• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.5
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• pp.1404-1409
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• 2004

Cheonmabanhwa-Tang(CBT) has been used in the Oriental Medicine for many centuries as a therapeutic agent for dizziness due to Poong-Dam. This Study was designed to investigate the mechanism of Prescription on cerebral hemodynamics [regional cerebral blood flow(rCBF) and pial arterial diameter(PAD)J in cerebral ischemia rats, The results in cerebral ischemic rats were as follows: Both rCBF and PAD were significantly and stably increased by CBT (10 ㎎/㎏, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. Pretreatment with indomethacin(1 ㎎/㎏, i.p.), an inhibitor of cyclooxygenase significantly but unstably increased the CBT-induced increases in PAD as well as rCBF during the period of cerebral reperfusion. Pretreatment with methylene blue(10 (.1.㎍/㎏, i.p.), an inhibitor of guanylate cyclase significantly but unstably increased the CBT-induced increases in PAD as well as rCBF during 150 minutes of cerebral reperfusion, but decreased stably the CBT-induced increases in rCBF and PAD after 180 minutes of cerebral reperfusion. In conclusion, the present authors thought that CBT caused effect on cerebral hemodynamics via mediation of cyclooxygenase.

• Biomedical Science Letters
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• v.11 no.3
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• pp.355-363
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• 2005

This study aimed to investigate the cerebroprotective effect of vascular endothelial growth factor (VEGF) on permanent focal cerebral ischemia in Sprague-Dawley rats. Right middle cerebral artery (MCA) was occluded for 6 and 24 hours by an intraluminal monofilament technique. An open cranial window was made on the right parietal bone for determination of continuous changes in regional cerebral blood flow (rCBF) by laser-Doppler flowmetry. The infarct size was morphometrically determined using the 2,3,5-triphenyltetrazolium chloride technique. Brain edema was determined by measuring brain water content. In normal rats, rCBF was significantly increased by intravenous infusion of VEGF for 10 minutes. The VEGF-induced increase in rCBF was significantly inhibited by pretreatment with suramin, a heparin-binding growth factor inhibitor as well as $N^{\omega}-nitro-L-arginine$, a nitric oxide synthase inhibitor. In focal cerebral ischemic rats, the amplitude of decrease in rCBF during ischemic period was significantly less in VEGF-treated group, compared with that in vehicle-treated group. The cerebral infarct size was reduced by VEGF in a dose-dependent manner. The brain edema formation was dose-dependently reduced by VEGF in 24-hour MCA occlusion group but not in 6-hour MCA occlusion group. It is suggested that VEGF not only improves the rCBF during cerebral ischemic period but also reduces the brain edema formation, and thereby exert a protective effect on focal cerebral ischemia in rats.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.6
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• pp.601-606
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• 2014

The purpose of this study is to research the effects of acupuncturing BL40 and ST36 and to determine the mechanism of action of acupuncturing BL40 and ST36 by measuring the changes of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats. To determine the mechanism of action of acupuncturing BL40 and ST36, pretreatment with indomethacine and methylene blue was performed. Acupuncturing BL40 and ST36 significantly increased rCBF, and the increased rCBF by acupuncturing BL40 and ST36 was significantly inhibited by pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase, and methylene blue($10{\mu}g/kg$, i.p.), an inhibitor of guanylate cyclase. Acupuncturing BL40 and ST36 decreased MABP, and decreased MABP by acupuncturing BL40 and ST36 was not changed by pretreatment with indomethacin and methylene blue. This result suggested that acupuncturing BL40 and ST36 might significantly increase rCBF by dilating arterial diameter and mechanism of acupuncturing BL40 and ST36 might be mediated by cyclooxygenase and guanylate cyclase.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.5
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• pp.657-664
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• 2012

The aim of this study is to investigate the effects of onion vinegar on the cerebral blood flow by measuring the changes of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) and by observing the recovery of focal ischemic brain injury in rats. Rats are divided into thee groups depending on the medication; control group (no medication), 8.8-OV group (vinegar using 8.8 brix onion medication), 14.6-OV group (vinegar using 14.6 brix onion medication). The medication of onion vinegar significantly increased rCBF but decreased MABP. This result suggests that onion vinegar significantly increased rCBF by dilating arterial diameter. In addition, focal ischemic brain injury is induced in rats by middle cerebral arterial occlusion. The recovery from focal ischemic brain injury is more significantly improved in the groups using onion vinegar compared to the control group. The amount of recovery is measured by the GAP-43 and the medication of onion vinegar significantly increased GAP-43. This result suggests that onion vinegar is effective on the nerve regeneration. After the medication, the change of body weight, outcomes of renal and liver function test, and outcomes of CBC are analysed for safety examination. There are no statistical differences among control group and all experimental groups in the body weight, renal and liver function test, and CBC. In conclusion, these results suggest that onion vinegar can increase rCBF in normal state, and improve the stability of rCBF in ischemic state.

