• Journal of Korean Medicine Rehabilitation
• /
• v.18 no.1
• /
• pp.65-74
• /
• 2008

Objectives : This experimental study was designed to investigate the effects of Lumbricus extract (LE) on the changes in regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats, and further to determine the mechanism of action of LE. Methods : The changes of rCBF were observed by Laser-Doppler flowmetry (LDF) and the changes of MABP were recorded by a data acquisition system assembled with MacLab and Macintosh. Results : LE significantly increased rCBF in a high dosage(10.0 mg/kg, i.p), but MABP was somewhat increased as compared with baseline. This result suggests that LE significantly increased rCBF by dilating pial arterial diameter. Increase of LE-induced rCBF was significantly inhibited by pretreatment with indomethacin (1 mg/kg, i.p), an inhibitor of cyclooxygenase, but was not significantly inhibited by pretreatment with methylene blue ($10{\mu}g/kg$, i.p), an inhibitor of guanylate cyclase. Conclusions : LE increased rCBF by dilating pial arterial diameter, and the action of this response was mediated by cyclooxygenase.

• Biomolecules & Therapeutics
• /
• v.13 no.2
• /
• pp.95-100
• /
• 2005

This study was performed to investigate the mechanism of cerebral blood flow of adenosine $A_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by nitric oxide (NO) and guanylate cyclase. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebral cortex was measured using laser-doppler flowmetry. Topical application of an adenosine $A_{2B}$ receptor agonist, 5'-N-ethylcar-boxamidoadenosine (NECA; $4{\mu}mol/l$) increased cerebral blood flow. This effect of NECA ($4{\mu}mol/l$) was blocked by pretreatment with NO synthase inhibitor, $N^G$-nitro-L-argine methvlester (L-NAME; $40{\mu}mol/l$) and guanylate cyclase inhibitor, LY-83,583 ($10{\mu}mol/l$). These results suggest that adenosine $A_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine $A_{2B}$ receptor is mediated via the NO and the activation of guanylate cyclase in the cerebral cortex of the rats.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.18 no.4
• /
• pp.1014-1020
• /
• 2004

The study was designed to investigate the effects of Palmul-Tang(PMT) 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. The change of rCBF and MABP were determinated by laser-doppler flowmetry(LDF), and the change of PAD was determinated by video-microscopy. The results in normal rats were as follows ; PMT significantly increased rCBF and PAD in a dose-dependent, and PMT increased MABP in a dose-dependent. This results were suggested that PMT significantly increased rCBF by dilating PAD. The results in cerebral ischemic rats were as follows ; Both rCBF and PAD were significantly and stably increased by PMT(10㎎/㎏, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. The present authors thought that PMT had an anti-ischemic effect through the improvement of cerebral hemodynamics.

• The Journal of Internal Korean Medicine
• /
• v.26 no.3
• /
• pp.596-604
• /
• 2005

Objectives : Geopungjeseub-tang(Gufengchushi-tang) has been used in oriental medicine for many centuries as a therapeutic agent for hemiplegia caused by deficiency of qi(氣虛) and damp phlegm(濕痰). This study was performed to evaluate effects of Geopungjeseub-tang extract(GJT) on hemodynamics[regional cerebral blood flow(rCBF), pial arterial diameter(PAD), mean arterial blood pressure(MABP), heart rate(HR)] in normal rats and in rats with cerebral ischemia by middle cerebral artery(MCA) occlusion. Also, effects of adrenergic ${\beta}-receptor$, cyclooxygenase on response to GJT were evaluated. Methods : Laser-doppler flowmetry(LDF) measured changes of rCBF, MABP and HR. Video microscope and width analyzer measured changes in PAD. Results : rCBF and PAD increased after treatment with GJT(10mg/kg, i.v.) during the period of cerebral reperfusion, and pretreatment with indomethacin raised rCBF and PAD increased after treatment with GJT during the same period as above. Pretreatment with propranolol decreased rCBF, but increased after GJT treatment, but raised PAD increased after GJT treatment during this period of reperfusion. Conclusion : CR caused diverse responses were observed in rCBF and PAD after treatment with GJT. ACF action is mediated by adrenergic ${\beta}-receptor$ and cyclooxygenase. Result suggest that GJT has an anti-ischemic effect through the improvement of cerebral hemodynamics and has theraputic potential for cerebral apoplexy.

