Evaluation of esophageal motility in laryngectomized patients

Laryngectomy for treatment of laryngeal-pharyngeal carcinomas may impair the sensation in the larynx and epiglottis, with consequent impairment of esophageal motility. Our aim in the present study was to investigate the esophageal motility of laryngectomized patients. Esophageal manometry was performed on 17 patients submitted to laryngectomy 2 to 71 months (median 29 months) before the examination. Eleven were rehabilitated with esophageal voice and six could not speak. Ten swallows of a 5 ml bolus of water were recorded at the lower esophageal sphincter and at 5, 10 and 15 cm above it. The lower esophageal sphincter pressure was measured by the rapid pull-through method and the upper esophageal sphincter pressure by the station pull-through method. The results were compared with those obtained for a control group of 40 healthy volunteers. The amplitude of contractions was lower and the number of nonperistaltic contractions was higher in laryngectomized patients than in volunteers (P < 0.05). The duration of lower esophageal sphincter relaxation (7.4 +/- 1.5 s) was shorter in laryngectomized patients than in volunteers (8.8 +/- 1.6 s, P < 0.05). The upper esophageal sphincter pressure was lower (34.9 +/- 29.1 mm Hg) in laryngectomized patients than in volunteers (61.2 +/- 20.8 mm Hg, P < 0.05). There was no difference between groups in contraction duration or velocity, in the numbers of multipeaked or failed contractions, lower esophageal sphincter pressure or in the number of swallows followed by complete lower esophageal sphincter relaxation. In conclusion, laryngectomy causes esophageal motility impairment characterized by low contraction amplitude, nonperistaltic contraction and shorter lower esophageal sphincter relaxation duration.     

食管运动功能在重度反流性食管炎中的地位

目的　通过对重度反流性食管炎(RE)治愈前后食管体部运动功能的研究,了解食管体部运动功能在重度RE中的地位。方法　对70例胃食管反流病患者进行食管压力测定。从中筛选23例重度RE(内镜诊断为洛杉矶C和D级食管炎);且24h食管内pH监测证实为病理性酸反流;食管压力测定证实有食管体部运动障碍患者。给予兰索拉唑30mg/d治疗3~6个月至内镜下食管炎完全愈合后,再行食管压力测定,观察下食管括约肌静息压(LESP)及食管体部运动功能的变化。以湿咽成功率、食管远端收缩波幅和食管蠕动的传导速度作为食管体部运动功能的指标。结果　食管炎治愈前后,LESP[ (6 00±0 86 )mmHg比(5 10±0 87)mmHg, 1kPa=7 5mmHg, P=0 476],食管远端收缩波幅[ (34 1±4 1)mmHg比(37 2±4 0)mmHg,P=0 593]、湿咽成功率[ (33 5±6 5)%比(38 6±7 1 )%,P=0 592 ]比较差异均无统计学意义,其均值仍显著低于正常对照组。结论　治愈食管炎并不能提高LESP及改善食管体部的运动功能。食管体部运动功能障碍和酸反流是RE的重要发病机制,尤其是重度RE。     

Clinical and experimental studies on the efficiency of nifedipine on smooth muscle strips of the esophagus (author's transl)

Based on in vivo studies on isolated muscle strips of the LES and on manometric in vivo studies on 8 mongrel dogs, 6 healthy volunteers, 6 patients with achalasia and 3 subjects with diffuse esophageal spasm we could demonstrate that nifedipine causes a long-lasting relaxation of smooth muscle, the esophagus and LES. In 8 dogs resting pressure at the LES was decreased by 20 mg nifedipine from 18.5 +/- 1.8 mm Hg to 8.2 +/- 0.9 mm Hg. This pressure decrease could not be reversed by pentagastrin stimulation (3.0 microgram/kg KG PG). The resting pressure in LES was decreased from 26.8 +/- 3.8 mm Hg to 16.4 +/- 2.1 mm Hg in healthy volunteers and from 45.5 +/- 2.6 mm Hg to 14.5 +/- 0.4 mm Hg in patients with achalasia. In 3 patients with diffuse esophageal spasm nifedipine (20 mg) caused a mean decrease of 38% of the contraction amplitude. Further clinical studies have to be done to clarify if the spasmolysis by nifedipine may be important in the treatment of spastic or hypertonic motility disorders of the LES and the esophagus.     

