Improvement in injury induced hypocalcia by high-dose naloxone intervention

Stokes, Bradford T.; Hollinden, Gary E.; Fox, Phillip R.

doi:10.1016/0006-8993(84)90753-4

Cited by 77 publications

(6 citation statements)

References 23 publications

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“…There are several hypotheses about the mechanism of naloxone, for instance, an action at the opioid receptors (14), an antagonism with excitatory amino acids (15), a blockade of calcium influx (16,17), but the exact mechanism has not yet been determined. Up to the present, however, most investigators have attributed the beneficial effects of the drug to an improvement in spinal cord blood flow.…”

Section: Discussionmentioning

confidence: 99%

Effects of Naloxone and Levallorphan on the Spinal Cord Reflex Potentials under the Spinal Ischemic Condition in Cats

Okamoto

Suzuki

Murayama

1992

Japanese Journal of Pharmacology

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ABSTRACT-The spinal reflex potentials elicited by electrical stimulation of the tibial nerve were re corded from the lumbo-sacral ventral root in spinal cats. When the thoracic aorta and the bilateral in ternal mammary arteries were occluded for 10 min, the potentials were completely depressed. Reap pearance of these potentials could be observed at about 10 min after removal of the occlusion and they gradually recovered. Intravenous injection of naloxone (1 or 10 mg/kg) or levallorphan (0.1 mg/kg) together with removal of occlusion significantly promoted the recovery of the polysynaptic reflex poten tial. Morphine (5 mg/kg) showed no particular effect on the recovery of potentials. Furthermore, pre treatment with morphine (5 mg/kg) did not influence the effects of these opioid antagonists. These re sults suggest that naloxone and levallorphan may preserve or potentiate the interneuronal activities of the lumbo-sacral spinal cord under the ischemic condition and that the effects may not be mediated through morphine-like opioid receptors.

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Section: Discussionmentioning

confidence: 99%

Effects of Naloxone and Levallorphan on the Spinal Cord Reflex Potentials under the Spinal Ischemic Condition in Cats

Okamoto

Suzuki

Murayama

1992

Japanese Journal of Pharmacology

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“…Naloxone is a multi-opioid receptor antagonist that also attenuates NMDA receptor-mediated neurotoxicity in cell cultures involving Ca 2+ , magnesium and Na + , K + -ATPase activity [326,327,328,329]. However, the effects of naloxone in experimental injuries to the CNS are controversial ( Table 11) and clinical trials of naloxone in human SCI failed to reveal any improvement in the neurological outcome.…”

Section: Naloxone and Scimentioning

confidence: 97%

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Sharma¹

2005

CPD

154

218

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Blood-spinal cord barrier (BSCB) plays an important role in the regulation of the fluid microenvironment of the spinal cord. Trauma to the spinal cord impairs the BSCB permeability to proteins leading to vasogenic edema formation. Several endogenous neurochemical mediators and growth factors contribute to trauma induced BSCB disruption. Studies carried out in our laboratory suggest that those drugs and neurotrophic factors capable to attenuate the BSCB dysfunction following trauma are neuroprotective in nature. Whereas, agents that do not exert any influence on the BSCB disruption failed to reduce cell injury. These observations are in line with the idea that BSCB disruption plays an important role in the pathophysiology of spinal cord injuries. The probable mechanism(s) of trauma induced BSCB dysfunction and its contribution to cell injuries are discussed.

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“…Mechanisms of the beneficial effect of naloxone have been postulated to be the antagonism of neurotoxicity produced by excitatory amino acids (20) and the inhibition of transmembrane Ca 2t influx (8,21). However, GABAergic antagonisms, potentially observed in this study, might in part contribute to the acceleration of functional recovery.…”

Section: Effects Of Gabaergic Drugs On the Recovery Of Spinal Reflex mentioning

confidence: 67%

Effects of GABAergic Drugs on the Recovery of Reflex Potentials after Spinal Cord Ischemia in Cats

Suzuki¹,

Okamoto

Sekikawa

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-Effectsof GABAergic drugs on the recovery of reflex potentials after spinal cord ischemia were examined in anesthethized spinal cats. Monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials, elicited by electrical stimulation of the tibial nerve in spinal cats, were recorded from the Jumbo-sacral ventral root. The spinal reflex potentials were immediately depressed by occlusion of the thoracic aorta and the bilateral mammary arteries for 10 min. The potentials recovered gradually to the control level within 90 min after reperfusion. Pretreatment with bicuculline (0.3 mg/kg, i.v.), a GABA antagonist, or semicarbazide (200 mg/kg, i.v.), an inhibitor of GABA synthesis, accelerated the recovery of PSR potentials after the removal of the arterial occlusion. In contrast, pretreatment with aminooxyacetic acid (10 mg/kg, i.v.), an inhibitor of GABA degradation, retarded the recovery of PSR potentials, and this effect was overcome by the addition of the opioid antagonist naloxone (10 mg/kg, i.v.). These results suggest that the GABAergic system retards the recovery of PSR potentials after a brief spinal cord ischemia, which can be antagonized by naloxone.

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Improvement in injury induced hypocalcia by high-dose naloxone intervention

Cited by 77 publications

References 23 publications

Effects of Naloxone and Levallorphan on the Spinal Cord Reflex Potentials under the Spinal Ischemic Condition in Cats

Effects of Naloxone and Levallorphan on the Spinal Cord Reflex Potentials under the Spinal Ischemic Condition in Cats

Pathophysiology of Blood-Spinal Cord Barrier in Traumatic Injury and Repair

Effects of GABAergic Drugs on the Recovery of Reflex Potentials after Spinal Cord Ischemia in Cats

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