Objective: The aim of this study was to investigate anti-ischemic effect of LR1 HT8 Reduction in Acupuncture Methods: I designed to investigate whether LR1 HT8 Reduction in Acupuncture affects cerebral hemodynamics [regional cerebral blood flow(rCBF), pial arterial diameter(PAD), mean arterial blood pressure(MABP)] in normal rats and to make manifest whether LR1 HT8 Reduction in Acupuncture is mediated by cyclooxygenase or guanylate cyclase. The changes of rCBF and MABP were determinated by laser-doppler flowmetry(LDF), and the change of PAD was de terminated by video microscope and width analyzer. Results: The results were as follows; 1. LR1 Reduction in Acupuncture was increased rCBF and PAD, but decreased MABP. 2. HT8 Reduction in Acupuncture was significantly increased rCBF, but decreased MABP, and increased PAD. 3. LR1 HT8 Reduction in Acupuncture was significantly increased rCBF, PAD, but decreased MABP after withdrawing of the needle. This results suggest that LR1 HT8 Reduction in Acupuncture increased significantly rCBF by dilating PAD. 4. Pretreatment with indomethacin(1mg/kg, i,v.) was significantly inhibited LR1 HT8 Reduction in Acupuncture induced increase of rCBF and PAD, but increased LR1 HT8 Reduction in Acupuncture induced decrease of MABP after withdrawing of the needle. 5. Pretreatment with methylene blue($10{\mu}g/kg$, i,v.) was decreased LR1 HT8 Reduction in Acupuncture induced increase of rCBF and PAD, but accelerated LR1 HT8 Reduction in Acupuncture induced decrease of MABP. Conclusions: I suggest that LR1 HT8 Reduction in Acupuncture has an anti-ischemic effect through the improvement of cerebral hemodynamics, and the mechanism is mediated by cyclooxygenase.
Pulmonary artery sarcoma (PAS) is a rare and fatal disease that often mimics chronic thromboembolic pulmonary hypertension (CTEPH); therefore, diagnosis of PAS is often delayed. Herein, a healthy 74-year-old man was presented with a 4-month history of dyspnea. Chest computed tomography showed wall thickening and stenosis in the main pulmonary artery as well as in both proximal pulmonary arteries. In order to differentiate between unusual CTEPH, vasculitis, and PAS, we performed right heart catheterization and pulmonary angiography. The mean pulmonary arterial pressure was 21 mmHg, and there was severe pulmonary artery stenosis. Thrombi on the pulmonary arterial wall lesions were observed in intravascular ultrasound and optical coherence tomography. Furthermore, the patient had a history of deep vein thrombosis. Therefore, we diagnosed unusual CTEPH. After 6 months of rivaroxaban anticoagulation therapy, a chest X-ray revealed a left lower lobe lung mass, and a positron emission tomography later showed hypermetabolic lesions in the main pulmonary artery wall, in both pulmonary arteries walls, in the lung parenchyma, and in the bones. A biopsy of the right proximal humerus lesion revealed undifferentiated intimal sarcoma. Pulmonary sarcoma is rare, but should be considered when differentially diagnosing main pulmonary artery wall thickening and stenosis. A positron emission tomography may aid in this diagnosis.
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.
Jaeumgenby-tang(JGT) have been used in oriental medicine for many centuries as a therapeutic agent of vertigo caused by deficiency of qi(氣) and blood(血). Effect of Aurantii Fructus(AF) take off the phlegm by promoting the circulation of qi, Gastrodae Rhizoma(GR) has effects treating for headache, vertigo by calming the liver and suppressing hyperactivity of the liver-yang(陽). And, We reported that JGT adding AFㆍGR extract(JGTAG) was significantly increased regional cerebral blood f1ow(rCBF) by dilating pial arterial diameter(PAD). Therefor we designed to investigate whether JGTAG is mediated by adrenergic β-receptor, cyclooxygenase or guanylate cyclase in normal rats. The changes of rCBF and mean arterial blood pressure(MABP) were determinated by laser-doppler flowmetry(LDF), and the change of PAD was determinated by video microscope and width analyzer. The results were as follows in normal rats; Pretreatment with propranolol(1mg/kg, i.v.) was significantly inhibited JGTAG induced increase of rCBF, PAD and MABP, and pretreatment with indomethacin(1 mg/kg, i.v.) was significantly inhibited too. But pretreatment with methylene blue(10μg/kg, i.v.) were accelerated JGTAG induced increase of rCBF and MABP, but pretreatment with methylene blue was inhibited JGTAG induced increase of PAD. This results suggest that the mechanism of JGTAG is mediated by adrenergic β-receptor and cyclooxygenase.
