balloon pump support. When patient's heartbeat exceeded a pacemaker rate, blood pressure decreased to below 60 mmHg. We tried to perform CRT by adjusting its program above his heart rate, and then blood pressure returned to normal levels. After coronary arterial bypass had been established, it was difficult to wean the patient from cardiopulmonary bypass (CPB) because his own heart rate was over 100 beats min(-1). For the purpose of controlling the heart rate, we administered landiolol intravenously. After injecting a total of 2.5 mg of landiolol, his heart rate was reduced and subsequently CRT started to work, which induced a stable hemodynamic condition enough to wean from CPB. According to our clinical experience, it is important to perform a rapid treatment against tachycardia in a patient with CRT Thus, landiolol is useful for such a rapid treatment against tachycardia with maintaining the hemodynamics.

Intravenous infusion of dexmedetomidine can prevent the degeneration of spinal ventral neurons induced by intrathecal morphine after a noninjurious interval of spinal cord ischemia in rats.

BACKGROUND: In recent studies, we demonstrated that neuraxial morphine after noninjurious spinal cord ischemia in the rat could induce spastic paraplegia and degeneration of selective spinal ventral neurons. Our objective was to investigate the impact of dexmedetomidine infusion on the degeneration of spinal ventral neurons induced by intrathecal (IT) morphine after spinal cord ischemia. METHODS: Male Sprague-Dawley rats were given repetitive doses of IT morphine (40 microg x 2) at 1 and 5 h after a noninjurious interval (6 min) of spinal cord ischemia. The animals were assigned to one of the following four groups after the first IT injection (n = 8/group): Group S, IV infusion of saline (mL/h); Group Dex 0.1, dexmedetomidine (0.1 microg . kg(-1) x h(-1)); Group Dex 1, dexmedetomidine (1 microg x kg(-1) x h(-1)); Group Dex 3, dexmedetomidine (3 microg x kg(-1) x h(-1)). Follow-up evaluation included a sedation scale, the Motor Deficit Index to determine neurological dysfunction and histopathology of the spinal cord at 72 h of reperfusion. RESULTS: IV dexmedetomidine produced a dose-dependent increase in the sedation index. Repetitive IT morphine injection induced paraplegia and degeneration of the spinal ventral neurons. IV dexmedetomidine at a sedative dose in comparison with saline significantly attenuated neurological dysfunction and histopathological consequences. CONCLUSION: These data show that repetitive administration of IT morphine can induce paraplegia with degeneration of spinal ventral neurons, which can be attenuated by IV dexmedetomidine at a sedative dose. The use of dexmedetomidine may provide beneficial effects on neurological outcome after IT morphine after spinal cord ischemia in rats.

Intrathecal nicorandil and small-dose morphine can induce spastic paraparesis after a noninjurious interval of spinal cord ischemia in the rat.

We investigated the interaction between nicorandil, a K(+)ATP channel opener, and morphine on motor function after a noninjurious interval of spinal cord ischemia in the rat. Spinal ischemia was induced by aortic occlusion for 6 min with a balloon catheter in Sprague-Dawley rats. All animals received intrathecal (IT) injection of morphine (1-60 microg) 1 h after ischemia. In addition to IT injection of morphine, group M (control), group MN (combination of morphine and nicorandil), and group MNG (combination of morphine, nicorandil, and glibenclamide) received IT saline, nicorandil (10 microg), and both glibenclamide (10 microg) and nicorandil (10 microg) after 150 min of reperfusion, respectively. A quantal bioassay for the effect of IT morphine on neurological function after ischemia was performed to calculate 50% effective dose values (ED50) for inducing paraparesis at 3 h of reperfusion. The ED50 in group M and group MN was 15.1 +/- 4.9 microg and 2.9 +/- 1.0 microg of IT morphine, respectively (P < 0.05). In Group MNG, the dose-response curve shifted back to the right and the ED50 for inducing paraparesis was 11.6 +/- 4.7 microg of IT morphine. The present study demonstrates that IT small-dose morphine combined with nicorandil induces spastic paraparesis after noninjurious interval of spinal cord ischemia in the rat.

