Journal of Physiology & Pathology in Korean Medicine
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제20권6호
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pp.1612-1619
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2006
This Study was designed to investigate the mechanism of Mixture of Bambusae Caulis in Liquamen and Bamboo Extract on the change of regional cerebral blood flow (rCBF) and blood pressure (BP) in normal rats, and further to investigate cytokines production in serum of cerebral ischemic rats. Mixture were as follows ; Bamboo Extract extracted with distilled water at 98 $^{\circ}C$ for 3 hrs, Mixture of Bambusae Caulis in Liquamen and bamboo Extracts (MLE) mixed at the ratio 1 to 100 (MLE100), 1 to 50 (MLE50), 1 to 20 (MLE20), 1 to 10 (MLE10), 1 to 5 (MLE5). The results were as follows ; The MLE-induced increase in rCBF was significantly inhibited by pretreatment with indomethacin (1 mg/kg, I.p.), an inhibitor of cyclooxygenase as well as methylene blue (10 $^{\mu}g/kg$, I.p.), an inhibitor of guanylate cyclase. The MLE-induced increase in BP was significantly inhibited by pretreatment with methylene blue. In cytokines production in the serum drawn from femoral arterial 1 hr after middle cerebral artery occlusion, MLE5 significantly increased production of TGF-${\beta}$ and increased production of IL-10, but significantly decreased production of TGF-${\alpha}$ compared with control group. In cytokines production in the serum drawn from femoral arterial 1 hr after reperfusion, MLE5 significantly increased production of TGF-${\beta}$ and IL-10, but significantly decreased production of TGF-${\alpha}$ compared with control group. AS results above. And MLE5 had anti-ischemic effect by inhibiting TGF-${\alpha}$ production, and by accelerating IL-10 and TGF-${\beta}$ production.
1) The relationship of arterial blood pressure and heart rate with raised intracranial pressure induced by the epidural balloon method was investigated in anesthetized rabbits and cats. 2) In both animals marked increase of the blood pressure was observed when the intracranial pressure became close to the blood pressure. 3) In both animals marked decrease in the blood pressure and transitory marked decrease in the heart rate were observed, when the level of the intracranial pressure exceeded that of the blood pressure. 4) In reserpinized animals raised intracranial pressure produced decrease in the blood pressure and heart rate. 5) During raised intracranial pressure, the 6-hydroxydopamine-treated (by intracerebral administration) animals showed increase of the blood pressure less than control animals. 6) The depressor response to raised intracranial pressure in the reserpinized animals was reversed to the marked pressor one by the administration of norepinephrine into the lateral ventricle. 7) These results suggest that the pressor response to raised intracranial pressure is due to the increase of norepinephrine release resulted from local stimulation of the central sympathetic neurons by the raised intracranial pressure.
We have designed a new type of bubble oxygenator (KOREA-KIM VENOTHERM OXYGENATOR) made of PVC sheet and deforming mesh incorporated in the heat exchanger, and evaluated in experimental animal for the analysis of it`s efficiency. The Oxygenator has low priming volume with high flow rate up to 6 L/rain, and efficiency of heat exchanger was excellent as 1-$1.5^{\circ}C.$ using total cardiopulmonary bypass method under moderate to deep hypothermia. Average priming volume of 1317 ml with 30% hemodilution method was perfused with an average of 1.1-3.0 L/min.$M^2$of arterial blood and pure oxygen at a rate of 2-3.4 L/min for 49.6 minutes continuously in average. During total cardiopulmonary bypass, average $PaO_2$ was $159.8{\pm}60$mmHg, $PaCO_2$$41.0{\pm}3$mmHg respectively under $SaO_2$ over 96% with systolic arterial pressure of 70 mmHg and CVP of 5-10 cm$H_2O$. Plasma free Hemoglobin was $7.0{\pm}4$ mg/dl with 25% drop of hemoglobin and hematocrit at the end of cardiopulmonary bypass. This KKV Oxygenator was observed to have excellent capabillty of oxygen and carbon dioxide gas transfer with small amount of blood trauma, and the efficiency of heat exchanger was satisfactory during cooling and rewarming of the bubbled blood. Disadvantages have included the somewhat poor deforming effect due to loose PVC fiber mesh, the extracompact character of Teflon filters, and the rough inner surface of the heat exchanger copper pipes.
