Objectives : Increasing evidence suggests that parasympathetic vagus nerve activity plays a role in modulating acupuncture-induced anti-inflammatory reaction, but the function of sympathetic nerve is not known. Here, we investigated whether splanchnic sympathetic nerve activity was involved in the regulation of splenic expression of $TNF-{\alpha}$ mRNA by electroacupuncture (EA) in LPS-injected animals. Methods : DiI was injected into the stomach or celiac ganglion (CG) for retrograde labeling of the target tissues. EA was given at ST36 and the electrical stimulation on the sciatic nerve in LPS-injected mice. c-Fos signals in the tissues were analyzed by immunofluorescence staining, and $TNF-{\alpha}$ mRNA was analyzed by real-time PCR. Results : Application of EA at ST36 or electrical stimulation on the sciatic nerve induced c-Fos expression in neurons of the spinal cord and celiac ganglion (CG). Then, the vagotomy reduced c-Fos levels in CG neurons but not in the spinal cord in animals given EA. Expression of $TNF-{\alpha}$ mRNA which was induced in the spleen after LPS was significantly inhibited by EA, then the vagotomy elevated $TNF-{\alpha}$ mRNA level similar to that in LPS-injected animals. Splanchnectomy in animals given LPS and EA also increased $TNF-{\alpha}$ mRNA though it was less effective than vagotomy. Conclusions : Our data suggest that EA delivered to the spleen via the splanchnic sympathetic nerve may be involved in attenuating splenic inflammatory responses in LPS-injected animals.
Yan, Hai-Dun;Kim, Charn;Kim, Ji-Mok;Lim, Won-Il;Kim, Sang-Jeong;Kim, Jun
The Korean Journal of Physiology
/
v.30
no.1
/
pp.105-116
/
1996
Rendering the brain ischemic would evoke the cerebral ischemic reflex which is characterized by an arterial pressor response, apnea and bradycardia. Since the rostral ventrolateral medulla (RVLM) is known to play a key role in the maintenance of normal cardiopulmonary activity, during the cerebral ischemic reflex some cardiac related cells should be excited and respiration related cells inhibited. In this context, the responses of RVLM neurons to systemie and focal hypoxia were analyzed in the present study. Twenty-five adult cats of either sex were anesthetized with ${\alpha}-chloralose$ and the single neuronal activities were identified from RVLM area. For the induction of focal hypoxia in the recording site, sodium cyanide was applied iontophoretically and for systemic hypoxia the animal was ventilated with nitrogen gas for a twenty-second period. Cellular activities were analyzed in terms of their discharge pattern and responses to the hypoxia by using post-stimulus time and single-pass time histograms. Of eighteen cardiac related cells recorded from the RVLM area, twelve cells were excited by iontophoresed sodium cyanide and of twenty-five respiration related cells, fourteen cells were excited by iontophoresed sodium cyanide. Remaining cells were either inhibited or unaffected. Eight of fifteen cells tested with iontophoresed sodium lactate were excited and remaining seven cells were inhibited. Systemic hypoxia induced by nitrogen gas inhalation elevated the arterial blood pressure, but excited, inhibited or unaffected the single neuronal activities. Some cells showed initial excitation followed by inhibition during the systemic hypoxia. Bilateral vagotomy resulted in a decrease of arterial pressor response to the systemic hypoxia, and a slight decrease in the rhythmicity related to cardiac and/or respiratory rhythms. The single neuronal responses to either systemic or focal hypoxia were not affected qualitatively by vagotomy. From the above results, it was concluded that the majority of the cardiac- and respiration- related neurons in the rostral ventrolateral medulla be excited by hypoxia, not through the mediation of peripheral chemoreceptors, and along with the remaining inhibited cells, all these cells be involved in the mediation of cerebral ischemic reflex.
Evidence from the last 10 years have been suggested that melatonin mainly produce a depressant effect on the cardiac system, but we found an activating effect of melatonin on heart rate in this research. To determine the hypothesis that melatonin has dual effects on physiological behaviour of cardiac system, we investigated the effects of melatonin on heart rate in isolated rat atria and anesthetized rats. Regardless of concentration, melatonin produced bradycardia in the 84 cases of 148 experiments (57 %) and tachycardia in the 64 cases of 148 experiments (43 %). And in atrium, melatonin produced a decrease automaticity in 52 cases of 86 experiments (60 %) and increase automaticity in 40 % (34/86 cases). Also, these effects are not significnat relationship with concetration of melatonin. The melatonin-induced bradycardia in vivo was inhibited by pretreatment of atropine or bilateral cervical vagotomy. Also, in isolated atrium the melatonin-induced decrease in automaticity was inhibited by pretreatment of atropine. These melatonin-induced responses were potenitated by pretreatment of propranolol. The melatonin-induced tachycardia in vivo was inhibited by pretreatment of propranolol, nifedipine or bilateral cervical vagotomy, but not by pretreatment of atropine. The melatonin-induced incease in automaticity in isolated atrium was converted to decrease in automaticity by pretreatment of propranolol. In addition, the change in heart rate caused by adrenoceptor agonists was inhibited by pretreatment of melatonin. These results indicate that melatonin-induced bradycardia may be related to a muscarinic receptor activation and melatonin-induced tachycardia may be related to a $\beta$-adrenoceptor stimulation.
