• Journal of Yeungnam Medical Science
• /
• v.12 no.2
• /
• pp.260-268
• /
• 1995

Ischemia results when the decrease in tissue perfusion exceeds the tissues ability to increase an oxygen extraction from the blood. Brain edema has been defined as an abnormal accumulation of fluid within brain parenchyma associated with a volumetric enlargement of the brain tissue. In most instances, the labelling of edema as vasogenic or cytotoxic is only relative. For cerebral protection, there were many possible techniques which could increase or maintain cerebral perfusion and reduce cerebral metabolic demand for oxygen. This study was carried out the effect of mild brain hypothermia which was induced by infusion with cold saline into the carotid artery, during brief episodes of transient global ischemia on postischemic brain edema in rabbit. Eight rabbits were anesthetized with halothane and mechanically ventilated with oxygen. For isolated cerebral perfusion, polyethylene catheter was inserted left carotid artery for infusion of cold saline, external carotid artery was ligated, vertebral arteries were cautherized, right carotid artery was snared for ischemia and femoral artery and vein were also canulated for monitoring and drug treatment. At 3 hours After transient global ischemia, specific gravity of cerebral cortex and hippocampus was compared with no-perfusion group , perfusion with cold saline group and normal group. There was no significant differences in physiologic variables among the groups before transient global ischemia. But during transient global ischemia, brain temperature of perfusion group was decreased when compared to no perfusion group. Specific gravity of cerebral cortex and hippocampus of no-perfusion group and perfusion group was statistically significant when compared to normal group (p<0.01). The results of this study suggested that mild brain hypothermia with intracarotid cold saline infusion during brief episodes of transient global ischemia had decreased postischemic brain edema in rabbit.

• Journal of the East Asian Society of Dietary Life
• /
• v.15 no.5
• /
• pp.606-612
• /
• 2005

This study was performed to provide basic data that predict the application of Saengmaegsan(SMS) as medicinal food. SMS has been used in oriental medicine for many years as a therapeutic agent for cerebral disease. We examined the effects of SMS on physiological function in isolated abdominal aorta and femoral artery from rabbit and measured the changes of regional cerebral hood flow(rCBF), which was continually monitored by laser-doppler flowmeter and pressure transducer in anesthetized adult Spargue-Dawley rats through the data acquisition system composed of MacLab and Macintosh computer. The contraction forces by injection of norephinephrine in isolated abdominal aorta and femoral artery were significantly decreased in each concentration of SMS treatment compared with control. rCBF was increased by SMS in a dose-dependent manner. These results suggest that SMS causes a diverse response of rCBF and arterial diameter. These mechanism in rCBF increase may be mediated by prostaglandis, cyclic GMP and adrenergic $\beta-receptor$. Also mechanism in artery contraction decrease is also mediated by prostaglandis and cyclic GMP. These results indicate that SMS can be nsed as a safe and clinically applicable as a supplementation of diet therapy for cerebral cardiovascular disease patients.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.3
• /
• pp.313-322
• /
• 1998

In a myocyte freshly isolated from rabbit cerebral artery, the characteristics of $Ca^{2+}$ release by histamine or caffeine were studied by microspectrofluorimetry using a $Ca^{2+}-binding$ fluorescent dye, fura-2. Histamine (5 ${\mu}M$) or caffeine (10 mM) induced a phasic rise of cytoplasmic free $Ca^{2+}$ concentration $([Ca^{2+}]_C)$ which could occur repetitively with extracellular $Ca^{2+}$ but only once or twice in $Ca^{2+}-free$ bathing solution. Also, the treatment with inhibitor of sarcoplasmic reticulum $Ca^{2+}-ATPase$ suppressed the rise of $[Ca^{2+}]_C$ by histamine or caffeine. In $Ca^{2+}-free$ bathing solution, short application of caffeine in advance markedly attenuated the effect of histamine, and vice versa. In normal $Ca^{2+}-containing$ solution with ryanodine (2 ${\mu}M$), the caffeine-induced rise of $[Ca^{2+}]_C$ occurred only once and in this condition, the response to histamine was also suppressed. On the other hand, in the presence of ryanodine, histamine could induce repetitive rise of $[Ca^{2+}]_C$ while the amplitude of peak rise became stepwisely decreased and eventually disappeared. These results suggest that two different $Ca^{2+}-release$ mechanisms (caffeine-sensitive and histamine-sensitive) are present in rabbit cerebral artery myocyte and the corresponding pools overlap each other functionally. Increase of $[Ca^{2+}]_C$ by histamine seems to partially activate ryanodine receptors present in caffeine-sensitive pool.

