• 제목/요약/키워드: esophageal sphincter

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Reflux Following Esophagectomy for Esophageal Cancer

  • Cho, Jong Ho
    • Journal of Chest Surgery
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    • 제53권4호
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    • pp.217-221
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    • 2020
  • Gastroesophageal reflux is a common problem after gastroesophageal resection and reconstruction, despite the routine prescription of proton pump inhibitors (PPIs). Resection of the lower esophageal sphincter and excision of the vagus nerve are generally thought to be the main factors that interfere with gastric motor function. However, physiological studies of reflux symptoms after esophagectomy are still lacking. Gastroesophageal reflux occurs frequently after esophagectomy, but there is no known effective method to prevent it. Therefore, in order to manage gastroesophageal reflux after esophagectomy, strict lifestyle modifications and gastric acid suppression treatment such as PPIs are needed, and further clinical studies are required.

유동식 및 고형식을 이용한 동위원소 식도통과검사의 임상적 의의에 대한 연구 (Clinical Evaluation of Radionuclide Esophageal Transit Studies using Liquid and Solid Foods)

  • 최재걸;이민재;서원혁;송치욱;현진해
    • 대한핵의학회지
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    • 제29권1호
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    • pp.61-72
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    • 1995
  • The author performed radionuclide esophageal transit studies(RETS) with liquid and solid boluses using the same day protocol in 90 normal controls and 164 patients with various primary esophageal motility disorders who were diagnosed by manometric criteria and clinical courses. The authors calculated mean esophageal transit time(MTT) and mean residual retention(MRR) in each of the liquid and solid studies, and classified time-activity curve(TAC) patterns. The normal criteria of RETS with liquid bolus were MTT<24 sec, MRR<9%, and the TAC pattern that showed rapid declining slope and flat low residual(Type 1). The normal criteria of RETS with solid bolus were MTT<35 sec, MRR<9% and TAC of type 1. With these normal criteria, the sensitivity and the specificity of the liquid study were 62.2 % and 97.8%, respectively. The sensitivity increased to 75.4% with the solid study. The author also found that the RETS was highly reproducible. The achalasia typically showed no effective emptying of both liquid and solid boluses during the whole study period, and was well differentiated by its extremely long transit time and high retention from the other motility disorders. The diffuse esophageal spasm (DES) and nonspecific esophageal motility disorder(NEMD) showed intermediate delay in transit time and increased retention. In the groups of hypertensive lower esophageal sphincter(LES), hypotensive LES and nutcracker, there noted no significant difference with the normal control group in terms of MTT and MRR. The DES and NEMD could be more easily identified by solid studies that showed more marked delay in MTT and increased MRR as compared with the liquid study. In conclusion, esophageal scintigraphy is a safe, noninvasive and physiologic method for the evaluation of esophageal emptying.

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인후두 역류질환으로 오인된 식도 이완불능증 1예 (A Case of Esophageal Achalasia Misconceived as Laryngopharyngeal Reflux Disease)

  • 노승호;이용우;박진수;이상혁
    • 대한후두음성언어의학회지
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    • 제28권1호
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    • pp.43-47
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    • 2017
  • Laryngopharyngeal reflux disease (LPRD) is common in laryngologic practice. In Korea, up to 1 out of every 5 patients who visit otorhinolaryngology clinic is supposed to have LPRD with symptoms and physical findings. Major symptoms of LPRD include hoarseness, cough, reflux symptom and mild dysphagia. Even though LPRD is common, its diagnosis may be difficult, because its symptoms are nonspecific and the laryngeal findings are not always associated with symptom severity. In Recent study, 66.4% of Patient who has LPRD also associated with esophageal motility disorders. Esophageal achalasia is a disease of unknown etiology characterized by an absence of peristalsis in the body of esophagus and nonrelaxing hypertension of the lower esophageal sphincter. Common cause is loss of ganglion cells in Auerbachs plexus. The classic triad of symptoms in achalasia includes dysphagia, regurgitation and weight loss. LPRD and esophageal achalasia have similar symptoms but have different treatment of choice. The Differentiation diagnosis of theses disease is important and should be established by history, radiologic examination and endoscopic examination. We recently assessed a 59-year-old female patient who complained of an epigastric pain, dysphagia and chronic cough. LPRD was initially diagnosed on Laryngoscopic examination and Reflux Symptom Index, but patient was not relieved of any symptoms after treatment of Proton Pump Inhibitor for 3 months. After high resolution manometry, esophageal achalasia was finally diagnosed. We report this case regarding the diagnosis and treatment with review of literatures because we have to think about esophageal motility disorders as a differential diagnosis in laryngology.