Measurement of peripheral muscle resistance in rats with chronic ischemia-induced paraplegia or morphine-induced rigidity using a semi-automated computer-controlled muscle resistance meter.

In experimental and clinical studies, an objective assessment of peripheral muscle resistance represents one of the key elements in determining the efficacy of therapeutic manipulations (e.g. pharmacological, surgical) aimed to ameliorate clinical signs of spasticity and/or rigidity. In the present study, we characterize a newly developed limb flexion resistance meter which permits a semi-automated, computer-controlled measurement of peripheral muscle resistance (PMR) in the lower extremities during a forced flexion of the ankle in the awake rat. Ischemic paraplegia was induced in Sprague-Dawley rats by transient aortic occlusion (10 min) in combination with systemic hypotension (40 mm Hg). After ischemia the presence of spasticity component was determined by the presence of an exaggerated EMG activity recorded from gastrocnemius muscle after nociceptive or proprioceptive afferent activation and by velocity-dependent increase in muscle resistance. Rigidity was induced by high dose (30 mg/kg, i.p.) of morphine. Animals with defined ischemic spasticity or morphine-induced rigidity were then placed into a plastic restrainer and a hind paw attached by a tape to a metal plate driven by a computer-controlled stepping motor equipped with a resistance transducer. The resistance of the ankle to rotation was measured under several testing paradigms: (i) variable degree of ankle flexion (40 degrees, 50 degrees, and 60 degrees), (ii) variable speed/rate of ankle flexion (2, 3, and 4 sec), (iii) the effect of inhalation anesthesia, (iv) the effect of intrathecal baclofen, (v) the effect of dorsal L2-L5 rhizotomy, or (vi) systemic naloxone treatment. In animals with ischemic paraplegia an increased EMG response after peripheral nociceptive or proprioceptive activation was measured. In control animals average muscle resistance was 78 mN and was significantly increased in animals with ischemic spasticity (981-7900 mN). In ischemic-spastic animals a significant increase in measured muscle resistance was seen after increased velocity (4 > 3 > 2 sec) and the angle (40 degrees > 50 degrees > 60 degrees) of the ankle rotation. In spastic animals, deep halothane anesthesia, intrathecal baclofen or dorsal rhizotomy decreased muscle resistance to 39-80% of pretreatment values. Systemic treatment with morphine induced muscle rigidity and corresponding increase in muscle resistance. Morphine-induced increase in muscle resistance was independent on the velocity of the ankle rotation and was reversed by naloxone. These data show that by using this system it is possible to objectively measure the degree of peripheral muscle resistance. The use of this system may represent a simple and effective experimental tool in screening new pharmacological compounds and/or surgical manipulations targeted to modulate spasticity and/or rigidity after a variety of neurological disorders such as spinal cord traumatic or ischemic injury, multiple sclerosis, cerebral palsy, or Parkinson's disease.

Transcranial motor-evoked potentials monitoring can detect spinal cord ischemia more rapidly than spinal cord-evoked potentials monitoring during aortic occlusion in rats.

In this study, we evaluated the efficacy of transcranial motor-evoked potentials (tc-MEPs), compared with segmental spinal cord-evoked potentials (SCEPs), for detecting spinal cord ischemia (SCI) and assessed the relationship between neurological outcome and tc-MEPs or SCEPs in the rat aortic occlusion model. In the rats, SCI was induced by aortic occlusion for 10 min with a balloon catheter. At first, tc-MEPs (Group A: n = 6) or segmental SCEPs (Group B: n = 6) was recorded during SCI. Second, in using the quantal bioassay for the relationship between an interval of aortic occlusion and the probability of positive response in tc-MEPs or segmental SCEPs, the P50(MEP) and P50(SCEP) which represent the interval of aortic occlusion associated with 50% probability of assessment of ischemic spinal cord dysfunction by tc-MEP and SCEP were analyzed. The amplitude of tc-MEPs decreased significantly at 30 s and disappeared completely at 2 min after aortic occlusion. In Group B, it took about 6 min after aortic occlusion to diminish SCEP signal amplitude by approximately 50%. P50(MEP) obtained in the quantal analysis was 0.3 +/- 0.1 min. P50(SCEP) was calculated as 6.2 +/- 0.5 min that was significantly (P < 0.01) longer than P50(MEP). Our data indicated that tc-MEP monitoring could detect the onset of SCI so rapidly in comparison with segmental SCEP monitoring, which could provide therapeutic windows in a surgical approach that includes spinal cord protection.