Scolopendra corpus has been used as anticonvulsants and antispasmodics in the oriental medicine. It was previously shown that water extract of Scolopendra corpus had an inhibitory action on ileum in mouse. To investigate the anticonvulsant and antispasmodic activity of Scolopendra corpus, pharmacological studies have been carried out with the water extract of Scolopendra subspinipes mutilans $L.\;K_{OCH}$, which is widely distributed in Korea. 1. The extract depressed convulsions induced by picrotoxin and strychnine. 2. Sedative and antipyretic analgesic action were observed. 3. In mouse and rabbit, tone of intestinal smooth muscle was suppressed with the treatment of the extract and intestinal contraction induced by $BaCl_2$ was also inhibited, suggesting that the extract has a papaverine-like effect. Whereas, in guinea pig, intestinal and tracheal smooth muscle were stimulated, and the effect was antagonized by pre-and after-treatment of diphenhydramine, suggesting that the extract has a histamine-like effect. 4.Flow rate was increased when hind-limb of Toad was perfused with saline containing the extract, but returned to normal within 10 min. Hypotensive effect was observed in rabbit and the effect was abolished by vagotomy.
By the intravenous infusion of saline solution through the postcaval vein, the effects of increasing the venous return on the heart rate were studied in the water turtle (Amyda japonica). The following results were obtained: 1) Prior to saline infusion, when the initial heart rate was below $50{\sim}55/min$ the heart rate was increased by the infusion. When the initial rate was above this value no changes in heart rate were observed following the infusion. 2) When the heart rate was decreased by vagal stimulation, the infusion elicited a remarkable increase in the heart rate. 3) Increased heart rate caused by tile infusion was not affected by vagotomy or sympathectomy. 4) These results suggest that the increase in heart rate secondary to increased venous return is under the control of a myogenic regulatory mechanism, not a neural mechanism.
Park, Hyoung-Jin;Lee, Yun-Lyul;Kwon, Hyeok-Yil;Shin, Won-Im
The Korean Journal of Physiology
/
v.20
no.1
/
pp.1-7
/
1986
It has been well documented that the peripheral autonomic nervous system plays an important role in exocrine pancreatic secretion. However, the role of the central nervous system in pancreatic function is still obscure even though the central nervous system has been known to control gastrointestinal functions through the autonomic nervous system. Since the reticular formation in the mesencephalone seems to integrate the autonomic function, the present study was undertaken to investigate a possible influence of the reticular formation upon the exocrine pancreatic secretion. Twenty·two albino rats fasted for 24 hours were anesthetized by intraperitoneal injection of urethane in a dose of 1 g/kg, The pancreatic duct was cannulated to collect pancreatic juice and bile juice was diverted to the jejunum. The gastroduodenal junction was ligated to Prevent passage of gastic juice into the duodenum. A pair of electrodes were bilaterally inserted in the reticualr formation of the mesencephalone with aid of a stereotaxic apparatus. When the volume of pancreatic juice secreted for 10 min became constant, the reticular formation was electrically stimulated for 10 min. Parameters of the electical stimulation was 1.3V, 40 Hz and 2 msec. When the pancreatic secretion returned to the level before the electrical stimulation, cervical vagotomy (11 rats) or administration of propranolol (11 rats) in a dose of 0.1 mg/kg through the jugular vein was carried out. Ten minutes after the treatment, the electrical stimulation of the reticular formation was repeated. The brain was fixed by perfusion of 10% formaline solution through the heart, and then placement of the electrode tip was examined histologically. Protein concentration and amylase activity in samples of Pancreatic secretion were measured. The electrical stimulation of the reticular formation significantly increased in volume $({\mu}l/10\;min)$, Protein output $({\mu}g/10\;min)$ and amylase output (U/10 min) in the pancreatic secretion. The stimulatroy effects were not affected by the cervical vagotomy but completely abolished by propranolol. Meantime, it was also observed that both vagotomy and propranolol significantly reduced the pancreatic secretory function. These results indicate that the reticular formation in the mesencephalone may exert a stimulatory effect upon the Pancreatic secretory function not through the vagus nerve but through the sympathetic pathway in anesthetized rats.