Histamine, 0.5 mg as histamine base in 4 ml of normal saline solution, was injected into rabbits anesthetized with nembutal and the mean blood pressure was kept in the range of $52{\sim}80\;mmHg$ for over one hour by supplemental additions. Following the injection of the test substances, 300 mg of urea and 200 mg of antipyrine intravenously, serial blood samples were obtained from the femoral artery and the internal jugular vein at $0.5{\sim}3$ minutes interval. The decreasing patterns in the concentrations of arterial and venous blood plasma samples were compared with each other. The ratio of the concentration of brain tissue to that of the final arterial plasma was also studied. By these measures the degrees of penetration of the test substances in the brain in the control and in the histamine treated rabbits were observed. The concentrations of antipyrine and urea in the arterial blood plasma were decreasing exponentially with respect to the time elapsed. The venous concentrations were anticipated to increase initially and to cross the arterial concentration curve in the point of equlibrium between the plasma and the tissue. On the contrary to the expectation venous concentration also revealed the decreasing tendency similar to that of arterial plasma. The similarity between these two curves, arterial and venous, would be atributable to the fact that the cerebral blood flow rate was large enough and the rising phase in the venous concentration curve was instantly over before serial blood samples were taken. Inspite of some similarity in the decreasing tedency in both concentration curves there were appreciable discrepancies between the arterial and venous plasma which would reflect the situation far from the equlibria among several compartments in the brain. Changes in plasma potassium levels caused by the injection of histamine or bleeding were observed, too. Using 8 rabbits as the control and 12 rabbits for the histamine treated group following results were obtained: 1. Both of the concentration curves, arterial and venous, declined rapidly at_first and slowly later on and approached same equilibrium concentration with the passage of time after a single injection. The time at which attained the same concentration was $2.0{\pm}0.54\;min.$ in the control and $4.3{\pm}1.92\;min.$ in the histamine treated group with respect to antipyrine. On the other hand in the case of urea they were $2.4{\pm}0.59\;min.$ in the control and $4.4{\pm}1.31\;min.$ in the histamine group, respectively. In the histamine treated group enlarged spaces for distribution of test substances were postulated. 2. The concentration of antipyrine in the brain tissue water revealed no significant differences between the control and experimental groups, showing $212{\pm}40.2\;mg/l$ in the control and $206{\pm}64.1\;mg/l$ in the histamine treated group. On the other hand urea revealed higher value in the histamine treated group than in the control, showing an enhanced penetration of urea into the tissue after injection of histamine. Urea concentration in the brain water was $32.3{\pm}3.36\;mg%$ in the control and $39.2{\pm}4.25\;mg%$ in the histamine treated group. 3. The distribution ratio of antipyrine in the brain tissue was very close to unity in the histamine treated animals as well as in the control. 4. The average of the distribution ratio of urea in the control animals was 0.77 and it showed the presence of blood-brain barrier with regard to urea. However in the histamine treated animals the distribution ratios climbed up to 0.86 and they were closer to unity than in the control animals. Out of 12 cases 5 were greater than 0.9 and 8 exceeded 0.85. It appeared that histamine enhanced the penetration of urea through the barrier. 5. Histamine injection and or hemorrhage caused an elevation of the concentration of potassium in plasma. In the event that histamine and hemorrhage were applied together the elevation of potassium exceed the elevation seen at the histamine alone. There was no evidence that the leakage of potassium from the brain tissue was dominant in comparison with the general leakage from the whole body.
Hemodynamic information in the carotid artery bifurcation is very important for understanding the development and progression mechanisms of cerebrovascular disease and for its early diagnosis and prediction of the progress. In this paper, we constructed a mock pulsatile blood circulation system using an anthropomorphic elastic vessel of the carotid artery bifurcation and ex vivo pig blood to acquire ultrasound images from blood and vessels synchronized with internal pressure while controlling the blood flow. Echogenicity, blood flow velocity, and blood vessel wall motion from the ultrasound images, and internal blood pressure were extracted over a cycle averaged from five cycles when the pulsatile pump rates are 20 r/min, 40 r/min, and 60 r/min. As a result, respectively, the peak systolic blood flow velocities were 20 cm/s, 25 cm/s, and 40 cm/s, the blood pressure differences were 30 mmHg, 70 mmHg, and 85 mmHg, the arterial walls were expanded to 0.05 mm, 0.15 mm, and 0.25 mm. Time-delayed cyclic variation of echogenicity compared to blood flow and pressure was observed, but the variation was minimal at 20 r/min. Time-synchronized cyclic variations of these parameters are important information for accurate input parameters and validation of the computational hemodynamic experiments which will provide useful information for the development and progress mechanisms of carotid artery stenosis.
