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Biomedical subjects

K Omote

Publications and source records attributed to K Omote.

At least 37 records · Page 2Linked to original sources
PubMed1999

Self-guided robotic camera control for laparoscopic surgery compared with human camera control.

BACKGROUND: In laparoscopic surgery, the surgeon no longer has direct visual control of the operation area, and a camera assistant who maneuvers the laparoscope is essential. Problems of cooperation between the two naturally arise, and a robotic assistant that automatically controls the laparoscope can offer a highly desirable alternative to this situation. METHODS: A self-guided robotic camera control system (SGRCCS) based upon a color tracking method has been developed and its use evaluated in 20 cases of laparoscopic cholecystectomy and compared with using human camera control. RESULTS: In 83% of the patients the procedures were successfully completed with the SGRCCS. Set-up time for the robot averaged 21 minutes; and the surgical time with and without the robot averaged 54 and 60 minutes, respectively. Using the robot instead of a human camera assistant significantly reduced both the frequency of the camera correction, 2.2 per hour compared with 15.3 per hour, and frequency of the lens cleaning, 1.0 per hour compared with 6.8 per hour. Subjective assessment by the surgeon revealed that the robot performed better than the human assistant in 71 % of the cases. CONCLUSIONS: In laparoscopic surgery, the SGRCCS offered optimal camera guidance and helped to maintain the surgeon's concentration during the operation.

Cholecystectomy, Laparoscopic↗
PubMed1999

Pretherapeutic laparoscopic staging in advanced gastric carcinoma.

BACKGROUND AND STUDY AIMS: Direct visualization of the abdominal cavity by laparoscopy prior to multimodal treatment may be capable of improving the diagnostic precision of gastric cancer staging. The aim of this study was to evaluate whether diagnostic laparoscopy can influence treatment strategies in gastric cancer staged T3 and T4 by preoperative diagnostic tests. PATIENTS AND METHODS: Extended diagnostic laparoscopy (EDL) was carried out in 111 patients with advanced gastric cancer staged T3 or T4 by computed tomography (CT) and endoluminal ultrasound (EUS). On Lauren's classification of gastric cancer, 46% of the lesions were of the intestinal type and 54% of the nonintestinal type. EDL was carried out with the patients under general anesthesia, and included visual inspection of the abdomen, with surgical exploration of initially inaccessible regions, laparoscopic ultrasound examination, peritoneal lavage, and biopsies. The information provided by laparoscopy was classified as 1) no additional information, 2) important additional findings independent of the tumor stage, 3) downgrading of the tumor to a more favorable stage, and 4) upgrading of the tumor to a less favorable stage. The results of EDL were then compared with those obtained by sonography, CT and EUS in combination. RESULTS: EDL was performed successfully in 107 patients. In 56 of the 111 patients (50.5%), no additional findings were obtained. In 5.4% of cases, additional unforeseen information was found, not connected with the tumor but altering the management. EDL altered the preoperative diagnosis in 51 of the 111 patients (46.0%), leading to changes in management in 45 of them (40.5%). EUS provided additional information in eight cases (7.2% of the whole group, or 15.7% of those in whom the diagnosis had to be changed). Four metastases were detected using EDL. It was possible to rule out peritoneal spread in four patients, but it was newly detected in 26. CONCLUSIONS: Additional information by EDL about the tumor stage in gastric cancer led to a modification of the therapeutic strategy in 40% of patients, in spite of earlier comprehensive diagnostic work-up using modern imaging procedures. EDL should therefore be mandatory if neoadjuvant treatment is planned, in order to avoid either undertreatment or overtreatment of this type of tumor.

Adult↗
PubMed1999

Analgesic effect of intrathecal desipramine on carrageenan-induced thermal hyperalgesia in the rat.