• Herbal Formula Science
• /
• v.6 no.1
• /
• pp.187-197
• /
• 1998

The study was aimed to investigate the effect cuscutae semen(CS) on the vascular systems including changes in blood pressure (BP), regional cerebral blood flow(rCBF) and pial arteriolar diameter of male Sprague-Dawely rats. The changes in rCBF were determinated by laser-Doppler flowmetry, and the changes in diameter of pial arteriole were measured through a closed crainal window. 1. Blood pressure was not affected by CS in rats. 2. rCBF was increased by CS in a dose-dependent manner. 3. Pretreatment with methylene blue(Img/kg), and propranolol(1mg/kg) significantly inhibited CS induced increased in rCBF. 4. Pretreatment with indomethacin(1mg/kg) did not inhibited CS induced increased in rCBF. 5. Pial arterial diameter was increased by CS in a dose-dependent manner. These results suggest that CS causes a diverse response of blood pressure, regional cerebral blood flow(rCBF), and pial arteral diameter. The increased in rCBF is also mediated by adrenergic ${\beta}-receptor $ and guanylate cyclase.

• Biomolecules & Therapeutics
• /
• v.12 no.2
• /
• pp.68-73
• /
• 2004

This study was performed to investigate the regulatory mechanism of cerebral blood How of adenosine $A_2$ receptor agonist in the rats, and to define whether its mechanism is mediated by nitric oxide (NO), adenylate cyclase and guanylate cyclase. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebal cortex was measured using laser-Doppler flowmetry. Topical application of an adenosine $A_2$ receptor agonist [5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA; 4 umol/l)] increased cerebral blood flow. This effect of CPCA (4 umol/l) was blocked by pretreatment with NO synthase inhibitor [$N^G$-nitro-L-argine methylester (L-NAME; 140 umol/l)] and adenylate cyclase inhibitor [MDL-12,330 (20 umol/l)]. But the effect of CPCA (4 umol/l) was not blocked by pretreatment with guanylate cyclase inhibitor [LY-83,583 (10 umol/l)]. These results suggest that adenosine $A_2$ receptor increases cerebral blood How. It seems that this action of adenosine $A_2$ receptor is mediated via the NO and the activation of adenylate cyclase in the cerebral cortex of the rats.

• Biomolecules & Therapeutics
• /
• v.12 no.2
• /
• pp.108-113
• /
• 2004

This study was performed to investigate the regulatory mechanism of cerebral blood flow of adenosine $A_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by adenylate cyclase and guanylate cyclase. in pentobarbital-anesthetized, pentobrabital-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood How from cerebral cortex was measured using laser-Doppler flowmetry. Topical application of an adenosine $A_{2B}$ receptor agonist, 5'-N-ethylcar-boxamidoadenosine (NECA; 4 umol/l) increased cerebral blood flow. This effect of NECA (4 umol/l) was not blocked by pretreatment with adenylate cyclase inhibitor, MDL-12330 (20 umol/l). But effect of NECA (4 umol/l) was blocked by pretreatment with guanylate cyclase inhibitor, LY-83383 (10 umol/l). These results suggest that adenosine $A_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine $A_{2B}$ receptor is mediated via the activation of guanylate cyclase in the cerebral cortex of the rats.

