• Proceedings of the Korea Electromagnetic Engineering Society Conference
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• 1999.07a
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• pp.117-129
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• 1999

Acute effects of locally applied of static magnetic field (SMF) and extremely low frequency electromagnetic field(ELF-EMF) to the cutaneous tissue within a rabbit ear chamber (REC)were evaluated under conscious conditions. Rabbits with the REC were subjected to intravital microscopical investigation by use of microphotoelectric plethysmography(MPPG). There was no dose-response relationship between the extent of vasomotion changes and frequencies(0,20,50, 100Hz)or power levels (1, 5, 10, 25, 50, 100, 200 mT). Under low vascular tone the both fields induce vasodilatation. The effects of SMF (1 mT) on the cutaneous microcirculatory system induced the vasodilatation with enhanced vasomotion under nor-adrenaline-induced high vascular tone as well as the vasoconstriction with reduced vasomotion under acetylcholine-induced low vascular tone. This suggests that the SMF can modulate vascular tone due to the modification of vasomotion biphasically in the cutaneous tissue.

• Proceedings of the KOSOMBE Conference
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• v.1993 no.11
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• pp.51-54
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• 1993

The purpose of this research is to investigate the relationship between the blood flow and autonomic nervous system which regulates the circulation system. After the oral glucose tolerance test(GTT) the velocity changes of the blood flow were measured from the normal, hyperglycemia and diabetic neuropathy using the laser doppler. The FFT analyses showed that the spectrums were concentrated around the particular bands(0.02-0.166Hz, 0.8-1.1Hz) for the normal, while almost uniform distribution of the spectrums was observed for the abnormal. The blood glucose affects the compliance of the blood vessels and viscosity and finally causes the resistance problem in the blood vessels. An index PG was introduced, which was determined by the ratio of the change or the integral power spectrum in the range between 0.02 and 0.166Hz to change of the blood glucose before and after GTT. The index shows 1.0. 0.3 and 0.1 for the normal, hyperglycemia and diabetic neuropathy, respectively. As a conclusion, this spectrum analysis shows the potential of checking the progress or the diabetic, also car be used to evaluate the vasomotion which are regulated by the autonomic nervous system.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.573-580
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• 1998

The study aims to identify the mechanism (s) underlying the altered vasodilatory responses of the pial artery of spontaneously hypertensive rats (SHR) under a hypothesis that calcitonin gene-related peptide (CGRP) exerts a modulator role in the autoregulation of cerebral blood flow (CBF). The animals were divided into four groups: 1) Sprague-Dawley rats (SDR), 2) Wistar rats (WR), 3) SHR with high blood pressure $(BP{\ge}150\;mmHg),$ and 4) SHR with normotensive BP $({\le}150\;mmHg).$ The lower limit of CBF autoregulation in SHR shifted to a higher BP $(82.8{\pm}9.3\'mmHg,\;P<0.05)$ than that in SDR $(58.9{\pm}5.7\;mmHg)$. In SHR, whether the BP levels were high or normotensive, the vasodilator responses to a stepwise hypotension were significantly attenuated unlike with SDR and WR. When artificial cerebrospinal fluid (CSF) containing capsaicin $(3{\times}10^{-7}\;M)$ was suffused over the cortical surface, a transient increase in pial arterial diameter was observed in the SHR with high or normotensive BP. In contrast, SDR and WR showed a large increase in diameter, and the increase was sustained for over 10 minutes. In line with these results, the basal releases of CGRP-like immunoreactivity (CGRP-LI) in the isolated pial arteries from SHR with high and normotensive BP were $12.5{\pm}1.4\;and\;9.8{\pm}2.8\;fmole/mm^2/60\;min\;(P<0.05)$, while those from SDR and WR were $25.5{\pm}3.1\;and\;24.6{\pm}3.1\;fmole/mm^2/60\;min,$ respectively. The isolated basilar arteries showed similar results to those of the pial arteries in SHR. Thus, it is summarized that, in the SHR, the reduced autoregulatory vasodilator responses to stepwise hypotension and capsaicin may be, in part, ascribed to the decreased release of CGRP from the perivascular sensory nerve fibers of the pial arteries, and that altered vasomotor activity in SHR may not be related with the hypertensive tone.