Influence of the descending thoracic aortic cross clamping on bispectral index value and plasma propofol concentration in humans.

BACKGROUND: In this study, the authors investigated changes in Bispectral Index (BIS) values and plasma propofol concentrations (Cp) after aortic cross clamping in the descending thoracic aortic aneurysm repair surgery during propofol anesthesia. METHODS: Prospectively, in 10 patients undergoing thoracic aortic surgery during total intravenous anesthesia with propofol, BIS values were recorded during cross clamping of the descending thoracic aorta. In this study, the rate of propofol infusion was controlled to keep the BIS value between 30 and 60 throughout surgery. Simultaneously, Cp values in the blood samples taken from the right radial artery (area proximal to cross clamping) and the left femoral artery (area distal to cross clamping) were measured. RESULTS: Approximately 15 min after initiating aortic cross clamping, BIS values in all cases started to decrease abruptly. Cp values of samples taken from the radial artery after cross clamping of the aorta were significantly (P < 0.05) increased compared with pre-cross clamp values (1.8 +/- 0.4 microg/ml), and the mean Cp after aortic cross clamping varied between 3.0 and 5.3 microg/ml. In addition, there were significant differences in the Cp values between radial arterial and femoral arterial blood samples throughout aortic cross clamping. Cp values in samples from the radial artery were approximately two to seven times higher than those from the femoral artery. CONCLUSIONS: This study showed that Cp values increased and BIS values decreased rapidly after aortic cross clamping in thoracic aortic aneurysm repair surgery during propofol anesthesia. These findings suggested that all anesthesiologists should control the infusion rate carefully, taking the abrupt changes in its pharmacokinetics into consideration, especially during cross clamping of the descending thoracic aorta.

Emergence from propofol anesthesia in a nonagenarian at a Bispectral Index of 52.

In this case report, we describe a nonagenarian patient who could respond completely to verbal commands at a Bispectral Index (BIS) value of 52 after epidural lidocaine and IV propofol anesthesia. Measured blood lidocaine and propofol concentrations were 0.69 microg/mL and 0.74 microg/mL, respectively. Intraoperative awareness even in the recommended BIS range of 40-60 remains possible.

Primary gastric small cell carcinoma: report of a case and review of the literature.

A 52-year-old man suffering from a pure-type primary gastric small cell carcinoma was treated with surgery and combination chemotherapy. The small cell carcinoma, approximately 6.5 cm in diameter, was situated in the posterior wall of the antrum and there were no distant metastases. Total gastrectomy and regional lymph node dissection was carried out. Histological examination revealed a solid pattern of proliferation of small cells with hyperchromatic, round nuclei and scant cytoplasm. Neoplastic cells infiltrated into the subserosal layer with severe lymphatic and vascular invasion. Regional lymph node cells were mostly replaced by tumor cells that stained positive for Grimelius, neuron-specific enolase (NSE), and synaptophysin. Accumulations of electron-dense core granules in the small neoplastic cells were seen by electron microscopy. Following surgery, the patient was treated with adjuvant chemotherapy consisting of cisplatin and etoposide. The patient is alive and recurrence free 3 years after surgical operation. We review 107 published cases of primary gastric small cell carcinoma, an extremely rare disease first reported in 1976. Small cell carcinoma is an aggressive, malignant tumor. Intensive chemotherapy is essential for patient survival even when curative surgical resection is carried out.

The effect of gamma-aminobutyric acid (GABA) receptor drugs on morphine-induced spastic paraparesis after a noninjurious interval of spinal cord ischemia in rats.