We examined if intrathecal desipramine, a selective norepinephrine reuptake inhibitor, would modulate peripheral inflammation-induced hyperalgesia. Rats were chronically implanted with a lumbar intrathecal catheter and paw withdrawal latency (PWL) to noxious heat stimuli was assessed. Unilateral hindpaw inflammation was induced by intraplantar carrageenan injection. Carrageenan injection significantly (P < 0.05) reduced PWL of the injected paw (from mean 11.4 (SEM 0.6) s to 3.5 (0.2) s, 3 h after carrageenan), but not of the contralateral side (from 11.6 (0.2) s to 11.2 (0.5) s). Intrathecal desipramine 10, 30, 60 and 100 micrograms, which did not produce analgesic effects in untreated rats, dose-dependently reversed the shortened PWL on the ipsilateral side (3.3 (0.2), 5.3 (0.4), 6.2 (0.3) and 9.6 (0.2) s, respectively) without affecting the contralateral side. Pretreatment with intrathecal yohimbine 10 micrograms did not antagonize the anti-hyperalgesic effects of desipramine (from 9.6 (0.2) to 9.8 (0.3) s). Our results suggest that the mechanism underlying the analgesic effect of desipramine on inflammation-induced hyperalgesia is unlikely to be inhibition of norepinephrine reuptake within the spinal cord.

Adrenergic Uptake Inhibitors↗
PubMed1999

Activation of spinal N-methyl-D-aspartate receptors stimulates a nitric oxide/cyclic guanosine 3,5-monophosphate/glutamate release cascade in nociceptive signaling.

BACKGROUND: Increasing evidence has suggested the possibility that the activation of N-methyl-D-aspartate (NMDA) receptors modulates spinal nociceptive transmission via a nitric oxide (NO)/cyclic guanosine 3',5'-monophosphate (cGMP) pathway. However, the existence and the role of an NO/cGMP pathway in the modulation of spinal nociceptive transmission has been unclear. The authors hypothesized that the activation of NMDA receptors stimulates an NO/cGMP pathway, and this pathway evokes glutamate release within the spinal cord, modulating spinal nociceptive transmission. METHODS: The authors have examined the effects of an NO synthase inhibitor and a soluble guanylate cyclase inhibitor on the concentrations of NO metabolites (NO2-/NO3-) and glutamate in the cerebrospinal fluid after intrathecal perfusion of NMDA, concomitantly observing pain-related behavior (scratching, biting, and vocalization) in unanesthetized, free-moving rats using an intrathecal microdialysis method. The contents of cGMP in the dorsal horn were also measured using enzyme immunoassay method. RESULTS: Intrathecal perfusion of NMDA produced pain-related behavior and increased glutamate and NO2-/NO3-concentrations in a dose-dependent manner. A competitive NMDA receptor antagonist, D,L-2-amino-5-phosphonovaleric acid, completely blocked the NMDA-induced responses. An NO synthase inhibitor, N(G)-monomethyl-L-arginine acetate, at a dose that completely blocked the increase in NO2-/NO3-, inhibited both the NMDA-induced pain-related behavior and the increase in glutamate concentration. In addition, a soluble guanylate cyclase inhibitor, 1H-[1,2,4]oxadiazole[4,3-a]quinoxaline-1-one, also inhibited significantly NMDA-induced pain-related behavior and the increase in glutamate concentration. NMDA induced an increase in cGMP in the dorsal half of the spinal cord, which was blocked by N(G)-monomethyl-L-arginine acetate. CONCLUSIONS: The results of this study support the hypothesis that the activation of NMDA receptors modulated pain-related behavior via an NO/cGMP/glutamate release cascade within the spinal cord.

2-Amino-5-phosphonovalerate↗
PubMed1999

[Low-dose CPT-11 against a recurrent rectal cancer--a case report].

We attempted a new regimen of low-dose CPT-11 on a 5-FU resistant recurrent rectal cancer patient with multiple lung metastases and a paraaortic lymph node metastasis. CPT-11 was administered at 25 mg/m2/day x 3/week by intravenous infusion. Serum CEA level decreased gradually with a half time of approximately 4 weeks. The lung metastases almost disappeared and the paraaortic lymph node was also reduced more than 50%. There were no adverse effects except slight alopetia. This treatment could be continued on an outpatient basis. These results suggest that low-dose CPT-11 may be more effective and tolerable than the conventional, CPT-11 therapy.

Antineoplastic Agents, Phytogenic↗
PubMed1998

Formalin-induced nociception activates a monoaminergic descending inhibitory system.

