Effects of nicorandil on the recovery of reflex potentials after spinal cord ischaemia in cats

Suzuki, Toshio; Sekikawa, Toshihiko; Nemoto, Tetsuharu; Moriya, Hideshige; Nakaya, Haruaki

doi:10.1111/j.1476-5381.1995.tb16668.x

Cited by 12 publications

(9 citation statements)

References 37 publications

(38 reference statements)

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“…Recently we have found that nicorandil and pinacidil, K + channel openers, accelerate the recovery of reflex potentials after a transient spinal cord ischemia in anesthetized spinal cats (Suzuki et al 1995). In contrast, nitroprusside, a NO donor, retarded the recovery of reflex potentials (Suzuki et al 1995).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, nitroprusside, a NO donor, retarded the recovery of reflex potentials (Suzuki et al 1995). These findings prompted us to evaluate the pathophysiological role of NO in the functional recovery after spinal cord ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…We have recently observed that nitroprusside, a NO donor, retarded the functional recovery from transient spinal cord ischemia in cats (Suzuki et al 1995). Therefore, NO production may be deleterious for ischemic injuries of the spinal cord.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of nitric oxide synthesis accelerates the recovery of polysynapitc reflex potentials after transient spinal cord ischemia in cats

Nemoto

Sekikawa

Suzuki

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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Nitric Oxide (NO) has been implicated as a mediator of neuronal injury in vascular stroke. On the other hand, NO is suggested to play a neuroprotective role by increasing blood flow during cerebral ischemia. In order to evaluate the role of NO in the spinal cord ischemia, effects of nitric oxide synthase (NOS) inhibition on the recovery of reflex potentials after a transient spinal cord ischemia were examined in urethane-chloralose anesthetized spinal cats. Spinal cord ischemia was produced by occlusion of the thoracic aorta and the both internal mammary arteries for 10 min. Regional blood flow (RBF) in the spinal cord was continuously measured with a laser-Doppler flow meter. The monosynaptic (MSR) and polysynaptic reflex (PSR) potentials elicited by electrical stimulation of the tibial nerve, were recorded from the L7 or S1 ventral root. The recovery process of spinal reflex potentials was reproducible when the oclusion was repeated twice at an interval of 120 min. Pretreatment with N(G)-monomethyl-L-arginine (L-NMMA, 10 mg/kg), a NOS inhibitor significantly accelerated the recovery of PSR potentials after spinal cord ischemia. The accelerating effect of L-NMMA on the recovery of PSR potentials was abolished by co-administration of L-arginine (1 mg/kg/min) but not by that of D-arginine (1 mg/kg/min). L-NMMA failed to improve RBF in the spinal cord during ischemia and reperfusion. Nitroprusside (10 microg/kg/min), a NO donor, retarded the recovery of PSR potentials after spinal cord ischemia. These results suggest that NO production has a significant influence on the functional recovery after transient spinal cord ischemia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibition of nitric oxide synthesis accelerates the recovery of polysynapitc reflex potentials after transient spinal cord ischemia in cats

Nemoto

Sekikawa

Suzuki

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Wind et al 32 found protection of cultured neurons against chemically induced hypoxia by bimakalim, a K ATP activator. Suzuki and coworkers 33 showed that pretreatment with pinacidil, a partial K ATP agonist, shortened the recovery time of spinal reflexes after spinal ischemia in cats. When glibenclamide, an inhibitor of K ATP , was coadministered, the protective effect was absent.…”

Section: Discussionmentioning

confidence: 99%

Potassium Channel Activators Protect the N -Methyl- d -Aspartate–Induced Cerebral Vascular Dilation After Combined Hypoxia and Ischemia in Piglets