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개 하부식도괄약근의 비아드레날린성, 비콜린성 이완반응에 있어서 Cyclic Nucleotide의 역할 (Regulatory Role of Cyclic Nucleotides in Non-Adrenergic Non-Cholinergic Relaxation of Lower Esophageal Sphincter from Dogs)

  • 김영태;임병용
    • The Korean Journal of Physiology and Pharmacology
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    • 제1권3호
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    • pp.303-313
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    • 1997
  • The role of the lower esophageal sphincter(LES) is characterized by the ability to maintain tone and to relax allowing the passage of a bolus. It is known that LES relaxation during swallowing may be induced by the cessation of the tonic neural excitation and the activation of non-adrenergic, non-cholinergic(NANC) inhibitory neurons. Furthermore, it is generally accepted that the relaxation of the smooth muscle is mediated primarily by the elaboration of adenosine 3',5'-cyclic monophosphate(cyclic AMP) and guanosine 3',5'-cyclic mono-phosphate(cyclic GMP) via activation of adenylate cyclase and guanylate cyclase, respectively. It is thus possible that cyclic nucleotides might be a second messenger involved in neural stimulation-induced relaxation of LES, although a relationship between relaxation and changes in cyclic nucleotides after neural stimulation has not been established. The present study was performed to define the participation of cyclic nucleotides in the relaxation of LES of dog in response to neural stimulation. Electrical field stimulation(EFS) caused relaxation of the canine isolated LES strips in a frequency-dependent manner, which was eliminated by pretreatment with tetrodotoxin$(1{\mu}M)$, but not by atropine$(100{\mu}M)$, guanethidine$(100{\mu}M)$ and indomethacin$(10{\mu}M)$. The nitric oxide synthase inhibitors, $N^G-nitro-L-arginine$, $N^G-nitro-L-arginine$ methyl ester and $N^G-monomethyl-L-arginine$ inhibited EFS-induced relaxation. Additions of sodium nitroprusside, a nitrovasodilator and forskolin, a direct adenylate cyclase stimulant, caused a dose-dependent relaxation of LES smooth muscle. Effects of sodium nitroprusside and forskolin were selectively blocked by the corresponding inhibitors, methylene blue for guanylate cyclase and N-ethylmaleimide(NEM) for adenylate cyclase, respectively. Dibutyryl cyclic AMP and dibutyryl cyclic GMP caused a concentration-dependent relaxation of the LES smooth muscle tone, which was not blocked by NEM or methylene blue, respectively. However, both NEM and methylene blue caused significant antagonism of the relaxation in LES tone in response to EFS. EFS increased the tissue cyclic GMP content by 124%, whereas it did not affect the tissue level of cyclic AMP. Based on these results, it is suggested that one of the components of canine LES smooth muscle relaxation in response to neural stimulation is mediated by an increase of cyclic GMP via the activation of guanylate cyclase. Additionally, an activation of cyclic AMP generation system was, in part, involved in the EFS-induced relaxation.

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Interaction of Calmodulin- and PKC-Dependent Contractile Pathways In Cat Lower Esophageal Sphincter (LES)

  • Kang, Hee-Yun;Lee, Tai-Sang;Lee, Yul-Pyo;Lee, Doo-Won;La, Hyun-O;Song, Hyun-Ju;Sohn, Uy-Dong
    • Archives of Pharmacal Research
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    • 제24권6호
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    • pp.546-551
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    • 2001
  • We have previously shown that, in circular muscle cells of the lower esophageal sphincter (LES) isolated by enzymatic digestion, contraction in response to maximally effective doses of acetylcholine (ACh) or Inositol Triphosphate ($IP_3$) depends on the release of $Ca^{2+}$ from intracellular stores and activation of a $Ca6{2+}$-calmodulin (CaM)-dependent pathway. On the contrary, maintenance of LES tone, and response to low doses of ACh or $IP_3$ depend on a protein kinase C (PKC) mediated pathway. In the present investigation, we have examined requirements for $Ca6{2+}$ regulation of the interaction between CaM- and PKC-dependent pathways in LES contraction. Thapsigargin (TG) treatment for 30 min dose dependently reduced ACh-induced contraction of permeable LES cells in free $Ca6{2+}$ medium. ACh-induced contraction following the low level of reduction of $Ca6{2+}$ stores by a low dose of TG ($10^{-9}{\;}M$) was blocked by the CaM antagonist, CCS9343B but not by the PKC antagonists chelerythrine or H7, indicating that the contraction is CaM-dependent. After maximal reduction in intracellular $Ca{2+}$ from $Ca6{2+}$stores by TG ($10^{-6}{\;}M$), ACh-induced contraction was blocked by chelerythrine or H7, but not by CCS9343B, indicating that it is PKC-dependent. In normal $Ca^{2+}$medium, the contraction by ACh after TG ($10^{-9}{\;}M$) treatment was also CaM-dependent, whereas the contraction by ACh after TG ($10^{-9}{\;}M$) treatment was PKC-dependent. We examined whether PKC activation was inhibited by activated CaM. CCS 7343B Inhibited the CaM-induced contraction, but did not inhibit the DAC-induced contraction. CaM inhibited the DAC-induced contraction in the presence of CCS 9343B. This inhibition by CaM was $Ca{2+}$dependent. These data are consistent with the view that the switch from a PKC-dependent pathway to a CaM dependent pathway can occur and can be regulated by cytosolic $Ca{2+}$ in the LES.