This experimental study was designed to investigate the effects of Sagunja-tang(SGJT), Ijin-tang(IJT), Yukgunja-tang(YGJT) on the change of cerebral hemodynamics [regional cerebral blood f1ow(rCBF), mean arterial blood pressure(MABP), and pial arterial diameter (PAD)] in normal rats, and further to determine the mechanism of action of YGJT. And, this Study was designed to investigate whether YGJT inhibit lactate dehydrogenase(LDH) activity in neuronal cells. The results were as follows ; 1. SGJT significantly increased rCBF but MABP was not changed comparing with normal MABP(l00 %). This results were suggested that SGJT significantly increased rCBF by dilating PAD. 2. IJT significantly decreased rCBF in a dose-dependent, but significantly increased MABP in a dose-dependent. This results were suggested that IJT significantly decreased rCBF by contracting PAD. 3. YGJT significantly increased rCBF and PAD in a dose-dependent, and YGJT increased MABP compared with normal MABP(100 %). This results were suggested that YGJT significantly increased rCBF by dilating PAD. 4. The YGJT-induced increase in rCBF was significantly accelerated by pretreatment with indomethacin (IDN, 1 mg/kg, i.p.), an inhibitor of cyclooxygenase but was significantly inhibited by methylene blue (MTB, 10 ㎍/㎏ i.p.), an inhibitor of guanylate cyclase. 5. The YGJT-induced increase in PAD and MABP were accelerated by pretreatment with IDN but was significantly inhibited by MTB. This results suggested that the mechanism of YGJT is mediated by guanylate cyclase. 6. YGJT inhibited significantly LDH activity in neuronal cells. This results were suggested that YGJT prevented the neuronal death. I thought that YGJT should have improvement of cerebral hemodynamics and inhibitive effect on the brain damage.
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.
Adult rabbits were anesthetized with nembutal, 30 mg/kg. Carotid artery and jugular vein were exposed surgically and cannulated with polyethylene tubing. Arterial blood pressure was recorded via pressure transducer on the physiograph and $100{\mu}g/ml$ of histamine solution was infused through the jugular vein by using the constant infusion pump with a rate of 0.92 ml/min or 1.40 ml/min. Mean arterial blood pressure was maintained at $40{\sim}70 mmHg$ and hypotension was kept for 2 hours. After the termination of this period, blood was taken and osmotic fragility was mea sured immediately. Also, every sample of normal blood and shocked blood was incubated for 1 hour or 2 hours at $37^{\circ}C$ in order to see whether or not there was some influence of incubation. Furthermore to clarify which component was responsible for the change on the fragility, the mixtures of normal blood cells with shocked plasma and shocked blood cells with normal plasma were also incubated at $37^{\circ}C$ for one or two hours and fragility in such cases was measured. The data obtained were analysed by probit-plot method and the concentration of saline solution at which the hemolysis started to occur, 50% of blood cells were hemolysed and that at which the red blood cells hemolysed completely were determined. The values for the blood of hypotension stage were compared with those of the control blood. The results obtained were as fellows: 1. Osmotic fragility of red blood cell was increased in hypotensive state induced by histamine. 2. The differences of osmotic fragility after two hours of incubation were negligible both in normal blood and in that of hypotensive state. 3. Osmotic resistance of normal red blood cell incubated in shock plasma was less than that of shock red blood cell incubated in normal plasma. It was suggested that plasma in hypotensive state caused by histamine might be primarily responsible for the alteration of red blood cell fragility.
This experimental study was designed to investigate the effects of Acanthopanax sessiliflorus $S_{EEM}$ extracts following gamma-ray irradiation on the change of weight, the serum total cholesterol, HDL-cholesterol, LDL-cholesterol, triglyceride, free fatty acid, total lipid, phospholipid level in obese mice induced by high fat diet, and the change of regional cerebral blood flow (rCBF) and blood pressure (BP) in normal rats. Experimental materials were as follows ; 10AS was the bark powder of Acanthopanax sessiliflorus $S_{EEM}$ stems which was exposed in 10 kGy electron beam, 10AS was the bark powder of Acanthopanax sessiliflorus $S_{EEM}$ roots which was exposed in 10 kGy electron beam, 100S was the bark powder of Acanthopanax sessiliflorus $S_{EEM}$ stems which was exposed in 100 kGy electron beam, Experimental groups were as follows ; Normal group was fed with normal diet and administered with distilled water during 5 weeks, Control group was fed with high fat diet and administered with distilled water during 5 weeks, Sample A group was fed with high fat diet and administered with 10AS of 300 mg/kg/mouse/day during 5 weeks, Sample B group was fed with high fat diet and administered with 10AR of 300 mg/kg/mouse/day during 5 weeks, Sample C group was fed with high fat diet and administered with 100AS of 300 mg/kg/mouse/day during 5 weeks. The results were as follows ; Sample A group, Sample B group and Sample C group were significantly decreased body weight and the serum LDL-cholesterol, triglyceride, total lipid level in comparison with Control group. Sample A group, Sample B group and Sample C group were significantly increased the serum HDL-cholesterol level in comparison with Control group. Sample B group and Sample C group were significantly decreased the serum total cholesterol, free fatty acid and phospholipid level in comparison with Control group. This results were suggested that all experimental materials were able to be used for the obesity. 10AS did not changed rCBF and MABP in a dose-dependent manner. 10AR significantly increased rCBR in a dose-dependent manner, and BP did not change in a dose-dependent manner. 100AS decreased rCBF and BP in a dose-dependent manner. This results were suggested that 10 AR significantly increased rCBF by dilating pial arterial diameter. According to above results, the authors suggested that 10AR was able to be used for the obesity and ischemic disease.
Zainalabidin, Satirah;Budin, Siti Balkis;Ramalingam, Anand;Lim, Yi Cheng
The Korean Journal of Physiology and Pharmacology
/
제18권5호
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pp.411-418
/
2014
Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p<0.05). Nicotine-treated group showed significant (p<0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group ($ED_{50}=1.44{\times}10^5M$ vs. $4.9{\times}10^6M$) (p<0.05~0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group ($ED_{50}=6.17{\times}10^7M$ vs. $2.82{\times}10^7M$) (p<0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p<0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.
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