• Biomolecules & Therapeutics
• /
• v.13 no.1
• /
• pp.35-40
• /
• 2005

This study was performed to investigate the regulatory mechanism of cerebral blood flow of adenosine A$_{2B}$ receptor agonist in the rats, and to define whether its mechanism is mediated by adenylate cyclase, guanylate cyclase and potassium channel. In pentobarbital-anesthetized, pancuronium-paralyzed and artificially ventilated male Sprague-Dawley rats, all drugs were applied topically to the cerebral cortex. Blood flow from cerebral cortex was measured using laser-Doppler flowmetry. Topical application of an adenosine A$_{2B}$ receptor agonist, 5'-N-ethylcarboxamidoadenosine (NECA; 4 umol/I) increased cerebral blood flow. This effect of NECA (4 umol/I) was not blocked by pretreatment with adenylate cyclase inhibitor, MDL-12,330 (20 umol/I). But effect of NECA (4 umol/I) was blocked by pretreatment with guanylate cyclase inhibitor, LY-83,583 (10 umol/I) and pretreatment with ATP-sensitive potassium channel inhibitor, glipizide (5 umol/I). These results suggest that adenosine A$_{2B}$ receptor increases cerebral blood flow. It seems that this action of adenosine A$_{2B}$ receptor is mediated via the activation of guanylate cyclase and ATP-sensitive potassium channel in the cerebral cortex of the rats.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.16 no.6
• /
• pp.1127-1133
• /
• 2002

Cheonghunhwadam-tang(CHT) have been used in oriental medicine for many centuries as a therapeutic agent of vertigo by wind, fire and phlegm. CHTGR was CHT adding Gastrodae Rhizoma. The effects of CHTGR on the regional cerebral blood flow(rCBF) and mean arterial blood pressure(MABP) is not known. A comparative Study of action-mechanism of CHT and CHTGR on the cerebral hemodynamics is not known too. Therefore, purpose of this Study was to investigate effects of CHT and CHTGR on the rCBF and MABP, compare action-mechanism of CHT and CHTGR on the rCBF and MABP. The changes of rCBF and BP was determinated by Laser-Doppler Flowmetry(LDF). The results were as follows ; CHT extract was increased rCBF in a dose-dependent, but was not changed MABP compared with CHT non-treated group. CHTGR extract was decreased rCBF and MABP compared with CHTGR non-treated group in a dose-dependent. Action of CHT is not related with adrenergic β-receptor, cyclooxygenase and guanylate cyclase, but action of CHTGR is related with guanylate cyclase.

• Biomedical Science Letters
• /
• v.11 no.3
• /
• pp.375-382
• /
• 2005

This study aimed to investigate whether nociceptin is implicated in the, trigeminovascular responses to electrical stimulation of trigeminal ganglion in rats. An open cranial window was prepared on the right parietal bone of male Sprague-Dawley rats. Trigeminovascular system was stimulated by electrical stimulation of trigeminal ganglion (ETS; 5ms, 5Hz, 3V). Neonatal capsaicin treatment was performed with subcutaneous administration of capsaicin (50mg/kg) within the first 24 hours after birth. Changes in regional cerebral blood flow were continuously measured through the cranial window by laser-Doppler flowmetry, and the expression of nociceptin-like immunoreactivity was determined by immunohistochemistry. ETS caused increases in regional blood flow of pial arteriole in a voltage-dependent manner. ETS markedly and voltage-dependently increased the expression of nociceptin-like immunoreactivity in dura mater ipsilateral rather than contralateral to ETS. The nociceptin-like immunoreactivity was markedly reduced by pretreatments with calcitonin gene-related peptide(8-37) ($CGRP_{8-37},\;a\;CGRP_1$ receptor antagonist), L-733060 (a $NK_1$ receptor antagonist), and $[Nphe^1]$ nociceptin(1-13)$NH_2$ (a selective and competitive nociceptin receptor antagonist) as well as by neonatal capsaicin treatment. These results suggest that the electrical stimulation of trigeminal ganglion causes prominent expression of nociceptin within dura mater, in which not only neuropeptides inducing substance P and CGRP but also nociceptin are implicated in the trigeminovascular responses to electrical trigeminal ganglion stimulation.