UNLABELLED: We have previously demonstrated that intrathecal morphine given after a noninjurious interval of spinal cord ischemia induced transient spastic paraparesis in a rodent model. However, the mechanism of this paraparesis is unknown. We hypothesized that morphine inhibits gamma-aminobutyric acid (GABA)ergic interneurons that control the tonus of spinal cord alpha-motoneurons and that inhibition of spinal cord interneurons may cause spastic paraparesis. In this study, we investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarified the mechanism of the spastic paraparesis induced by intrathecal morphine. Spinal cord ischemia was induced by aortic occlusion lasting 6 min. We first determined whether intrathecally administered GABA agonists (muscimol or baclofen) improve the spastic paraparesis in this model. GABA agonists did not improve the paraparesis. Next, we examined the effect of GABA antagonists (bicuculline or 5-aminovaleric acid) and determined the interaction between morphine and GABA antagonists. In an isobolographic analysis, the 50% effective dose decreased below the theoretical additive line, indicating a synergistic interaction between morphine and GABA antagonists. These results indicate that the spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors. IMPLICATIONS: The purpose of this study was to investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarify the mechanism of the spastic paraparesis induced by intrathecal morphine. The spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors.

Intrathecal morphine, but not buprenorphine or pentazocine, can induce spastic paraparesis after a noninjurious interval of spinal cord ischemia in the rat.

In this study, we sought to determine the effect of intrathecal (IT) pentazocine or buprenorphine on the neurological outcome after a short interval of spinal cord ischemia in rats. Although IT morphine (30 microg) induced spastic paraparesis after 6 min of aortic occlusion, neither pentazocine (150 microg) nor buprenorphine (4 microg) produced neurological dysfunction. Our results indicate that the effect of various opioids on the motor function after a noninjurious interval of spinal cord ischemia is opioid-specific.

Propofol reduces spinal motor neuron excitability in humans.

IMPLICATIONS: We investigated in humans whether changes in spinal motor neuron excitability correlate with the predicted propofol concentration (Cpt) achieved by a target-controlled infusion system. Propofol suppressed F-wave persistence in a Cpt-dependent manner, indicating that propofol depresses spinal motor neuron excitability at clinically relevant concentrations.

Intrathecal administration of morphine, but not small dose, induced spastic paraparesis after a noninjurious interval of aortic occlusion in rats.

UNLABELLED: We sought to investigate the dose-response relationship for the effect of intrathecal morphine on the transient spastic paraparesis after short-lasting spinal ischemia in rats. Spinal ischemia was induced by aortic occlusion for 6 min with a balloon catheter in rats previously implanted with an intrathecal catheter for drug delivery. After ischemia, the animals were allowed to recover, and 3, 10, or 30 microg of morphine or saline was injected intrathecally at 30 min after reperfusion. In a separate group, the quantal bioassay for the effect of intrathecal morphine on neurological function after ischemia was performed to calculate 50% effective dose values for inducing paraparesis at 2 h of reperfusion. Subsequently, histopathology of the spinal cord was assessed at 48 h of reperfusion. Intrathecal injection of 30 or 10 micro g of morphine, but 3 micro g of neither morphine nor saline, caused a progressive development of hindlimb spasticity. The 50% effective dose values for inducing paraparesis were 16.1 +/- 1.5 microg in assessing behavioral analysis at 2 h after intrathecal morphine. Histopathological analysis of spinal cords in the 30- microg group revealed the presence of dark-staining alpha-motoneurons in lumbosacral segments. We conclude that spinal administration of a large dose of morphine after transient aortic occlusion may be associated with a potential risk of paraparesis and the corresponding development of neurological dysfunction. Careful attention should be paid when intrathecal morphine is used for pain control after thoracoabdominal aortic aneurysm repair. IMPLICATIONS: Spinal administration of large-dose morphine after transient aortic occlusion may be associated with a potential risk of irreversible spinal neuronal degeneration and the corresponding development of neurological dysfunction.