Nobuhisa Iriuchijima

Gunma University, Maebashi-shi, Gunma-ken, Japan

Are you Nobuhisa Iriuchijima?

Claim your profile

Publications (5)13.26 Total impact

  • Source
    [show abstract] [hide abstract]
    ABSTRACT: Purpose: Several different anti-hypertensive regimens have been introduced for the prevention of systemic hyperdynamic responses after electrically induced seizures. In the present study, the effects of anti-hypertensive medications on cerebral circulation were studied. Methods: Systemic blood pressure was controlled by several anti-hypertensive medications, nicardipine, prostaglandin EI, alprenolol and nitroglycerin, in 30 patients (150 electroconvulsive therapy trials). Changes in cerebral blood flow velocity were measured by transcranial Doppler sonography of the right middle cerebral artery from the start of anesthesia to 10 min after the electrical shock. Results: Administration of a Ca2+ antagonist, nicardipine, or prostaglandin EI did not alter the augmented cerebral blood flow velocity after the seizure. However, a ß-adrenergic blocking agent, alprenolol (P<0.05) or nitroglycerin (P<0.01) partially inhibited the increase in cerebral blood flow velocity. Maximal blood flow velocity was 133% larger than the pre-anesthesia value in the control group, 109% in the nicardipine group, 113% in the prostaglandin EI group, 72% in the alprenolol group, and 45% in the nitroglycerin group, respectively. The increase in cerebral blood flow velocity after electrically induced seizure was independent of systemic blood pressure. Internal jugular venous saturation (SjO2) was increased, and difference in arterial and venous concentrations of lactate was not altered in all groups. Conclusions: Cerebral hemodynamics is altered by ECT, even when systemic hemodynamics are stabilized by antihypertensive medication. Although the effects of antihypertensive medicine on cerebral hemodynamics are variable, systemic blood pressure control by these agents does not induce cerebral ischemia after ECT. Objectif: Différentes thérapies antihypertensives ont été proposées comme moyen de prévention des réponses hyperdynamiques généralisées à la suite d’électrochocs. Dans la présente étude, on a analysé les effets de médicaments antihypertenseurs sur la circulation cérébrale. Méthode: La pression sanguine générale a été contrôlée par différents médicaments antihypertenseurs, la nicardipine, la prostaglandine El, l’alprénolol et la nitroglycérine, chez 30 patients lors de 150 essais d’électrochocs. Les changements de vitesse circulatoire cérébrale ont été mesurés par échographie Doppler transcrânienne de l’artère cérébrale moyenne droite, du début de l’anesthésie jusqu’à 10 min après l’électrochoc. Résultats: L’administration d’un antagoniste de Ca2+, la nicardipine, ou la prostaglandine El n’ont pas modifié la vitesse circulatoire cérébrale augmentée après les convulsions. Toutefois, un agent ß-bloquant, l’alprénolol (P<0,05) ou la nitroglycérine (P<0,01) ont partiellement inhibé l’augmentation de vitesse circulatoire cérébrale. La vitesse circulatoire maximale a été 133 % de la valeur préanesthésique mesurée dans le groupe témoin, de 109 % dans le groupe nicardipine, de 113 % dans le groupe prostaglandine El, de 72 % dans le groupe alprénolol et de 45 % dans le groupe nitroglycérine, respectivement. L’augmentation de la vitesse circulatoire cérébrale à la suite d’électrochocs a été indépendante de la pression sanguine générale. La saturation en oxygène de la veine jugulaire interne (SjO2) a été augmentée et les différences de concentration artérielle et veineuse de lactate n’ont pas été modifiées, dans aucun groupe. Conclusion: L’hémodynamie cérébrale est modifiée par l’électrochoc, même quand la stabilité de l’hémodynamie générale est conservée par une médication antihypertensive. Quoique les effets des antihypertenseurs sur l’hémodynamie cérébrale soient variables, la pression sanguine contrôlée par ces médicaments n’induit pas d’ischémie cérébrale après l’électrochoc.
    Canadian Journal of Anaesthesia 04/2012; 47(8):767-774. · 2.13 Impact Factor
  • Kunie Nakajima, Hideaki Obata, Nobuhisa Iriuchijima, Shigeru Saito
    [show abstract] [hide abstract]
    ABSTRACT: Antidepressants are often used for the treatment of neuropathic pain. Clinical studies suggest that the efficacy of serotonin (5-HT) and noradrenaline (NA) reuptake inhibitors (SNRIs) for neuropathic pain is greater than that of selective 5-HT reuptake inhibitors (SSRIs). In the present study, we determined the efficacy and mechanisms involved in the antihyperalgesic effects of milnacipran, an SNRI, compared with paroxetine, an SSRI, and maprotiline, a selective NA reuptake inhibitor, using a rat model of neuropathic pain. Male Sprague-Dawley rats underwent spinal nerve ligation (SNL), and the withdrawal threshold to paw pressure was measured. Intraperitoneal injection of milnacipran (3-30mg/kg) produced a dose-dependent antihyperalgesic effect. The effect was reversed by intrathecal injection of the α(2)-adrenoceptor antagonist idazoxan (30μg), but not by various 5-HT receptor antagonists. Paroxetine produced an antihyperalgesic effect only at the highest dose tested (10mg/kg). This effect was reversed by intrathecal injection of both idazoxan and ondansetron (30μg), a 5-HT3 receptor antagonist. Maprotiline produced an antihyperalgesic effect (10 and 30mg/kg), and the effect was reversed by intrathecal idazoxan. In microdialysis studies, NA and 5-HT concentrations in the spinal dorsal horn were increased after injection of either milnacipran or paroxetine, and only NA was increased after maprotiline. Furthermore, the NA content in the spinal cord of SNL rats was greater than that in normal animals. These findings suggest that an increase in NA in the spinal cord plays an important role in the antihyperalgesic effects of not only NA reuptake inhibitors but also SSRIs.
    Pain 03/2012; 153(5):990-7. · 5.64 Impact Factor
  • Anesthesia and analgesia 11/2009; 109(5):1416-8. · 3.08 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: We previously demonstrated that cAMP-dependent protein kinase was reduced in the dendrites of MAP2-deficient mice. In this study, we compared the expression of various protein phosphatases (PPs) between wild-type and map2(-/-) dendrites. Kinase-associated phosphatase (KAP) was the only PP which showed difference between the two phenotypes: (1) the expression of KAP was reduced in map2(-/-) cortical dendrites, and (2) the amount of KAP bound to microtubules was reduced in map2(-/-) brains. We also demonstrated in cultured neuroblastoma cells that KAP is not only expressed in dividing cells, but also in the neurites of differentiated cells. Our findings propose that KAP, which has been reported to function in cell-cycle control, has an as yet uncovered role in regulating dendritic functions. We also propose MAP2-deficient mice as an ideal system for identifying protein phosphatases essential for dendritic functions.
    Biochemical and Biophysical Research Communications 01/2006; 338(2):1216-21. · 2.41 Impact Factor
  • [show abstract] [hide abstract]
    ABSTRACT: A 49-year-old man developed severe headache after spinal anesthesia. We found diffuse meningeal enhancement on gadolinium enhanced MRI and diffuse meningeal thickening on plain MRI. These MRI findings and postural headache suggest intracranial hypotension. Injection of autologous blood 10 ml into his epidural space was effective to ameliorate the headache. MRI findings were useful for the diagnosis of postspinal headache.
    Masui. The Japanese journal of anesthesiology 08/2003; 52(7):789-91.