• Archives of Reconstructive Microsurgery
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• v.6 no.1
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• pp.1-8
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• 1997

Recently prostaglandin $E_1(PGE_1)$ has been shown to ensure flap survival by producing vasodilation of the peripheral vessels and platelet disaggreation. However, direct observation and detailed quantitative studies of the effects of $PGE_1$ on the cutaneous microcirculation have not been reported. In the present study, we investigated cutaneous microcirculatory changes in the rabbit ear chamber(REC) with an intravital microscope following intravenous administration of $PGE_1$. The results obtained in this study indicate that $PGE_1$ administered intravenously at a rate of 200ng/kg/min might act directly on the vessels and cause dilatation of metarterioles and capillaries without affecting vasomotion and systemic blood pressure. Clinically in order to evaluate the effect of an intravenous administration of $PGE_1$ on the cutaneous microcirculation, cutaneous blood flow, skin temperature and transcutaneous $Po_2$ in the pedicle or free flap of operated patients were evaluated by the combination of several measurements following the administration of $PGE_1$. The present study suggests that improvement of cutaneous microcirculation by $PGE_1$ may enhance the survival rate of flap or replantation. Both vessel arterial ischemia and venous congestion are main factors of tissue necrosis in the flap surgery. Vasodilatory or antithrombotic agents have been used in salvage of flap necrosis. However, the therapeutic effects of those drugs are still not well elucidated. Recently prostaglandin $E_1(PGE_1)$ has been shown to ensure flap survival by producing vasodilatation of the peripheral vessels and platelet disaggregation[1-3]. Emerson and sykes[4] have obtained significant improvement in the flap survival in the rat using $PGI_2$. Suzuki et al.[5] have reported prolonged flap survival length by using $PGE_1$ in the rabbit and concluded that $PGE_1$ improved the microcircuration in the flap. However, direct observation and detailed quantitative studies of the effects of $PGE_1$ on the cutaneous microcirculation have not been reported. In the present study, we investigated microcirculatory changes in the rabbit ear chamber[6,7] with an intravital microscope following intravenous administration of $PGE_1$.

• International Journal of Industrial Entomology and Biomaterials
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• v.22 no.1
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• pp.17-20
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• 2011

The average life expectancy has continuously increased with the development of medical industry. As women get older, they experience the deficit of estrogen caused by decreased function of ovarian. Specifically, they suffer from temporary fever because of unstable vasomotion and, in the long term experience, degeneration of urogenital organs, tooth loss, arteriosclerosis, demantia, snores and so on. Because of these symptoms the estrogen medical supply is getting required. Along with this, many studies have conducted to find out substitutional medicals without any side effects. This research was carried out to find out such substitutable materials. For the purpose of study, we examined the change of estrogen using the rats fed with the pupa powder immediately before the eclosion, eclosed adult, the pupa extract immediately before the eclosion, and the silkworm powder prepared at $3^{rd}$ day of $5^{th}$ instar. The result showed no significant chance in weight, feeding and water intake quantity among variables. However, the estrogen hormone secretion effects was very high at 73 pg/ml in the rats fed with the freeze-dried powder of the Yeonnokjam male pupa prepared immediately before the eclosion, compared with the control at 59 pg/ml. The next was Yangwonjam male adult at 71 pg/ml.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.139-149
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• 1989

Although tail flick reflex (TFR) in rats has been used as a classic model of the nociceptive test to evaluate the action of analgesics, there have been few studies on the origin of the latent period of TFR. Present study was performed to elucidate the mechanism of increase in latency of TFR by morphine in anesthetized rats. Tail skin and dorsolateral tail nerve were stimulated electrically and EMG activities were recorded from abductor caudae dorsalis muscle participating in tail flick reflex. In the case of noxious radiant heat stimulation to tail, the tail flick tension was recorded before and after administration of morphine. Then changes in latency and conduction velocity of peripheral nerve were evaluated. The results obtained were as follows: 1) The latencies of TFR evoked by the electrical stimulation of tail skin and dorsolateral tail nerve were all within 40 ms and were elongated by several milliseconds from control after the administration of morphine. Peripheral conduction velocities of tail flick afferent nerve were within the range of 10-25 m/s. 2) The conduction velocity of peripheral nerve was significantly reduced after morphine administration, therefore the afferent time (utilization time+conduction time to spinal cord) was significantly increased. But the time for central delay and efferent time was not affected by morphine. 3) The conduction velocity under room temperature $(20-25^{\circ}C)$ was significantly reduced after morphine while that under vasodilation state $(40{\sim}42^{\circ}C)$ increased, 30 min and 45 min after morphine. The conduction velocity under vasodilation state without treatment of morphine increased continuously 4) The latency in tension response of TFR evoked by electrical stimulation was elongated by several milliseconds from control while the latency evoked by noxious radiant heat was elongated by several seconds compared with that of control. From the above results, it could be concluded that: 1) the increased latency of TFR evoked by electrical stimulation of the tail after morphine administration was due to the reducton in conduction velocity of peripheral nerve, which was the secondry effect of morphine on the peripheral vasomotion and 2) increased latency of TFR evoked by noxious radiant heat was also due to the same effect of morphine and the increase in cutaneous insulation to the noxious heat.