Neural plasticity of afferent pain pathways that is induced by prolonged or repeated noxious stimuli may contribute to activate intrinsic inhibitory mechanisms in CNS. In order to clarify the role of the monoaminergic descending inhibitory system in acute nociception and inflammatory pain, we examined if this inhibitory system would modulate the tonic response to formalin-induced nociception. Yohimbine, alpha2 adrenergic antagonist, or methysergide, serotonin antagonist was administered intrathecally before or after subcutaneous 2% formalin injection into the plantar of the hind paw in rats. In another series of the experiment, the tissue of the spinal dorsal half of the untreated rats and post-formalin-treated rats were sampled and analyses of monoamine levels were carried out by HPLC. The subcutaneous formalin evoked biphasic flinching behavior of the injected paw. Intrathecal pretreatment with yohimbine and methysergide produced a significantly greater increase in the number of flinches than in the control in phase 1, intermediate period and phase 2. Posttreatment with yohimbine and methysergide showed a significantly greater increase in the number of flinches in phase 2. Furthermore, formalin injection induced significant increases in noradrenaline, MHPG, serotonin (5-hydroxytryptamine; 5-HT) and 5-HIAA concentrations in both the ipsi- and contralateral dorsal halves. These results suggest that the pain state produced by formalin-induced chemical and/or inflammatory nociception is under the modulation of the monoaminergic (noradrenergic and serotonergic) descending inhibitory system.

Adrenergic alpha-Antagonists↗
PubMed1998

Partial structural functions of binary liquids estimated from anomalous X-ray scattering measurements.

A new apparatus has been built for structural studies of high-temperature liquids using the anomalous X-ray scattering (AXS) method with synchrotron radiation. AXS measurements were made in the asymmetrical reflection mode for a free liquid surface by changing the beam direction using an additional mirror system. The usefulness and capabilities of this new equipment were confirmed by obtaining the individual partial structural functions of liquid Bi(30)Ga(70) alloy.

Journal Article↗
PubMed1998

Formalin-induced release of excitatory amino acids in the skin of the rat hindpaw.

Application of glutamate to skin evokes pain-related behaviors [S.M. Carlton, G.L. Hargett, R.E. Coggeshall, Localization and activation of glutamate receptors in unmyelinated axons of rat glabrous skin, Neurosci. Lett., 197 (1995) 25-28; D.L. Jackson, C.B. Graff, J.D. Richardson, K.M. Hargreaves, Glutamate participates in the peripheral modulation of thermal hyperalgesia in rats, Eur. J. Pharmacol., 284 (1995) 321-325.] and peripherally-administered glutamate antagonists can prevent the nociception produced by inflammation [E.M. Davidson, R.E. Coggeshall, S.M. Carlton, Peripheral NMDA and non-NMDA glutamate receptors contribute to nociceptive behaviors in the rat formalin test, NeuroReport, 8 (1997) 941-946; Jackson et al., 1995.] In this study, the concentrations of glutamate and aspartate in the plantar of the rat hindpaws were measured before and after the subcutaneous administration of formalin. Increases in glutamate and aspartate concentrations were observed on the ipsilateral side, but not on the contralateral side, to the injection. This shows that nociception and inflammation caused by formalin injection induces the release of peripheral glutamate and aspartate, which would contribute to nociception and inflammatory pain.

Animals↗
PubMed1998

Direct evidence for the role of nitric oxide on the glutamate-induced neuronal death in cultured cortical neurons.

It has been reported that glutamate-induced neurotoxicity is related to an increase in nitric oxide (NO) concentration. An NO-sensitive electrode has been developed to measure NO concentration directly. Using this electrode, we examined NO concentration and neuronal survival after glutamate application in rat cultured cortical neurons. We also examined the effects of NMDA receptor antagonists, MK-801 and ketamine, and the NO synthetase inhibitor, L-NMMA on NO production and neuronal death. After 7 days in culture, application of glutamate (1 mM) or L-arginine (0.3 mM) to the cultured medium increased NO concentration, and decreased the number of anti-microtubule-associated protein 2 positive neurons. Both pretreatment with MK-801 (300 microns) and ketamine (300 microns) prevented glutamate-, but not L-arginine-induced increase in NO concentration and neuronal death. L-NMMA prevented both glutamate- and L-arginine-induced NO production and neuronal death. The nitric oxide donor, S-nitroso-N-acetyl-D,L-penicillamine (SNAP) also caused neuronal death, and MK-801, ketamine and L-NMMA did not prevent SNAP-induced toxicity. We have demonstrated excitatory amino acid-induced changes of NO concentration and the parallel relationship between changes of NO concentration and neuronal death. In conclusion, an increase in NO concentration does induce neuronal death, and the inhibition of the production of NO prevents glutamate-induced neuronal death.

