Journal of the Korean Society of Food Science and Nutrition
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제28권3호
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pp.607-612
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1999
Cigarette smoking is the potential risk factor for lung cancer and chronic pulmonary disease, as well as inflammatory bowel disease and reproductive malfunction. Nicotine and tar have been im plicated as a major factor in the pathogenesis of the diseases. Nicotine increases heart rate and blood pressure due to stimulation sympathetic neurotransmission and tar also accounts for the severe damage of peridontal diseases and osteoporosis in postmenopausal women. Portulaca oleracea, which contains significant amount of K+, noradrenaline and dopamine as well as various nutrients, has been used for many medicinal purposes and one of which is the detoxification of insect or snake toxins. The purpose of this study was to investigate the action of Portulaca oleracea extracts on the reduction of harmful materials of tabacco. The reduction percentages were measured in the presence and absence of each solvent extract of Portulaca oleracea using reversed C18 column of HPLC. Nicotine reduction effects were obtained from aqueous, methanol and chloroform extracts of Portulaca oleracea as 89%, 55% and 51%, respectively. The results suggest that the polar extracts of Portulaca oleracea affects the reduction of nicotine which is responsible for many diseases.
A large number of isolation systems are designed without considering the non-uniform friction distribution in space. In order to analyze the effects of non-uniform friction distribution on the structural response of isolation system, this paper presented a simplified rolling-damper-spring isolation system and analyzed the structural responses under earthquakes. The numerical results indicate that the calculation errors related to the peak values of structural acceleration, relative displacement and residual displacement are sequentially growing because of the ignorance of non-uniform friction distribution. However, the influence rule may be weakened by the spring and damper actions, and the unreasonable spring constant may lead to the sympathetic vibration of isolation system. In the case when the friction variability is large and the damper action is little, the non-uniform friction distribution should be taken into consideration during the calculation process of the peak values of structural acceleration and relative displacement. The non-uniform friction distribution should be taken into full consideration regardless of friction variability degree in calculating the residual displacement of isolation system.
Effects of a $M_1$ receptor antagonist, pirenzepine, a $M_2$ receptor antagonist, AF-DX116, and a nicotinic receptor antagonist, mecamylamine on the pressor responses to preganglionic sympathetic nerve stimulation (PNS) and McN-A-343 and DMPP in spinal (pithed) rabbits were investigated, in order to elucidate a functional role of $M_1$, $M_2$ and nicotinic receptors in ganglionic transmission. Pirenzepine and AF-DX116 selectively inhibited the McN-A-343-induced pressor response in chlorisondamine-treated rabbit and the BCh-induced bradycardia, respectively. Electrical stimulations of preganglionic sympathetic outflow at T8 level produced increases in blood pressure. Pirenzepine $(3\;{\mu}g/kg)$ significantly inhibited the PNS-induced pressor response and the degree of inhibition was not changed by increasing the doses to $100\;{\mu}g/kg$. AF-DX116 $(100\;{\mu}g/kg)$ had no effect on the PNS-induced pressor response. Mecamylamine inhibited the PNS-induced pressor response in a dose-dependent manner. The inhibitory action of mecamylamine was significantly augmented by combined-treatment with pirenzepine $(30\;{\mu}g/kg)$ but AF-DX116 $(100\;{\mu}g/kg)$ did not affect the inhibitory action of mecamylamine. McN-A-343 and DMPP elicited pressor response in the spinal rabbit. Pirenzepine and AF-DX116 dose-dependently inhibited the McN-A-343-induced pressor response but they did not affect DMPP-induced pressor response. Mecamylamine inhibited both pressor responses induced by McN-A-343 and DMPP. These results suggest that not only nicotinic receptors but also $M_1$ receptors play a facilitatory role in ganglionic transmission but $M_2$ receptors do not contribute the transmission in spinal (pithed) rabbits.