Veltkamp

Domoki²,

Bari³

et al. 1998

Stroke

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Background and Purpose-Cerebral arteriolar dilation to N-methyl-D-aspartate (NMDA) is a neuronally mediated multistep process that is sensitive to cerebral hypoxia and ischemia (H/I). We tested the hypothesis that topical pretreatment with the selective potassium channel agonists NS1619 and aprikalim preserves the vascular response to NMDA after consecutive H/I. Methods-Pial arteriolar diameters were measured in anesthetized piglets with the use of a closed cranial window and intravital microscopy. Arteriolar responses to NMDA (10 Ϫ5 , 5ϫ10 Ϫ5 , and 10 Ϫ4 mol/L) were recorded before and 1 hour after 10 minutes of hypoxia (8.5% O 2 in N 2 ) plus 10 minutes of ischemia (H/I). Ischemia was induced by increasing intracranial pressure. Subgroups were topically pretreated with 10 Ϫ5 mol/L NS1619, 10 Ϫ6 mol/L aprikalim, 10 Ϫ6 mol/L calcitonin gene-related peptide (CGRP), or 10 Ϫ5 mol/L papaverine. We also examined the effects of H/I on vascular responses to kainate (10 Ϫ4 mol/L) to assess specificity of neuronal injury. Results-Arteriolar responses to NMDA were significantly attenuated after H/I. Baseline compared with post-H/I arteriolar diameters were 9Ϯ4% versus 3Ϯ2% at 10 Ϫ5 mol/L, 22Ϯ4% versus 4Ϯ2% at 5ϫ10 Ϫ5 mol/L, and 33Ϯ4% versus 7Ϯ2% at 10 Ϫ4 mol/L (meanϮSE; all PϽ.05, nϭ7). Pretreatment with NS1619 and aprikalim preserved the arteriolar responses to NMDA after H/I. For NS1619 (nϭ6), values were as follows: 9Ϯ2% versus 6Ϯ4% at 10 Ϫ5 mol/L, 19Ϯ6% versus 21Ϯ5% at 5ϫ10 Ϫ5 mol/L, and 35Ϯ3% versus 31Ϯ5% at 10 Ϫ4 mol/L. For aprikalim (nϭ7), values were as follows: 6Ϯ2% versus 8Ϯ2% at 10 Ϫ5 mol/L, 22Ϯ6% versus 15Ϯ3% at 5ϫ10 Ϫ5 mol/L, and 41Ϯ5% versus 32Ϯ6% at 10

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“…The accelerated recovery of polysynaptic reflex potentials elicited by L-NMMA was abolished by coadministration of L-, but not D-arginine. Nitroprusside, an NO donor, retards the recovery of polysynaptic reflex potentials after transient spinal cord ischaemia (Suzuki et al 1995;Nemoto et al 1997). However, it is not known whether inhibition of NOS also improves neurological function in the chronic phase after spinal cord injury.…”

Section: Introductionmentioning

confidence: 99%

Beneficial effects of nitric oxide synthase inhibition on the recovery of neurological function after spinal cord injury in rats

Suzuki

Tatsuoka

Chiba

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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We have demonstrated recently that treatment with N(G)-monomethyl-L-arginine (L-NMMA) accelerates electrophysiological recovery after transient spinal cord ischaemia in anaesthetized cats. To determine whether nitric oxide synthase (NOS) inhibition in the acute phase of spinal cord injury results in better functional recovery in the chronic phase, we evaluated the influence of L-NMMA on the time course of changes of neurological function and the histopathological changes after spinal cord compression in rats. Experimental spinal cord injury was produced in anaesthetized rats by short-term (5 min) compression with a thread placed around the spinal cord at T13. The recovery of motor function was assessed by a treadmill test 10, 20 and 30 days after spinal cord compression. The latency of potentials evoked by hindlimb stimulation was measured at the funiculus posterior at C1 10 days after the spinal cord injury in anaesthetized rats. Histological examinations were also performed at the same time. The compression-induced spinal cord injury resulted in motor dysfunction of hindlimbs, an increase in the latency of the evoked potentials and neuronal degeneration in funiculus posterior at T13. Repeated administration of L-NMMA for 1 day significantly accelerated the recovery of the motor function, shortened the latency of the evoked potentials and attenuated the myelin vacuolization in the spinal cord. These beneficial effects of L-NMMA on neurological function and histopathological changes were abolished by coadministration of L- but not D-arginine. These results suggest that NOS inhibition during the early stage of spinal cord injury has beneficial effects on the recovery of neurological function and the histopathological changes in the chronic stage.

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Effects of nicorandil on the recovery of reflex potentials after spinal cord ischaemia in cats

Cited by 12 publications

References 37 publications

Inhibition of nitric oxide synthesis accelerates the recovery of polysynapitc reflex potentials after transient spinal cord ischemia in cats

Inhibition of nitric oxide synthesis accelerates the recovery of polysynapitc reflex potentials after transient spinal cord ischemia in cats

Potassium Channel Activators Protect the N -Methyl- d -Aspartate–Induced Cerebral Vascular Dilation After Combined Hypoxia and Ischemia in Piglets

Beneficial effects of nitric oxide synthase inhibition on the recovery of neurological function after spinal cord injury in rats

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