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

Suzuki, Toshio; Okamoto, Yoshiharu; Sekikawa, Toshihiko; Nemoto, Tetsuharu; Moriya, Hideshige; Murayama, S.; Nakaya, Haruaki

doi:10.1254/jjp.68.423

Cited by 4 publications

(3 citation statements)

References 25 publications

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“…Studies of the negative effects of excitatory and inhibitory neurotransmitters in spinal cord ischemia indicate that some of these effects can be antagonized by naloxone. [14][15][16][17][18][19] With the previously demonstrated predictive paraplegia model, the slope of the regression plot for estimated versus actual deficits for a particular technique of repair over time is an estimate of the paraplegia risk for that technique (Table IX and Fig. 3).…”

Section: Discussionmentioning

confidence: 99%

Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement

Acher

Wynn

Hoch

et al. 1998

Journal of Vascular Surgery

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Section: Discussionmentioning

confidence: 99%

Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement

Acher

Wynn

Hoch

et al. 1998

Journal of Vascular Surgery

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“…Previous reports from our and other laboratories indicated that acute spinal ischaemia followed by reperfusion reduced the GABA level of the spinal cord probably by increasing GABA release (Homma et al, 1979;Martiniak et al, 1991;Zhang et al, 1994). Since GABA receptor stimulation inhibited the recovery of PSR potentials after spinal cord ischaemia (Suzuki et al, 1995), nicorandil and pinacidil might inhibit the depolarization-induced GABA release from spinal cord neurones and enhance the recovery of PSR potentials.…”

Section: Resultsmentioning

confidence: 71%

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

Suzuki

Sekikawa

Nemoto

et al. 1995

British J Pharmacology

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1 The pathophysiological significance of ATP-sensitive K+ (KATP) channels in the central nervous system is not fully understood. In this study the effects of nicorandil (a hybrid vasodilator having a dual mechanism of action as a K+ channel opener and a nitrate) on the recovery of the spinal cord reflex potentials after spinal cord ischaemia were examined and compared with those of pinacidil and nitroprusside in anaesthetized spinal cats. 2 Spinal cord ischaemia was produced by occlusion of the thoracic aorta and the bilateral internal mammary arteries for 10 min. Regional blood flow 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 lumbo-sacral ventral root. The recovery process of spinal reflex potentials was reproducible when the occlusion was repeated twice at an interval of 120 min. 3 Pretreatment with nicorandil (30-100 gg kg-') accelerated the recovery of PSR potentials after spinal cord ischaemia. Such an accelerating effect on the recovery of PSR potentials was also shared by pinacidil (100 gg kg-'), another K+ channel opener. In addition, the accelerating effect of nicorandil (100 jIg kg-') on the recovery of PSR potentials was abolished by co-administration of glibenclamide (3 mg kg-'), a sulphonylurea KATP channel blocker. Nitroprusside (8 gg kg-'min-') retarded rather than improved the recovery of PSR potentials after spinal cord ischaemia. All of these drugs failed to improve the spinal cord blood flow during ischaemia and reperfusion. 4 These results suggest that nicorandil promotes the recovery of polysynaptic reflex potentials after spinal cord ischaemia by opening the KATP channels of neurones rather than by increasing local blood flow. K+ channel openers may exert a salutary effect on the functional recovery of the ischaemic spinal cord.

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“…The latter (i.v. bicuculline and semicarbazide [147]) mainly restored reflex potentials after spinal cord ischemia in cats. Thus, the complex mechanism of the role in spinal cord I/R injury exists and needs further distinguishing.…”

Section: The Role Of Gaba In Spinal Cord I/r Injurymentioning

confidence: 99%

The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs

Chen

Zhou

Jian

et al. 2019

Oxidative Medicine and Cellular Longevity

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Ischemia-reperfusion (I/R) injury is a common pathological process, which may lead to dysfunctions and failures of multiple organs. A flawless medical way of endogenous therapeutic target can illuminate accurate clinical applications. γ-Aminobutyric acid (GABA) has been known as a marker in I/R injury of the central nervous system (mainly in the brain) for a long time, and it may play a vital role in the occurrence of I/R injury. It has been observed that throughout cerebral I/R, levels, syntheses, releases, metabolisms, receptors, and transmissions of GABA undergo complex pathological variations. Scientists have investigated the GABAergic enhancers for attenuating cerebral I/R injury; however, discussions on existing problems and mechanisms of available drugs were seldom carried out so far. Therefore, this review would summarize the process of pathological variations in the GABA system under cerebral I/R injury and will cover corresponding probable issues and mechanisms in using GABA-related drugs to illuminate the concern about clinical illness for accurately preventing cerebral I/R injury. In addition, the study will summarize the increasing GABA signals that can prevent I/R injuries occurring in peripheral organs, and the roles of GABA were also discussed correspondingly.

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

Cited by 4 publications

References 25 publications

Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement

Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement

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

The Roles of GABA in Ischemia-Reperfusion Injury in the Central Nervous System and Peripheral Organs

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