When administered intracerebroventricularly (icv), cholinergic nicotinic agents, nicotine and DMPP, as well as cholinergic muscarinic agents, muscarine and bethanechol, produced pressor responses in urethane-anesthetized vagotomized rabbits. The response patterns to nicotine and to DMPP were similar, while the bethanechol response resembled the muscarine pattern. The pressor response to nicotine and DMPP was markedly inhibited by icv mecamylamine but not by icv pirenzepine, whereas the response to muscarine and bethanechol was inhibited by icv pirenzepine but not by icv mecamylamine, suggesting that both nicotinic and muscarinic receptors in the brain are involved in the action. Intravenous pretreatments of animals with regitine, reserpine, enalapril, saralasin, both regitine and enalapril, both regitine and saralasin, SK&F-100273 did not prevent the pressor response to nicotine and muscarine. Iv pretreatments with both regitine and SK&F-100273 inhibited the nicotine response without affecting the muscarine response, whereas pretreatments with three agents, regitine, enalapril and SK&F-100273, inhibited the muscarine response. The nicotine-induced elevated blood pressure as well as the muscarine-induced were lowered by regitine but not by enalapril or by SK&F-100273. Enalapril was without effect on the nicotine hypertension in rabbits treated with regitine or both regitine and SK&F-100273, whereas SK&F-100273 lowered the nicotine hypertension in regitine-treated animals. Enalapril did not enhance the lowering effect of SK&F-100273 in regitine-treated ones, nor did it cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and SK&F-100273. Likewise, SK&F-100273 did not cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and enalapril. These data suggest that the nicotine-induced hypertensive state is related to at least two systems in the periphery-sympathetic and vasopressin, whereas in the muscarine-induced hypertensive state three systems in the periphery are involved, i.e., the sympathetic, vasopressin and angiotensin system. The hypotensive effect of regitine on basal arterial blood pressure levels of rabbits was not influenced by pretreatment with either of enalapril or SK&F-100273, but significantly potentiated by treating with both enalapril and SK&F-100273, suggesting participation of the sympathetic and the renin-angiotensin system as well as the vasopressin system in maintenance of arterial blood pressure.
The effect of physostigmine (PS), which has been shown to act on the muscarinic receptors in the brains of the rat, dog and cat, on the arterial blood pressure (BP) was investigated in urethane-anesthetized rabbits. Intravenous (iv) PS, $25{\sim}300\;{\mu}g/kg$, caused little change in BP. However, after treatment of rabbits with either of chlorisondamine (CS), hexamethonium, intracerebroventricular (icv) clonidine, icv xylazine and icy reserpine iv PS produced a pressor response. Spinalization of the rabbit also caused iv PS to increase BP. The pressor effect of iv PS in CS-treated rabbits was markedly reduced after prazosin or pirenzepine. Iv PS inhibited the pressor response to McN-A-343 in CS-treated and in spinal rabbits; alternately during the infusion of McN-A-343 iv PS failed to produce the pressor response. The pressor response to DMPP was not affected by iv PS. Icv PS, $12{\sim}200\;{\mu}g/kg$, produced a pressor response which was accentuated after CS-treatment. This pressor effect was inhibited, though not complete, by prazosin or by pirenzepine. A simultaneous treatment of rabbits with both $[Sar^{1},\;Ala^{8}]-angiotensin$ II, an angiotensin II antagonist, and prazosin or pirenzepine almost completely abolished the pressor effect of icv PS, whereas the angiotensin II antagonist did not enhance the inhibitory effect of pirenzepine and prazosin on the pressor response to iv PS . Icv pirenzepine blocked the pressor response to icv PS without affecting that to iv PS. The present results show that the pressor response to iv PS in CS-treated and in spinal rabbits arises from stimulation of the muscarinic receptors in the sympathetic ganglia, whereas the pressor response by icv PS via activation of the muscarinic receptors in the brain which causes an enhancement in the outflow of sympathetic discharge and angiotensin. The results also suggest that iv PS is unable to produce a pressor response in the rabbit unless the sensitivity of the gangionic muscarinic receptors is altered by ganglionic nicotinic blockade, by the decrease of central sympathetic outflow on the sympathetic ganglia or by spinalization.