• The Korean Journal of Physiology and Pharmacology
• /
• v.4 no.4
• /
• pp.301-309
• /
• 2000

The purpose of our investigation was to examine the effects of prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ on membrane potentials, $Ca^{2+}-activated\;K^+\;(K_{Ca})$ channels, and delayed rectifier $K^+(K_V)$ channels using the patch-clamp technique in single rabbit middle cerebral arterial smooth muscle cells. $PGF_{2{\alpha}}$ significantly hyperpolarized membrane potentials and increased outward whole-cell K currents. $PGF_{2{\alpha}}$ increased open-state probability of $K_{Ca}$ channels without the change of the open and closed kinetics. $PGF_{2{\alpha}}$ increased the amplitudes of $K_V$ currents with a leftward shift of activation and inactivation curves and a decrease of activation time constant. Our results suggest that the activation of $K_{Ca}$ and $K_V$ channels, at least in part, may lead to attenuate or counteract vasoconstriction by $PGF_{2{\alpha}}$ in middle cerebral artery.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.6
• /
• pp.695-703
• /
• 1998

$[K^+]_o$ can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of $[K^+]_o$ in the range of $5{\sim}15$ mM may affect tensions of blood vessels and can change their sensitivity to various vasoactive substances. Therefore, it was examined in the present study whether the sensitivity of cerebral arteries to vasoactive substances can be changed with the moderate increase of $[K^+]_o$, using Mulvany-type myograph and $[Ca^{2+}]_c$ measurement. The contractions of basilar artery and branch of middle cerebral artery induced by histamine were not increased with the elevation of $[K^+]_o$ from 6 mM to 9 mM or 12 mM. On the contrary, the contractions induced by serotonin were significantly increased with the elevation of $[K^+]_o$. The contractions were also significantly increased by the treatment with nitro-L-arginine $(10^{-4}$ M for 20 minutes). In the nitro-L-arginine treated arteries, the contractions induced by serotonin were significantly increased with the elevation of $[K^+]_o$ from 6 mM to 12 mM. $K^+-induced$ relaxation was evoked with the stepwise increment of extracellular $K^+$ from 0 or 2 mM to 12 mM by 2 mM in basilar arterial rings, which were contracted by histamine. But $[K^+]_o$ elevation from 4 or 6 mM to 12 mM by the stepwise increment evoked no significant relaxation. Basal tension of basilar artery was increased with $[K^+]_o$ elevation from 6 mM to 12 mM by 2 mM steps or by the treatment with ouabain and the increase of basal tension was blocked by verapamil. The cytosolic free $Ca^{2+}$ level was not increased by the single treatment with serotonin or with the elevation of $[K^+]_o$ from 4 mM to 8 or 12 mM. In contrast to the single treatment, the $Ca^{2+}$ level was increased by the combined treatment with serotonin and the elevation of $[K^+]_o$. The increase of free $Ca^{2+}$ concentration was blocked by the treatment with verapamil. These data suggest that the sensitivity of cerebral artery to serotonin is increased with the moderate increase of $[K^+]_o$ and the increased sensitivity to serotonin is due to the increased $[Ca^{2+}]_i$ induced by extracellular $Ca^{2+}$ influx.

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.6
• /
• pp.705-714
• /
• 1998

Cerebral blood vessels relax when extracellular $K^+$ concentrations $([K^+])_e$ are elevated moderately $(2{\sim}15$ mM, $K^+-induced$ vasorelaxation). We have therefore studied the underlying mechanism for this $K^+-induced$ vasorelaxation in the isolated middle cerebral arteries (MCAs). The effects of ouabain and $Ba^{2+}\;on\;K^+-induced$ vasorelaxation were examined to determine the role of sodium pump and/or Ba-sensitive process (possibly, inward rectifier K current) in the mechanism. Mulvany myograph was used to study 24 rats, 18 rabbits, and 10 humans MCAs $(216{\pm}3\;{\mu}m,\;347{\pm}7\;{\mu}m,\;and\;597{\pm}39\;{\mu}m$ in diameter when stretched to a tension equivalent to 55 mmHg). High $K^+$ (125 mM) and $PGF_{2{\alpha}}\;(1{\sim}10\;{\mu}M)$ induced concentration-dependent contractions in all 3 species, while histamine $(10{\sim}50\;{\mu}M)$ evoked contraction only in the rabbits and induced relaxation in the rats and humans. Addition of $K^+\;(2{\sim}10\;{\mu}M)$ to the control solution induced vasorelaxations. These effects were inhibited by the pretreatment with both ouabain $(10\;{\mu}M)$ and $Ba^{2+}\;(0.1{\sim}0.3\;mM)$ in the rat, but only with ouabain $(10\;{\mu}M)$ in the rabbit and human. These results suggest that $K^+-induced$ vasorelaxation occurs via the stimulation of electrogenic Na pump in the rabbit and human MCAs, while in the rat MCAs via the activation of both Na pump and Ba-sensitive process.