In order to determine the dose-response relationship of ethanol on blood pressure and renal function, 2 doses of ethanol were intubated into albino rats. For a direct measurement of arterial blood pressure, a polyethylene catheter(PE 10) was implanted in the abdominal aorta, and the other end of the catheter was pulled out of the back of the neck. The experiment was conducted after the rats recovered from the surgery. After emptying their bladders, the rats were placed in a metabolism cage. Mean arterial pressure (MAP) was measured and arterial blood samples were collected through the catheter. Following the collection of the control urine sample, 1 ml of 10 g% (low dose), or 30 g% (high dose) of ethanol/100 g BW was intubated. 1 ml of water/100 g BW was intubated into the control group. MAP and blood samples were taken every hour, and urine samples were collected every 90 min for 3 hours. Blood alcohol concentrations reached a peak at 1 hour (low dose: $105.0{\pm}7.5$, high dose: $214.7{\pm}20.2\;mg%$) and decreased linearly thereafter. Following alcohol ingestion, MAP began to decrease at 15 min and remained at a significantly low level thoughout the 3 hours experimental period(low dose: $112{\pm}2{\rightarrow}102{\pm}4$, high dose: $117{\pm}2{\rightarrow}100{\pm}8\;mmHg$). Urine Flow increased markedly during the first 90 min of ethanol ingestion (low dose: $0.88{\pm}0.20{\rightarrow}1.04{\pm}0.22$, high dose: $0.56{\pm}0.11{\rightarrow}1.35{\pm}0.18\;ml/1.5\;hr$) and decreased during the second 90 min period(low dose: $0.25{\pm}0.06$, high dose: $0.22{\pm}0.06\;ml/1.5\;hr$). Urine flow of the control group decreased gradually during the experiment $(0.88{\pm}0.10{\longrightarrow}0.59{\pm}0.09{\rightarrow}0.45{\pm}0.09\;ml/1.5\;hr)$. These results indicate that the blood-pressure-lowering and diuretic effects of ethanol are dose-related: higher doses of ethanol produce a greater decrease in blood pressure and greater diuresis.
The aim of this study was to investigate trazodone's effect on vasorelaxation and blood pressure lowering and to examine its underlying mechanism of action in isolated thoracic aorta and anesthesized rats. Precontracted aortic rings with high KCl were relaxed with trazodone, at concentrations of $50{\mu}M$ or greater. However, precontracted rings with phenylephrine (PE) were relaxed with trazodone, at concentrations of $0.03{\mu}M$ or greater, in a concentration-dependent manner. These relaxant effects of trazodone on endothelium intact rat aortic rings were significantly greater than those on denuded rings. The trazodone-induced relaxations were suppressed by nitric oxide synthase (NOS) inhibitors, N(G)-nitro-L-arginine (L-NNA) and N(omega)-nitro-L-arginine methyl ester (L-NAME), guanylate cyclase inhibitors, methylene blue and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a $Ca^{2+}$-activated $K^+$ channel blocker, tetrabutylammonium (TBA), a $Ca^{2+}$ channel blocker, nifedipine, $Na^+$ channel blockers, lidocaine and procaine, and removal of extracellular $Na^+$, but not by aminoguanidine, 2-nitro-4-carboxyphenyl-n, n-diphenylcarbamate (NCDC), indomethacin, glibenclamide and clotrimazole. In vivo, infusion of trazodone elicited significant decrease in arterial blood pressure. Trazodone-induced decrease in blood pressure was markedly inhibited by pretreatment of intravenous injection of saponin, L-NNA, methylene blue, TBA, lidocaine or nifedipine. These findings suggest that the endothelium-dependent relaxation and decrease in blood pressure induced by trazodone is mediated by release of NO from the endothelium, activation of TBA-sensitive $Ca^{2+}$-activated $K^+$ channels or inhibition of $Ca^{2+}$ entry through voltage-gated channel.
The death of cattle from acute bracken poisoning has been recognized for many years. Acute bracken poisoning is characterized by mucoidal nasal and anal hemorrhage, severe anorexia. pyrexia, gastric ulcer and myocardial damage. In 1958 Evans first suggested that clinical picture of bracken poisoning was very much similar to that of radiation injuries such as aplastic anemia, leucopenia, thrombocytopenia and increased capillary fragility. Bracken has been clearly demonstrated to contain a carcinogen as well as thiaminase. However, the nature of carcinogen in bracken has not definetely elucidated. Also it was warned by several workers that bracken could be a causative factor for stomach cancer in Korean and Japanese. It appears that little is known on the e(feet of bracken on the function of cardiovascular system. Therefore the present study was designed to explore effects of ethanol extract of raw and toiled bracken (RBEE:BBEE) on blood pressure in cats. Also studied was the mechanism underlying changed in blood pressure of cats by bracken. The result obtained were as follows; 1) Mean arterial blood pressure was invariably decreased following administration of either RBEE or BBEE. Tn general depressor responses to RBEE persisted longer than that to BBEE. Generally, depressor responses were proportional to debases of RBEE and BBEE administered. 2) After administration of 60 mg/kg RBEB and BBEE, blood Pressure decreased by $62.1{\pm}1.7mmHg$ and $68.0{\pm}3.0mmHg$, respectively. No change was observed between depressor responses to RBEE and that to BBEE. 3) Depressor responses to BBEE and RBEE were not affected by vagotomy, propranolol and regitine. 4) In atropinized animal depressor responses to BBEE and RBEE were reduced by 30-40% showing part of depressor response was resulted from cholinergic effect of bracken.