The purpose of the present study is an attempt to investigate the effect of intraventricular taurine, which is a naturally occuring amino acid containing sulfur and has inhibitory action in brain, on heart rate and blood pressure in the urethane anesthetized rabbits and also to elucidate the mechanism of its cardiovascular actions. Taurine $(0.15{\sim}1.5\;mg)$ injected into the lateral ventricle of anesthetized normontensive rabbits produced a dose-related fall in arterial blood pressure and heart rate, which were marked and long-lasting along with considerable respiratory depression. However, the intravenous administration of taurine at the same dose with intraventricular injection did not induce any changes in blood pressure as well as heart rate. Depressor responses induced by taurine were inhibited significantly by pretreatment with chlorisondamine, clonidine, strychnine and bicuculline but not by atropine, vagotomy, propranolol and metoclopramide. Moreover, taurine did not affect the pressor responses of norepinephrine. Taurine-induced bradycardic effects were blocked clearly by pretreatment with chlorisondamine, propranolol, clonidine, strychnine and bicuculline, while they were not influenced by atropine, vagotomy and metoclopramide. These experimental results suggest that intraventricular taurine causes long-lasting hypotensive and bradycardic actions, and that these cardiovascular effects may be exerted through taurinergic (glycinergic) and GABAergic receptors which are associated with catecholaminergic neurons in brain.
This study was undertaken to investigate the relationship between the $Na^+$ channels of the cardiovascular regulation center and the responses to increased $Na^+$ concentration in the cerebrospinal fluid (CSF), by observing the effects of icv administration of the agents affecting $Na^+$ transport. Icv infusion of $200\;{\mu}l$ of 1 M NaCl produced hypertension and bradycardia in the urethane-anesthetized rabbit, and the bradycardia was inhibited and reversed to tachycardia by vagotomy. Amiloride, a $Na^+$ transport inhibitor, produced hypertension and bradycardia, which were not altered by vagotomy, and it did not affect the NaCl-induced responses. Benzamil, a derivative of amiloride with higher specificity, neither produced any cardiovascular effects by itself, nor affected the NaCl-induced responses. In vagotomized rabbits, icv amiloride reversed the NaCl-induced tachycardia to a bradycardia, but the bradycardiac effect was not altered by pretreating with NaCl. This study showed that although amiloride and benzamil slightly differ in their cardiovascular action, neither of them did affect the NaCl-induced responses. We suggest that the $Na^+$ channels which are sensitive to amiloride or benzamil in the cardiovascular regulation center are not involved in the NaCl-induced response.
In order to investigate the therapeutic effects on blood pressure and hyper cholesteremia, aqueous extract of Chin Gan Sik Pung Tang were studied. The result of the total cholesterol contents in serum and blood pressure of each group were as follows, 1. The aqueous extract of Chin Gan Sik Pung Tang inhibited increased Total cholesterol in serum of rabbits administrated with cholesterol rich diet. 2. Blood pressure manifested gradual response by the fall of 4, 3, 9.2, 19.9 percent in proportion to the administration of 10, 30, 100 mg/kg of Chin Gan Sik pung Tang, respectively 3. Administration of Chin Gan Sik Pung Tang to the rabbit pretreated with Vagotomy, Atropine and Regitine did not show any significant difference in the blood pressure, compare with that of the control group. 4. Administration of Chin Gan Sik Pung Tang to the rabbit pretreated with propranolol show significant difference in the blood pressure, compare with that of the control group. From the above results, it is suggested that Chin Gam Sik Pung Tang has the action on adrenergic ${\beta}-receptor$ and can he used therapeutic effect on the hypertension, and inhibit the increase of Total Cholesterol contents in serum.
The modified Hellers myotomy for esophageal achalasia is known as the best procedure. A properly performed transthoracic esophagomyotomy is essential to prevent complications. But it has some problems such as persistent achalasia due to inadequate myotomy, recurrence due to the healing of myotomy and reflux esophagitis due to destruction of the lower esophageal sphincter. The methods of the reoperation after esophagomyotomy for achalasia of the esophagus consist of 1 ] for persistent achalasia due to inadequate myotomy, additional myotomy feasible. 2] for esophageal reflux, a long-limb jejunal gastric drainage after vagotomy and hemigastrectomy, jejunal after conservative resection for stricture. We experienced 3 cases of reoperation after esophagomyotomy for achalasia of the esophagus. The 1st and 3rd case belongs to 30 cases which were undertaken the primary operation at the National Medical Center from 1961 to 1984. The 2nd case was undertaken the primary operation at other hospital. The 1st and 3rd case were reoperated because of persistent achalasia due to inadequate myotomy and 2rid case was caused by stricture due to reflux esophagitis. The methods of the reoperation were additional myotomy in 1st case, esophagogastrectomy and lower thoracic esophagogastrostomy in 2nd case, and esophagogastrectomy and mid-thoracic esophagogastrostomy in 3rd case. All three cases were complicated with postoperative reflux esophagitis.
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