start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=3
article-no=
start-page=292
end-page=298
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=201307
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Quantitative evaluation of the neuroprotective effects of a short-acting β-adrenoceptor antagonist at a clinical dose on forebrain ischemia in gerbils: effects of esmolol on ischemic depolarization and histologic outcome of hippocampal CA1.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=BACKGROUND:
Neuroprotective effects of esmolol in laboratory and clinical settings have been reported. The present study was designed to quantitatively evaluate the neuroprotective effects of esmolol using logistic regression curves and extracellular potentials.
MATERIALS AND METHODS:
In 42 gerbils, bilateral occlusion of common carotid arteries was performed for 3, 5, or 7 minutes (n=7 in each group). In treated animals, esmolol (200 µg/kg/min) was administered for 90 minutes, 30 minutes before the onset of ischemia. Direct current potentials were measured in the bilateral CA1 regions, in which histologic evaluation was performed 5 days later. Relations of neuronal damage with ischemic duration and duration of ischemic depolarization were determined using logistic regression curves.
RESULTS:
There was no significant difference in onset time between the 2 groups (the control group vs. the esmolol group: 1.65±0.46 vs. 1.68±0.45 min, P=0.76), and significant differences in durations of ischemic depolarization were not observed with any ischemic duration. However, logistic regression curves indicated that esmolol has a neuroprotective effect from 2.95 to 7.66 minutes of ischemic depolarization (P<0.05), and esmolol prolonged the duration of ischemic depolarization causing 50% neuronal damage from 4.97 to 6.34 minutes (P<0.05). Logistic regression curves also indicated that esmolol has a neuroprotective effect from 3.77 to 7.74 minutes of ischemic duration (P<0.05), and esmolol prolonged the ischemic duration causing 50% neuronal damage from 4.26 to 4.91 minutes (P<0.05).
en-copyright=
kn-copyright=

en-aut-name=DanuraTetsuya
en-aut-sei=Danura
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakedaYoshimasa
en-aut-sei=Takeda
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShiraishiKensuke
en-aut-sei=Shiraishi
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MizoueRyoichi
en-aut-sei=Mizoue
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatoSachiko
en-aut-sei=Sato
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritaKiyoshi
en-aut-sei=Morita
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School

affil-num=2
en-affil=
kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School

affil-num=3
en-affil=
kn-affil=Department of Anesthesiology, Maizuru Kyosai Hospital

affil-num=4
en-affil=
kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School

affil-num=5
en-affil=
kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School

affil-num=6
en-affil=
kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School

affil-num=7
en-affil=
kn-affil=Department of Anesthesiology and Resuscitology, Okayama University Medical School
en-keyword=esmolol
kn-keyword=esmolol
en-keyword=[beta]-adrenoceptor
kn-keyword=[beta]-adrenoceptor
en-keyword=ischemic depolarization
kn-keyword=ischemic depolarization
en-keyword=neuroprotective effect
kn-keyword=neuroprotective effect
en-keyword=brain ischemia.
kn-keyword=brain ischemia.
END