• The Journal of Internal Korean Medicine
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• v.27 no.4
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• pp.855-863
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• 2006

Objectives : This study was performed to evaluate effects of Yangsim-tang extract (YST) on hemodynamics (regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) ) in normal rats, and effects of cyclooxygenase and guanylate cyclase under YST. Methods : Laser-Doppler flowmetry (LDF) measured changes of rCBF, and a data acquisition system assembled with MacLab and Macintosh measured changes of MABP. Results : YST significantly increased rCBF, but did not change MABP. Pretreatment with indomethacin significantly inhibited rCBF increased by YST, but pretreatment with methylene blue did not significantly inhibit rCBF increased by YST. Conclusions : YST increases rCBF, and the action of this response is mediated by cyclooxygenase.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1083-1088
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• 2004

This Study was designed to investigate the mechanism of Prescription for Treatment Abundant Expectoration due to Deficiency of Qi(Yukgunja-Tang, YGT) on cerebral hemodynamics [regional cerebral blood f1ow(rCBF) and pial arterial diameter(PAD)] in cerebral ischemia rats. The results were as follows: Both rCBF and PAD were significantly and stably decreased by YGT (10㎎/㎏, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in Control group. Pretreatment with indomethacin(1㎎/㎏, i.p.), an inhibitor of cyclooxygenase and methylene blue(10㎍/㎏, i.p.), an inhibitor of guanylate cyclase significantly but unstably increased the YGT-induced increases in rCBF during the period of cerebral reperfusion. Pretreatment with indomethacin significantly and stably decreased the YGT-induced increases in PAD during the period of cerebral reperfusion, but pretreatment with methylene blue increased unstably the YGT-induced increases in PAD during the period of cerebral reperfusion. In conclusion, the present authors thought that mechanism of YGT on cerebral hemodynamics was connected with guanylate cyclase in cerebral ischemia rats.

• Biomolecules & Therapeutics
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• v.7 no.3
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• pp.234-241
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• 1999

The present study assessed the cerebroprotective effect of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rats. Right middle cerebral artery (MCA) of Sprague-Dawley rats was occluded for 2 hours using an intraluminal filament technique, and was reperfused for 6 hours following cerebral ischemia. The infarct area of seven coronal brain slices was measured morphometrically following stain ing in the 2% 2,3,5-triphenyltetrazolium chloride solution. The changes in regional cerebral blood flow (rCBF) and pial arteriolar diameter were measured by laser-Doppler flowmetry and by a videomicroscopy, respectively. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, which were administered i.p. 10 min before MCA occlusion. Pretreatment with PAF antagonists significantly restored the changes in pial arterial diameter as well as those in rCBF during the period of cerebral ischemia-reperfusion. PAF antagonists significantly inhibited the inducible nitric oxide synthase activity in the pial arteries ipsilateral to ischemia. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through an improvement of postocclusive cerebral blood flow.

• Herbal Formula Science
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• v.14 no.1
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• pp.105-119
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• 2006