Park, Woo-Young;Bae, Chun-Sik;Lee, Soo-Han;Park, Woo-Dae
Journal of Veterinary Clinics
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제26권3호
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pp.212-219
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2009
Anticholinergics, which are commonly given as a pre-anesthetic medication to prevent adverse effects in canine anesthesia, can cause cardiac adverse effects. To determine the effects of atropine and glycopyrrolate on the balance of sympathetic nervous tone and parasympathetic nervous tone of the heart during ketamine anesthesia in beagle dogs, heart rate variability(HRV), duration of anesthesia and behavioral changes were evaluated. There were no significant temporal domain differences between atropine and glycopyrrolate. Concerning the frequency domain component, atropine and glycopyrrolate effects were significantly lower(P<0.05) than the control saline-treated group. However, the root mean square of the interval differences between consecutive R peaks(RMSSD) and the standard deviation of Poincare plot perpendicular to the line-of-identity(SD1) in atropine were significantly decreased(P<0.05) from the baseline value, and the low frequency/high frequency ratio(LF:HF ratio) in glycopyrrolate was significantly increased from baseline value(P<0.05). The change of SD1 agreed with that of the high frequency(HF) in the frequency domain component and also with those of respiratory rate and $SpO_2-R$. Our results prove that glycopyrrolate is more suitable as a pre-anesthetic anticholinergic in ketamine anesthesia of dogs with respect to safety and duration of action.
Recent studies have shown that a GABAergic mechanism in the brain modulates arterial blood pressure (BP) through alterations of sympathetic activity in the brain. The purpose of the present study was to determine if this modulation is involved in the pressor response to raised intracranial pressure (ICP). The pressor response to raised ICP was abolished by pretreatment of anesthetized rabbits with intracerebroventricular (icv) muscimol (a GABA agonist) as well as with icv clonidine $(an\;{\alpha}_2-agonist)$. Raising ICP in the hypertensive state after icv yohimbine $(an\;{\alpha}_2-antagonist)$ did not cause an additional increase in the BP, whereas raising ICP in the hypertensive state following icv bicuculline (a GABA antagonist) produced a further increase. Bicuculline produced an increase of the BP which had been lowered by muscimol or by clonidine, whereas it failed to increase the hypertensive state induced by either previous yohimbine or raised ICP. Yohimbine reversed the BP which had been made low by clonidine but was incapable of raising the hypotensive state after muscimol. Yohimbine failed to increase the heightened BP due to raised ICP, whereas bicuculline-induced pressor state was further elevated by yohimbine. Muscimol, besides the bicuculline-antagonizing property, inhibited the pressor response to yohimbine, suggesting participation of a GABAergic mechanism in the pressor action of yohimbine. From these results it was inferred that there were three ways in which BP could be increased via raised ICP: inactivation of the inhibitory sympathetic activity through (1) ${\alpha}_{2}-adrenoceptors$, (2) bicuculline-sensitive GABA receptors, (3) yohimbine-sensitive, clonidine-acting GABAergic sites.
Neuropathic pain originating from multiple condition of nerve cell injury is common, but is difficult to treat. Even though many drugs such as anti-convulsants, anti-depressants, NSAIDs, opioids have been used, their clinical analgesic action were not satisfactory due to occur severe side effects. Gabapentin was introduced in 1994 as a novel antiepileptic drug and has been used to treat partial seizure. After 1995 gabapentin treatment for reflex sympathetic dystrophy (RSD) started, 45% of the reports about the analgesic efficacy of gabapentin were restricted to the treatments of non-epileptic pain syndrome. This drug is preferred to treat neuropathic pain because of a lower incidence of its side effects than those of other anti-convulsants and anti-depressants. For evaluating it's analgesic efficacy, the changes in the patients' subjective pain intensity was measured by the score on the visual analogue scale (VAS) and patient's objective pain intensity by measuring the skin temperature via infrared thermography were investigated respectively. Side effects of gabapentin were look into. We observed successful relief of neuropathic pain in the three patients which included post-herpetic neuraligia, complex regional pain syndrome (CRPS) and diabetic neuropathic pain, and the side effects of gabapentin were at acceptable levels.
