Hideki Taninishi

Quantitative evaluation of the neuroprotective effects of thiopental sodium, propofol, and halothane on brain ischemia in the gerbil: effects of the anesthetics on ischemic depolarization and extracellular glutamate concentration.

Although propofol and thiopental are commonly used as neuroprotective agents, it has not been determined which is more neuroprotective. This study was designed to quantitatively evaluate the neuroprotective effects of thiopental, propofol, and halothane on brain ischemia by determining P50, ischemic time necessary for causing 50% neuronal damage. Gerbils were anesthetized with thiopental, propofol, or halothane and underwent 2-vessel occlusion (0, 3, 5 or 10 min). Direct current potentials were measured in bilateral CA1 regions, in which histologic evaluation was performed 5 days later. In some animals, extracellular glutamate concentrations (microdialysis) were measured during 7.5 minutes of ischemia. P50 in the thiopental, propofol, and halothane groups were estimated to be 8.4, 6.5 (P<0.05, vs. thiopental), and 5.1 (P<0.05) minutes, respectively. Durations of ischemic depolarization were equally reduced in the thiopental and propofol groups compared with that in the halothane group. Severity of neuronal damage with identical duration of ischemic depolarization was attenuated by thiopental compared with the effect of propofol. Maximum glutamate concentrations in the thiopental and propofol group were significantly reduced compared with that in the halothane groups but were comparable. By using P50, we found that the neuroprotective effect of thiopental was greater than that of propofol. Although duration of ischemic depolarization was equally reduced in thiopental and propofol groups, thiopental has a greater suppressive effect on neuronal injury during identical duration of ischemic depolarization than propofol does. Glutamate concentration during brain ischemia tended to be attenuated more by thiopental than by propofol, but it was not statistically significant.

Dynamic changes in cortical NADH fluorescence in rat focal ischemia: evaluation of the effects of hypothermia on propagation of peri-infarct depolarization by temporal and spatial analysis.

Suppression of peri-infarct depolarizations (PIDs) is one of the major mechanisms of hypothermic protection against transient focal cerebral ischemia. Previous studies have shown the lack of hypothermic protection against permanent focal ischemia. We hypothesized the lack of hypothermic protection was due to the poor efficacy in suppression of PIDs. To examine the hypothesis, we elucidated the effects of hypothermia on the manner of propagation of PIDs with temporal and spatial resolutions using NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by illuminating the parietal-temporal cortex with ultraviolet light. Spontaneously hypertensive rats (n=14) were subjected to permanent focal ischemia by occlusion of the middle cerebral and left common carotid arteries. 2-h hypothermia (30 degrees C) was initiated before ischemia. Although hypothermia delayed the appearance of PIDs, it did not suppress their appearance. Furthermore, 54% of the PIDs enlarged the high-intensity area of NADH fluorescence in the hypothermia group, similar to the normothermia group (53%). The high-intensity area of NADH fluorescence widened by each PID was larger in the hypothermia group than in the normothermia group. These findings suggest that PIDs even in hypothermia are one of the major factors causing growth of infarction, emphasizing the importance of therapy that targets suppression of PIDs even during hypothermia.

Effect of nitrous oxide on neuronal damage and extracellular glutamate concentration as a function of mild, moderate, or severe ischemia in halothane-anesthetized gerbils.

Background:The effect of nitrous oxide on ischemic neuronal damage was quantitatively evaluated by use of logistic regression curves. Methods:Seventy-two gerbils were anesthetized with 1% halothane and randomly assigned to receive 70% nitrous oxide or 70% nitrogen. Forebrain ischemia was performed for 3, 5, or 7 min, and direct-current potential in the hippocampal CA1 region was recorded. Histologic outcome was evaluated 5 days later. Relations of neuronal damage with ischemic duration and duration of ischemic depolarization were determined by logistic regression curves. In some animals, extracellular glutamate concentration was measured every 60 s during forebrain ischemia. Results:Nitrous oxide increased neuronal damage only with 5 min of ischemia (nitrous oxide vs. nitrogen: 78.5 ± 23.0 vs. 37.3 ± 12.2%; P < 0.01). The percentages of neuronal damage with 3 and 7 min of ischemia were not different with or without nitrous oxide. Logistic regression curves indicated that nitrous oxide significantly increased neuronal damage during the period from 3.07 to 6.63 min of ischemia. Logistic regression curves also indicated that nitrous oxide increased neuronal damage in the condition of the same duration of ischemic depolarization. Nitrous oxide shortened the ischemic duration necessary for causing 50% neuronal damage by 0.82 min. Dynamic change in extracellular glutamate concentration was not different (mean maximum dialysate glutamate concentration: 4.29 ± 3.09 vs. 4.63 ± 1.83 &mgr;m). Conclusion:Administration of nitrous oxide caused an increase in ischemic neuronal damage, but a significant adverse effect was observed with a limited range of ischemic intervals.