Animals↗
PubMed1998

Premedication with oral dextromethorphan reduces postoperative pain after tonsillectomy.

UNLABELLED: The aim of the present study was to examine whether premedication with dextromethorphan, a clinically available N-methyl-D-aspartic acid (NMDA) receptor antagonist, could reduce postoperative pain after tonsillectomy. Thirty-six patients scheduled for elective bilateral tonsillectomy were investigated in a double-blinded, randomized study. The patients were randomly assigned to one of three groups: control, dextromethorphan 30 mg (Dex 30), and dextromethorphan 45 mg (Dex 45) groups. In the control group, premedication was with oral placebo and intramuscular (i.m.) midazolam and atropine. In the Dex 30 and Dex 45 groups, patients were premedicated with i.m. midazolam and atropine and oral dextromethorphan 30 mg and 45 mg, respectively. Pain was evaluated repeatedly throughout 7 postoperative days, at rest and on swallowing, using a self-rating visual analog scale (VAS). The total doses of analgesics administered postoperatively were also recorded. The Dex 45 group showed significantly lower VAS scores than the control group both at rest and on swallowing throughout the 7 days. The total doses of postoperative analgesics in the Dex 45 group were significantly less than those in the control group. The Dex 30 group showed significantly lower VAS scores than the control group at rest, but not on swallowing. These results indicate that premedication with Dex 45 reduces postoperative pain after tonsillectomy, not only at rest but on swallowing. IMPLICATIONS: Recently, it has been suggested that central sensitization caused by the activation of N-methyl-D-aspartic acid receptors may contribute to the postoperative pain. We found that premedication with 45 mg of dextromethorphan, a clinically available N-methyl-D-aspartic acid receptor antagonist, reduced postoperative pain after tonsillectomy.

Administration, Oral↗
PubMed1998

[Suppressive effects of ketamine on neuropathic pain].

We previously reported that ketamine analgesia in acute pain was produced by the activation of the monoaminergic descending inhibitory system. Recent studies have confirmed that the NMDA receptor antagonists attenuate the hyperalgesia in neuropathic pain. In this study, we investigated the suppressive effects of a clinically available NMDA antagonist, ketamine, and the mechanisms of its effects on neuropathic pain in rats with peripheral mononeuropathy. A unilateral chronic constriction injury (CCI) model was introduced by loose ligation of the sciatic nerve of the rats. The CCI rats showed hyperalgesia to thermal and mechanical pressure stimuli on the injured side of their hind paws. Intraperitoneal (IP) ketamine (25 or 50 mg.kg-1) and intrathecal (IT) ketamine (25-500 micrograms) reversed, dose-dependently, both thermal and mechanical hyperalgesia. Pretreatment with IT yohimbine (alpha-2 adrenergic antagonist) or IT methysergide (serotonergic antagonist) did not show the suppressive effects of IP ketamine (50 mg.kg-1) on hyperalgesia. Concentrations of norepinephrine (NE) and serotonin (5HT) in the spinal dorsal horn were measured using high performance liquid chromatography. The CCI rats showed increased NE and 5HT concentrations on both ligated and unligated sides of spinal dorsal horn, compared with shamoperated rats. IP ketamine (50 mg.kg-1) in the CCI rats did not boost the spinal NE or 5HT levels. These results indicate that the anti-hyperalgesic effect of ketamine is derived from a direct action on the spinal cord, but not from the activation of monoaminergic descending inhibitory systems.

Acute Disease↗
PubMed1997

Antinociceptive interaction of intrathecal alpha2-adrenergic agonists, tizanidine and clonidine, with lidocaine in rats.