• Proceedings of the Plant Resources Society of Korea Conference
• /
• 2023.04a
• /
• pp.39-39
• /
• 2023

The purpose of this study is to investigate vasodilatation effect of complex saponin separated from Scrophulariae radix, Asparagus cochinchinensis and Liriope platyphylla mixture extract on rabbit carotid artery. In this study, to determine vasodilatation effect of complex saponin separated from Scrophulariae radix, Asparagus cochinchinensis and Liriope platyphylla mixture extract on rabbit carotid artery, arterial rings with intact or damaged endothelium were used for experiment using organ bath, and were contracted by endothelin. complex saponin, major active constituents of Scrophulariae radix, Asparagus cochinchinensis and Liriope platyphylla mixture extract, showed a moderate vasodilatation effect on the basilar arteries of rabbits. Therefore, treatment with complex saponin separated from Scrophulariae radix, Asparagus cochinchinensis and Liriope platyphylla mixture extract may selectively accelerate cerebral blood flow through dilatation of the basilar artery. Theseis result suggest a potential role of complex saponin separated from Scrophulariae radix, Asparagus cochinchinensis and Liriope platyphylla mixture extract as source of vasodilatation agent.

• The Korean Journal of Physiology and Pharmacology
• /
• v.9 no.5
• /
• pp.299-304
• /
• 2005

Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO)-evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery, during ISO-induced cardiac hypertrophy compared to heart itself. The results show that the mRNA level of c-fos (not c-jun and c-myc) in heart and these genes in cerebral artery were considerably increased during cardiac hypertrophy. These results that the PKA activity and activations of Ras/Raf/ERK cascade as well as c-fos expression in rabbit heart during cardiac hypertrophy were consistent with previous reports. Interestingly, however, we also showed a novel finding that the decreased PKA activity might have differential effects on Ras and Raf expression in cerebral artery during cardiac hypertrophy. In conclusion, there are differences in molecular mechanisms between heart and cerebral artery during cardiac hypertrophy when stimulated with β2 adrenoreceptor (AR), suggesting a possible mechanism underlying cerebrovascular dysfunction during cardiac hypertrophy.

• Journal of Life Science
• /
• v.11 no.1
• /
• pp.62-69
• /
• 2001

This study was aimed to investigate the effect Chukdamtanggamibang on the vascular systems including changes in blood pressure and regional cerebral blood flow(rCBF) of male Sprague-Dawely rats, contractile force of guinea pig`s tracheal smooth muscle and abdominal aorta and femoral artery in rabbits. Blood pressure was not affected by Chukdamtanggamibang in rats. rCBF was significantly increased by Chukdamtanggamibang in a dose-dependent manner. Contractile force of isolated guinea pig`s tracheal smooth muscle evoked by His ({TEX}$ED_{50}${/TEX}) were inhibited significantly by Chukdamtanggamibang. Propranolol, indomethacin and methylene blue did not significantly alter the inhibitory effect of Chukdamtanggamibang. Contractile force of isolated rabbit`s abdominal aorta and femoral artery evoked by NE ({TEX}$ED_{50}${/TEX}) were inhibited significantly by Chukdamtanggamibang. ODQ and L-NNA significantly attenuated the inhibitory effects of Chukdamtanggamibang in abdominal aorta, whereas propranolol did not significantly alter the inhibitory effect of Chukdamtanggamibang. These results indicate that Chukdamtanggamibang can relax hitamine-induced contraction of guinea pig`s tracheal smooth muscle and that this inhibition involves, in part, the relation to the soluble guanylyl cyclase synthesis and nitric oxide (NO) synthesis.

• The Journal of Korean Medicine
• /
• v.23 no.3
• /
• pp.63-73
• /
• 2002

Objective : This study aimed to investigate the effects Samyoo-tang Extract (SE) on the vascular systems, including changes in blood pressure and regional cerebral blood flow (rCBF), of male Sprague-Dawley rats. Methods : The changes in rCBF were determined by Laser-Doppler flowmetry through the opened cranial method and norepinephrine (NE)-induced blood vessel contractions were determined by physiograph in the pulmonary artery of isolated rabbits. Results and Conclusion : 1. Contractions evoked by NE ($ED_{50}$) were inhibited significantly by SE in the pulmonary artery. 2. SE inhibited the relaxation of NE induced contractions pretreated with propranolol. 3. SE did not inhibit the relaxation of NE induced contractions pretreated with ODQ and L-NNA. 4. Blood pressure was not affected by SE in rats. 5. rCBF was increased by SE in a dose-dependent manner. 6. Pretreatment with propranolol was increased by SE in a dose-dependent manner in blond pressure. 7. Pretreatment with methylene blue, ODQ and L-NNA did not inhibit SE induced increased in rCBF. These results indicate that SE can relax NE-induced contraction of rabbit blood vessels and increased the changes of rCBF in rats, that relate to the sympathetic nerve system.