Ultrasound-guided peripheral nerve blocks for a patient receiving four kinds of anticoagulant and antiplatelet drugs: a case report

To the Editor: A 64-year-old man was scheduled to undergo right foot amputation because of necrosis caused by obstructive arteriosclerosis. He had undergone coronary arterial bypass grafting 5 years previously and had undergone implantation of a Cypher stent into the left main coronary artery and a device for cardiac resynchronization therapy 3 years previously. Echocardiography showed that the ejection fraction of his left ventricule was 18%. His right coronary branch and left anterior descending branch were completely occluded and these areas were perfused only by coronary bypass graft flow. Warfarin, cilostazol, ticlopidine, and acetylsalicylic acid were administered to maintain his coronary arterial patency. He had also been receiving hemodialysis because of diabetic nephropathy. Administration of cilostazol was stopped and administration of warfarin changed to continuous intravenous infusion of heparin (12000 units per day). Administration of ticlopidine was stopped and administration of acetylsalicylic acid was continued on the day of the surgery (Fig. 1). Intravenous infusion of heparin was stopped at the time our patient entered the operation room. Peripheral nerve blocks were applied for anesthesia. By ultrasoundguidance, popliteal block and femoral nerve block were performed in that order (Fig. 2a, c). Each block was performed by the out-of plane method, and spread of local anesthetics above and below the nerves was confirmed by placing an ultrasound probe parallel to the nerves (Fig. 2b, d). No hemorrhagic complication appeared in the region of the block needle insertion throughout the perioperative period. No consensus has yet been established regarding the indication of superficial peripheral nerve block for patients receiving anticoagulant and antiplatelet drugs [1], and there are several case reports of peripheral nerve block being performed in patients receiving heparin [2, 3]. The current case is the first report of peripheral nerve blocks being safely performed in a patient receiving more than two anticoagulant and antiplatelet drugs during the perioperative period. Left ventricular function of our patient was poor and he had been dehydrated because of his hemodialysis state. Our assessment was that general anesthesia should be avoided because decrease in blood pressure and subsequent hydration during induction of general anesthesia would lead to irreversible ischemic or congestive heart failure. Therefore, peripheral nerve block was the first choice despite the fact that administration of antiplatelet drugs could not be discontinued in our patient because of implantation of a Cypher stent [4]. Anticoagulant effect of heparin and irreversible inhibition of platelet aggregation of ticlopizine and acetylsalicylic acid were continued on the day of the operation. Ultrasound-guided peripheral nerve blocks have some advantages over the blind or nerve stimulation method, and the rate of vascular puncture during peripheral nerve blocks with ultrasound is lower than that without ultrasound [5]. In our case, the out-of plane method was used because the short distance from the skin to nerves might reduce the risk of accidental vascular puncture. Real-time visibility and confirmation of the H. Taninishi (&) K. Morita Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1, Shikata-cho, Kita-ku, Okayama 700-8558, Japan e-mail: tanishi@ops.dti.ne.jp

Ultrasound-assisted epidural anesthesia to amyotrophic woman

To the Editor: A 32-year-old woman (height 140 cm, weight 20.4 kg) was scheduled to undergo ileocecal colostomy for an intractable pelvic abscess caused by a perforated sigmoid diverticulum. She had congenital systemic amyotrophy of unknown cause. Her forced vital capacity was 0.65 l (percent of predicted vital capacity, 25.0 %), and intermittent noninvasive positive pressure ventilation (NIPPV) was performed because of severe hypercapnia (preoperative carbon dioxide tension, 70.1 mmHg). Her respiratory status could not guarantee safe perioperative management by general anesthesia. Because her backbone was not deformed radiologically (Fig. 1a, b), perioperative anesthetic management by epidural anesthesia was applied as a first choice. First, we tried to insert an epidural catheter by the landmark method. However, no spinous process was palpable because she could not hunch her back. Therefore, detection of intervertebral spaces was attempted with the assistance of ultrasound (M-turbo; Sonosite, WA, USA), and only one intervertebral space, probably T12, was detected (Fig. 1c). The distance from skin to epidural space was approximately 2 cm. After making a mark with sterilized ink on the area of the probe center, epidural catheter insertion was attempted. Loss of resistance was achieved at a depth of 2.5 cm from the skin, and the catheter was inserted in the head direction for 3 cm. Intraoperative anesthetic management was completed by 1 % (6 ml) and 0.75 % (2 ml) epidural lidocaine with intravenous infusion of dexmedetomidine for traction pain of peritonea. Oxygen saturation was kept above 97 % by use of NIPPV (room air). Continuous epidural infusion of 0.1 % ropivacaine (2–4 ml/h) for 6 days provided sufficient postoperative analgesia. Use of muscle relaxant and subsequent mechanical ventilation during general anesthesia or postoperative pain temporarily impairs pulmonary function. Because her forced vital capacity after a minor lower abdominal procedure decreased more than 20 % [1], postoperative forced vital capacity in our patient was predicted to be around 500 ml. Further respiratory impairment would reduce quality of life because of dependence on mechanical ventilation and loss of verbal communication by tracheostomy. Effect of epidural anesthesia on respiratory function is minor even if the sensory block has reached the T4 level [2]. We therefore selected epidural anesthesia. Although our patient’s height was that of a lady of small structure for a Japanese, her body weight was that of a child around 6 years of age. Our patient’s height-to-weight ratio, which was different from that of a normal child, and her extended back made it difficult to determine intervertebral spaces by the landmark method. Use of ultrasound makes it possible to noninvasively determine the point of needle insertion and the pathway and distance from the skin to epidural space [3]. Regrettably, ‘‘ultrasound-guided’’ epidural anesthesia was not performed in our patient because the intervertebral space disappeared from the ultrasound screen with minimal movement of the ultrasound probe. However, our experience suggested that only H. Taninishi (&) K. Kawano K. Morita Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1, Shikata-cho, Kita-ku, Okayama 700-8558, Japan e-mail: tanishi@ops.dti.ne.jp