Kim, Shang-Jin;Kim, Jeong-gon;Joe, Sung-gun;Kang, Hyung-sub;Kim, Jin-shang
Korean Journal of Veterinary Research
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제44권3호
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pp.357-366
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2004
We studied the effect of propofol (PPF) on the endothelium-dependent vascular responses in isolated rat thoracic aorta. In aortic rings with endothelium, PPF inhibited the phenylephrine (PE)-induced contraction in a concentration-dependent manner. In PE-precontracted preparations, PPF attenuated the endothelium-dependent relaxation by acetylcholine but not by A23187. And PPF did not attenuate the endothelium-independent relaxation by sodium nitroprusside (SNP). The relaxation induced by acetylcholine in PE-precontracted aortic rings was significantly augmented by zaprinast, a cGMP-specific phosphodiesterase inhibitor, and this augmentation was inhibited by PPF. Although SNP-induced relaxation was significantly augmented by zaprinast, this augmentation was not inhibited by PPF. In preparations preconstricted with PE, the PPF-induced relaxation was inhibited by atropine. In addition, PPF attenuated the vasorelaxation by phosphodiesterase inhibitors (IBMX, Ro20-1724 or zaprinast except milrinone). In vivo, the infusion of acetylcholine and SNP showed decreased arterial blood pressure in rats. The pre-injection of PPF inhibited the acetylcholine-induced blood pressure lowering, but not the SNP-induced blood pressure lowering. These results suggest that PPF can attenuate in part the acetylcholine-induced vasorelaxation and blood pressure lowering through the inhibition of the acetylcholine receptor-mediated endothelium-derived relaxing factor by acting on endothelium. It is considered that the inhibitory effect of PPF on the vasorelaxation is due to the decreased level of cGMP which can be attributed to the inhibition of the muscarinic receptor and/or receptor-G-protein interaction.
Many surgeons and anesthesiologists prefer using vasoconstrictor mixed with local anesthetic agent to reduce the incidence of side effects and prolong the duration of analgesia because most local anesthetic agents, except cocaine, were believed to possess vasodilating effect. However, some investigators recently reported vasoconstricting effect of local anesthetic agents. There is still controversy on the vasoactive effect of local anesthetic agents. So this study is aimed to clarify the vasoactive effect of local anesthetics in the animal model resembling clinical settings. Rabbits were anesthesized with ketamine and haloghane, and respirations were controlled with Harvard animal ventilator. Lidocaine (0.5%, 1.0%, 1.5%) and bupivacaine (0.125%, 0.25% and 0.5%) with or without 1:100,000 epinephrine were subdermaly injected on the femoral bupivacaine of the femoral artery were measured with Doppler flow meter in vivo. The mean arterial pressure, pulse rate, arterial blood gases, pH and level of serum electrolytes were measured at every 2 minute interval for 30 minutes. Results were as follows: 1) There was no significant vasoconstriction with 0.5% lidocaine and 0.125% bupivacaine. 2) Statistically significant (p<0.05) vasodilations were observed with lidocaine (1.0~2.0%) and bupivacaine (0.25~0.5%). 3) There were no changes on the duration of vasodilation induced by local anesthetic agents of various concentrations. 4) Onset of vasodilation induced by local anesthetic agents of high concentration were faster than that of lower concentrations. 5) In the mixed injection group of epinephrine and local anesthetic agent, the vasoconstriction induced by epinephrine was completely reversed by local anesthetics, approximately 5 minutes later. In conclusion, local anesthetic agents at dose exceeding 1.0% lidocaine and 0.25% bupivacaine increase local blood flow significantly in animal study in vivo which is applicable in human clinical settings. The increase blood flow may be due to dilatation of blood vessel. Further study on the analysis of association between amount of absorbed local anesthetics in blood vessels and dilatation of blood vessels is needed.
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