BACKGROUND: The intrathecal alpha2-adrenergic agonist, clonidine, has been shown to have considerable antinociceptive effect, although clonidine causes hypotension and bradycardia. The combination of intrathecal clonidine and local anesthetics enhances analgesic effects, whereas the combination may cause marked hypotension and motor blockade, which may limit the clinical application of the combination. Tizanidine, another alpha2-adrenergic agonist, has also provided antinociception without producing pronounced hemodynamic changes. This study was designed to evaluate the antinociceptive and hemodynamic interactions of tizanidine and clonidine with lidocaine. METHODS: Male Sprague Dawley rats were chronically implanted with lumbar intrathecal catheters. The tail-flick test was used to assess the thermal nociceptive threshold. The ability of intrathecal tizanidine, clonidine, lidocaine, or the combinations of alpha2-adrenergic agonist and lidocaine to alter the tail-flick latency was examined. To characterize the antinociceptive interaction, the isobolographic analysis was applied. Additionally, the motor function, blood pressure and heart rate after intrathecal administration of drugs and combinations were also monitored. RESULTS: Intrathecal tizanidine, clonidine, or the combinations increased the tail-flick latency in dose- and time-dependent fashion without affecting motor function. The order potencies (dose producing a 50% of peak effect, in microg) of tizanidine and clonidine were 1.8 and 0.75, respectively. With isobolographic analysis, tizanidine with lidocaine and clonidine with lidocaine showed significantly synergistic antinociceptive interaction. Potency ratio analysis and fractional analysis also confirmed the synergistic interaction. At the doses in the combinations showing comparable antinociception, tizanidine with lidocaine, unlike clonidine with lidocaine, did not affect motor function or blood pressure. CONCLUSION: The authors' results show that intrathecal tizanidine and clonidine synergistically interact with lidocaine so that the degree of antinociception to somatic noxious stimuli are enhanced. The antinociceptive synergistic interaction between tizanidine and lidocaine may be useful in clinical practice without affecting blood pressure, heart rate, or motor function.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1997

[A case of right cranial polyneuropathy following the onset of herpetic eruptions associated with severe pain on the left cranial and cervical regions].

We describe a case presenting herpetic eruptions and pain in the left cranial and cervical regions, followed by right cranial polyneuropathy. The patient, a 66-yr-old male, developed a diphasic syndrome which was first characterized by herpetic eruptions on the whole of his left cranial and cervical regions with severe pain and left facial nerve palsy. Two weeks later, right multiple cranial nerve palsies of III, V, and VII and an increase in CSF protein appeared in a second phase. Neuroimaging technique (MRI) did not provide any evidence of brain involvement. The immediate use of steroid therapy led to improvement of the symptoms of cranial polyneuropathy. The clinical course suggests that reactivation of a latent herpes simplex virus may have been the etiologic cause of the cranial polyneuropathy. Steroid therapy should be applied to the treatment of cranial polyneuropathy in patients showing a similar pattern to this case.

Aged↗
PubMed1996

Roles of monoaminergic, glycinergic and GABAergic inhibitory systems in the spinal cord in rats with peripheral mononeuropathy.

The current study was designed to determine if the monoaminergic descending inhibitory system and the glycinergic and GABAergic inhibitory systems were activated in the spinal cord in the presence of peripheral mononeuropathy produced by loose ligatures around the common sciatic nerve. The time course of withdrawal latencies to thermal stimuli were assayed in lesioned and sham-operated rats. The levels of monoamines (serotonin; 5-HT, noradrenaline, and dopamine), glycine and gamma-aminobutyric acid (GABA) in the dorsal half of the spinal cord were measured using HPLC with electrochemical detection. Furthermore, on day 7 after nerve ligation, intrathecal methysergide, yohimbine, strychnine or bicuculline was administered in order to investigate the roles of these inhibitory neuromodulators in this pathological pain state. The levels of 5-HT and noradrenaline significantly increased in both ipsi- and contralateral sides of the dorsal half of the lumbar spinal cord in the lesioned, but not sham-operated animals. The levels of glycine and GABA in the ipsilateral dorsal half of the spinal cord increased significantly and were significantly higher than in the contralateral side. Intrathecal antagonists of 5-HT, noradrenaline, glycine and GABA produced enhancement of the magnitude of hyperalgesia on the lesioned hindpaw. We also examined the effects of four daily single treatments with intrathecal MK-801 beginning 15 min prior to nerve ligation on the development of thermal hyperalgesia and on the contents of the neuromodulators in the ligation model. MK-801 treatment effectively abolished the increases in 5-HT, noradrenaline, glycine and GABA levels as well as preventing the development of hyperalgesia. The results of the present study suggest that the pathological pain state activates or increases the activity of these inhibitory systems.