This study was carried out in order to clarify whether the cardiovascular effect of prostaglandin(PG) $F_{2{\alpha}}$ might be centrally mediated. In unrestrained conscious rat, $PGF_{2{\alpha}}$ was administered into the lateral ventricle. The mechanism of action was also studied by observing the interaction with several adrenergic antagonists injected subcutaneously, Indomethacin was administered into lateral ventricle to investigate the role of endogenous $PGF_{2{\alpha}}$ on the central regulation of cardiovascular system. The results were as follows: 1) The intraventricular injection of $PGF_{2{\alpha}}$ produced an increase in blood pressure and heart rate. 2) The pretreatment with phenoxybenzamine (2 mg/g, s.c.) inhited pressor, but not heart rate responses to the intraventricular injection of $PGF_{2{\alpha}}$$(2{\mu}g/kg)$. 3) The pretreatment with propranolol (1 mg/kg, s.c.) inhibited tachycardia, but not pressor responses to the intraventricular injection of $PGF_{2{\alpha}}(2{\mu}g/kg)$. 4) The intraventricular injection of indomethacin $(40{\mu}g/kg)$ could not induce significant changes in blood preesure and heart rate. 5) The result indicates that intraventricular injection of $PGF_{2{\alpha}}$ produces pressor and tachycardia responses in the unanesthetized rat, and it is mediated primarily by centrally increased sympathetic outflow. But the endogenous $PGF_{2{\alpha}}$ synthetized in the brain seems to play minor role in the direct regulation of cardiovascular system.
Estate M. Sokhadze;Lee, kyung-Hwa;Lee, Jong-Mee;Oh, Jong-In;Sohn, Jin-Hun
Proceedings of the Korean Society for Emotion and Sensibility Conference
/
한국감성과학회 2000년도 춘계 학술대회 및 국제 감성공학 심포지움 논문집 Proceeding of the 2000 Spring Conference of KOSES and International Sensibility Ergonomics Symposium
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pp.290-300
/
2000
One of the most important topics in attentional and emotional modulation of cardiac responses is time course of cardiac chronotropic response. The reason lies in dual innervation of heart, which leads to occurrence of several phases of cardiac response during exposure to affective stimuli, determined by the balance of sympathetic and parasympathetic influences. Cardiac chronotropic reactivity thus represents quite effective measure capable to trace the moment when attending and orienting processes (i.e., sensory intake of stimulus) prime relevant behavioral response (ile., emotion with approach or avoidance tendencies). The aim of this study was to find the time course of heart rate (HR) responses typical for negative (disgust, surprise, fear, anger) and positive (happiness, pleasant erotic) affective pictures and to identify cardiac response dissociation for emotions with different action tendencies such as "approach" (surprise, anger, happiness) and "avoidance" (fear, sadness, disgust). Forty college students participated in this study where cardiac responses to slides from IAPS intended to evoke basic emotions (surprise, fear, anger, sadness, disgust, happiness, pleasant-erotic). Inter-beat intervals of HR were analyzed on every 10 sec basis during 60 sec long exposure to affective visual stimuli. Obtained results demonstrated that differentiation was observed at the very first 10s of exposure (anger-fear, surprise-sad, surprise-erotic, surprise-happiness paris), reaching the peak of dissociation at 30s (same pairs plus surprise-disgust and surprise-fear) and was still effective for some pairs (surprise-erotic, surprise-sad) even at 50s and 60s. discussed are potential cardiac autonomic mechanisms underlying attention and emotion processes evoked by affective stimulation and theoretical considerations implicated to understand the role of differential cardiac reactivity in the behavioral context (e.g., approach-avoidance tendencies, orienting-defense responses).
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