Objectives & Methods : This present study was performed to investigate the effect of Hwadamtongrak-Tang extract (HTT) on the regulation of cerebral hemodynamics in terms of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats. Also the effects of HTT on changes in local blood flow, inhibition of LD H activity in neuronal cells, and levels of cytokine production in the serum were determined in the ischemic rat model. The major findings are summarized below. Results : 1. HTT significantly increased rCBF in a dose-dependent manner, but MABP was not changed by HTT treatment. These results suggest that HTT may increase rCBF by dilating cerebral arterial diameter. 2. HTT-induced increase in rCBF was blocked by pretreatment with cyclooxygenase inhibitor indomethacin (IDN, 1 mg/kg, i.p.) and MABP was significantly increased by ID N. 3. Pretreatment of methylene blue $(MTB,\;10\;{\mu}g/kg,\;i.p.)$, an inhibitor of guanylate cyclase, significantly decreased both rCBP and MABP in HTT-treated rats. 4. HTT treatment significantly increased rCBP to a stable level during the period of cerebral reperfusion. 5. HTT significantly inhibited LD H activity in neuronal cells, suggesting a neuroprotection by HTT. 6. Serum interleukin $(IL)-1{\beta}$ and tumor necrosis factor $(TNF)-{\alpha}$ levels were significantly decreased in the femoral artery 1 hr after middle cerebral arterial occlusion in HTT-treated rats. IL-10 levels in the serum were significantly increased by HTT treatment whereas transforming growth factor $(TGF)-{\beta}$ levels were similar between HTT-treated and control groups. 7. Serum interleukin $(IL)-1{\beta}$ and tumor necrosis factor $(TNF)-{\alpha}$ levels were significantly decreased in the femoral artery 1 hr after reperfusion in HTT-treated rats. Serum IL-10 levels were significantly decreased in HTT-treated rats compared with the control group, and no significant changes in $(TGF)-{\beta}$ in the serum were observed by HTT treatment. Conclusions: The present data suggest that HTT may have an anti-ischemic effect via the improvement of cerebral hemodynamics and thus protect the brain from ischemic damage.

• Journal of Society of Preventive Korean Medicine
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• v.19 no.3
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• pp.155-170
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• 2015

Objective : Jaeumgeonbitang have been used in Korean medicine for many centuries as a therapuetic agent of vertigo. JAE was extract of Jaeumgeonbitang adding Evodiae Fructus. The effects of JAE on the cerebral blood flow and blood pressure is not known. This study was designed to investigate the effects of JAE on the ischemic crebral injuries. Method : We performed to investigate effects of JAE on the changes of regional cerebral blood flow(rCBF) and mean arterial blood pressure (MABP) in normal and ischemic rats, and further to determine the mechanism and cytokines production ($IL-1{\beta}$, $TNF-{\alpha}$, IL-10, $TGF-{\beta}$) of JAE. Results : In normal rats, JAE significantly increased rCBF and significantly decreased MABP in a dose-dependent manner. This result suggested that JAE significantly increased rCBF by dilating pial arterial diameter. Increase of JAE-induced rCBF was significantly inhibited by the pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase, and was significantly inhibited by methylene blue ($10{\mu}g/kg$, i.p.), an inhibitor of guanylate cyclase. Decrease of JAE-induced MABP was significantly increased by the pretreatment with indomethacin (1 mg/kg, i.p.), an inhibitor of cyclooxygenase. So, these results suggested that the mechanism of JAE was mediated by cyclooxygenase. In ischemic rat, the rCBF was significantly and stably increased by JAE (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in Control group. In cytokine production of serum by drawing from femoral arterial blood at 1 hr after reperfusion, Sample group (JAE 10 mg/kg treated group) was significantly decreased $IL-1{\beta}$ and $TNF-{\alpha}$ production compared with Control group. In cytokine production of serum by drawing from femoral arterial blood at 1 hr after reperfusion, Sample group was significantly increased IL-10 production compared with Control group. Conclusion : These results suggested that JAE was significantly and stably increased regional cerebral blood flow by inhibited $IL-1{\beta}$ and $TNF-{\alpha}$ production, and increased IL-10 production.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.6
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• pp.1546-1551
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• 2005

This Study was designed to investigate the effects of Nelumbinis Rhizomatis Nodus (NRN) on the change of cerebral hemodynamics [regional cerebral blood flow (rCBF), pial arterial diameter (PAD) and mean arterial blood pressure (MABP)] in normal and cerebral ischemic rats. And, this study was designed to investigate the inhibition of lactate dehydrogenase activity in neuronal cells The results were as follows NRN significantly increased rCBF and PAD in a dose-dependent manner, and NRN increased MABP in a dose-dependent manner. This results suggested that NRN significantly increased rCBF by dilating PAD. Both rCBF and PAD were significantly and stably increased by NRN (10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. NRN significantly inhibited lactate dehydrogenase activity in neuronal cells. This results suggested that NRN prevented the neuronal death. It is suggested that NRN had an anti-ischemic effect through the improvement of cerebral hemodynamics and inhibitive effect on the brain damage.