Analysis of Variance↗
PubMed1996

Potentiation of local lignocaine-induced sensory block by calcium channel blockers in rats.

We have studied the effects of three different types of calcium channel blockers (verapamil, diltiazem, and nicardipine) on local lignocaine sensory block. The standardized tail flick test was used to measure the duration and degree of lignocaine-induced conduction block in rats. After obtaining baseline tail flick latencies (mean 3.2 s), two 100-microliter doses of 0.3% lignocaine alone, a combination of verapamil 25, 100 or 200 micrograms, diltiazem 25, 100 or 200 micrograms, or nicardipine 0.5, 1.0 or 2.0 micrograms, and a large dose of calcium channel blockers (verapamil 200 micrograms, diltiazem 200 micrograms or nicardipine 2.0 micrograms) were injected on opposite sites of the tail base and the tail flick test was performed every 5 min for 45 min. A large dose of the calcium channel blockers showed no prolongation of tail flick latencies. Administration of 0.3% lignocaine alone produced a significant increase in tail flick thresholds and the peak effect of the percentage maximum possible effect (% MPE) was demonstrated at 5 min after drug injection (mean % MPE 28.8%; P < 0.01 vs baseline). Co-administration of 0.3% lignocaine and three doses of verapamil produced significant increases in area under the curve (AUC) in a dose-dependent fashion. Mean AUC values for 0.3% lignocaine alone and a combination of verapamil 25, 100 or 200 micrograms were 217.5, 502.5, 529.1 and 1600.3, respectively. Almost similar patterns of augmentation in AUC values were demonstrated after addition of different doses of diltiazem or nicardipine to 0.3% lignocaine. We conclude that the use of mixtures of local anaesthetic and calcium channel blocker potentiated lignocaine sensory block at the level of the peripheral nerves.

Anesthetics, Local↗
PubMed1996

Spinal antinociceptive action of an N-Type voltage-dependent calcium channel blocker and the synergistic interaction with morphine.

BACKGROUND: Four different voltage-dependent calcium channels (L-, N-, T-, and P-types) are distinguished in the central nervous system. Both L- and N-type calcium channels have been implicated in the release of neurotransmitters from sensory neurons in the spinal cord. It has been demonstrated that intrathecal L-type calcium channel blockers, which alone do not exhibit any antinociceptive effects, potentiate the antinociceptive effect of intrathecal morphine. The current study was designed to investigate the antinociceptive effects of the intrathecally administered N-type calcium channel blocker, omega-conotoxin GVIA (omega-CgTx). The interaction between morphine and omega-CgTx at the level of the spinal cord also was examined. METHODS: In male Sprague-Dawley rats, lumbar intrathecal catheters were chronically implanted. Tail flick and mechanical paw pressure tests were used to assess thermal and mechanical nociceptive thresholds, respectively. Morphine, omega-CgTx, or a combination of morphine and omega-CgTx was administered intrathecally, and the nociceptive thresholds were determined. Isobolographic analyses were used to define the nature of the functional interactions between morphine and omega-CgTx. RESULTS: Intrathecal omega-CgTx produced antinociception in a dose- and time-dependent manner. Isobolographic analyses revealed that intrathecal omega-CgTx and morphine interacted synergistically in both nociceptive tests. CONCLUSIONS: This study indicates the importance of the N-type calcium channel in the spinal cord on nociception and suggests the functional interaction between the N-type calcium channel blocker and opioid at the level of the spinal cord.

Analgesics↗