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인두신경증 환자에서 Esophageal manometry와 24hour double prove pH metry 검사 및 위식도 역류와의 관계 (The Relationship Between Esophageal Manometry and 24 Hour Double Prove pH-metry with Gastroesophageal Reflax in Pharyrngeal Neurosis Patients.)

  • 김선태
    • 대한기관식도과학회지
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    • 제2권1호
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    • pp.88-96
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    • 1996
  • In recently the gastroesophageal reflux disease(GERD) has been known to induce the otolaryngologic manifestations. Pharyngeal neurosis is a disease which we could have not found the cause frequently. So we have studied the relation between the pharyngeal neurosis and the GERD among 50 patients who were diagnosed as pharyngeal neurosis after esophagogram and laryngoscopic examination. We performed esophageal manometry and 24hour double-probe pH-metry and then compared with normal control group(n=30). The results are as follows 1 Among 50 patients, 12(24%) patients were diagnosed as GERD by DeMeester scoring. 2. In esophageal manometry, the upper and lower esophageal sphincter between the patients and the control group have no significant difference(p>0.05) and 9 among 50 pateints showed abnormal peristaltic movement in esophageal body contraction. 3. In 24hour double-probe pH-metry, the esophageal probe showed that in GERD group(n= 12) the number of reflux episode, episodes greater than 5 minutes and the percentage of time

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위식도역류질환과 인후두역류질환의 대한 최신지견 (Update of Pathophysiology in GERO/LPR)

  • 우정수
    • 대한기관식도과학회지
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    • 제16권2호
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    • pp.83-90
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    • 2010
  • The pathophysiology of Gastroesophageal reflux disease (GERD) has been known that it is developed when the offense-primarily the gastric acid-pepsin content of the refluxate-overcomes a 3-tiered esophageal protective defense. consisting of antireflux mechanisms, luminal clearance mechanisms, and tissue resistance. Laryngopharyngeal reflux (LPR), which is known as an extraesophageal variant of GERD, has been considered to be developed by transient lower esophageal sphincter relaxation (TLESR), direct mucosal injury by gastric contents, more sensitive mucosa compared to esophagus, and absence of buffering effect and aggravation of the injury due to pepsin. However, hypothesis of the pathophysiology in both entities are numerous and still lack of understanding for being a theory. There is no conflict that understanding the pathophysiology is necessary for resolving the problems of these diseases and numerous studies and results have been releasing. This review could provide clinicians dealing with GERD and LPR with applicable new information and help for overcoming the clinical obstruction.

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천연자(川練子)가 만성 역류성 식도염 흰쥐에 미치는 효과 (Effect of Toosendan Fructus on Chronic Acid Reflux Esophagitis Rats)

  • 이진아;신미래;최정원;노성수
    • 대한본초학회지
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    • 제36권3호
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    • pp.1-8
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    • 2021
  • Objective : Reflux esophagitis (RE), one of gastroesophageal reflux disease (GERD), is a disease that causes inflammation due to reflux of stomach contents such as stomach acid and pepsin due to the unstable gastroesophageal sphincter, and is currently increasing worldwide. The currently used treatment for reflux esophagitis has various side effects. Therefore, in this study the effect of Toosendan Fructus extract on chronic acid reflux esophagitis in rats was evaluated in order to find a new treatment material for reflux treatment. Methods : After inducing reflux esophagitis through surgery, the group was separated and the drug was administered for 2 weeks; Normal rats (Normal, n=8), chronic acid reflux esophagitis rats (Control, n=8), Toosendan Fructus 200 mg/kg body weight/day-treated chronic acid reflux esophagitis rats (TF, n=8). After, we were taken esophageal tissue and esophageal mucosa damage was identified, and analyzed the expression of NADPH oxidase, AP-1/MAPK-related proteins, and tight junction proteins by western blot in esophageal tissue. Results : Toosendan Fructus administration significantly protected the esophageal mucosal damage of reflux esophagitis. Also, Toosendan Fructus significantly reduced the expression of NADPH oxidases (NOX2 and p22phox) and AP-1/MAPK-related proteins (c-Fos, c-Jun, p-p38, p-ERK, and p-JNK). In addition, it significantly increased the expression of tight junction proteins (Occludin, Claudin-3, and Claudin-4). Conclusions : These results suggest that Toosendan Fructus reduced damage to the esophageal mucosa by protecting the esophageal mucosa by upregulating tight junctions proteins as well as inhibiting the AP-1/MAPK pathway through reducing NADPH oxidases expression.