Diltiazem Therapy for Symptoms Associated with Nutcracker Esophagus

A randomized double-blind, cross-over prospective trial in 22 patients was designed to evaluate possible effect of an oral calcium channel blocker, diltiazem, on symptoms of chest pain and/or dysphagia in patients with nutcracker esophagus. We studied 22 consecutive patients referred to an esophageal diagnostic center for evaluation of noncardiac chest pain or dysphagia having high amplitude esophageal contractions, 14 of whom completed the study. Diltiazem (60-90 mg qid) was compared with placebo, each being administered for 8 wk. Patients were evaluated with esophageal motility pre- and posttreatment periods and with regular symptom assessment throughout each 8-wk treatment. Active diltiazem therapy resulted in significantly lower (p less than 0.05) mean distal esophageal peristaltic pressure (128 +/- 20 mm Hg; +/- SE) than placebo (158 +/- 16 mm Hg). Mean chest pains scores were significantly (p less than 0.05) lower with diltiazem therapy than with placebo. Only nine of the 14 patients fulfilled presently acceptable criteria for diagnosing nutcracker esophagus, and the diltiazem effect was similar, although not significant, because of the smaller sample. Conclusions: In this preliminary study involving 14 patients, the oral calcium channel blocker, diltiazem, appeared to improve noncardiac chest pain associated with strong esophageal contraction, the nutcracker esophagus. These improved symptoms were associated with significant decreases in contraction pressure.     

Manometry and impedance characteristics of achalasia. Facts and myths

BACKGROUND: Achalasia is defined manometrically by an aperistaltic esophagus. Variations in the manometric findings occur in achalasia suggesting that all manometric features should not be required to diagnose achalasia. Combined multichannel intraluminal impedance and esophageal manometry (MII-EM) allows both a functional and a manometric evaluation of esophageal motility and identifies chronic fluid retention. AIM: To compare manometric and MII characteristics in patients with achalasia. METHODS: Retrospective review of 73 MII-EM tracings from patients with achalasia done in our laboratory between October 2001 and December 2004 (38 females; mean age=53.5 y). Patients with previous esophageal interventions were excluded. Manometric and MII characteristics were identified and compared during 10 liquid and 10 viscous swallows. Patients were also divided into 2 groups: vigorous achalasia (VA) and achalasia. RESULTS: Twenty-two of the seventy-one (31%) achalasia patients had a hypertensive lower esophageal sphincter (LES). The mean lower esophageal sphincter pressure (LESP) for the 71 patients with achalasia was 37.9+/-21.2 mm Hg compared with 27.3+/-9.3 mm Hg (P<0.05) in the 73 patients with normal motility. The mean LESP in patients with achalasia was 36+/-20.3 mm Hg compared with 47+/-23.2 mm Hg (P<0.05) in patients with VA. Elevated intraesophageal pressure (IEP) was noted in 45/73 (61.6%). The mean LESP in this group was 41.1+/-22.9 mm Hg compared with 32.5+/-17 mm Hg (P<0.05) with normal IEP. The mean baseline impedance for achalasia was 801+/-732 compared with 1265.2+/-829.5 Omega (P<0.05) for the VA patients. CONCLUSIONS: Most patients with achalasia have elevated IEP, elevated LES residual pressure, normal LES pressure, and low baseline impedance. All manometric features should not be required to diagnose achalasia. Patients with an elevated IEP are likely to have an elevated LES pressure and LES residual pressure. Low MII values identify chronic fluid retention and helps confirm the diagnosis.     

Reproducibility of the Rapid Pull-Through Technique for Categorizing Lower Esophageal Sphincter Pressure

Duplicate measurements of basal lower esophageal sphincter (LES) pressure using a triple-lumen catheter and the rapid pull-through technique (RPT) were performed in 250 consecutive patients to determine their reproducibility for categorizing LES pressures as normal, hypertensive, or hypotensive. For all subjects, mean LES pressure did not differ for the two measurements (25.3 +/- 1.0 vs. 26.2 +/- 1.0 mm Hg, p greater than 0.5), but the correlation coefficient was only modest (r = 0.73). Reproducibility of categorization was 92% (230 of 250 subjects), and was best for subjects with normal (170/179, 95%) or hypotensive (24/26, 92%) values (for hypertensives: 36/45, 80%). Interstudy variability was least for the hypotensive group (1.8 +/- 0.2 mm Hg) and greatest for the hypertensive group (16.4 +/- 1.9 mm Hg). Likewise, the range of individual values from the triple-lumen catheter was least for the hypotensive subjects (4.7 +/- 0.7 mm Hg) and greatest for those with hypertensive LES pressure (32.5 +/- 2.6 mm Hg). These data show that, despite its interstudy variability, the RPT reproducibly categorizes basal LES pressure in greater than 90% of cases. The technique appears least reliable in determining hypertensive LES pressure, where diaphragmatic contraction may most significantly contribute to measurement variability.     

Influence of Esophageal Motility on Esophageal Speech of Laryngectomized Patients

After laryngectomy for treatment of cancer of the larynx, the patient may have vocal rehabilitation by esophageal speech. Some patients fail to achieve the esophageal speech due to reasons involving surgery, radiotherapy, and psychological alterations. Our hypothesis is that the esophageal motility alterations consequent to laryngectomy may be involved in the failure to achieve esophageal speech. Using manometry with continuous perfusion, we studied the esophageal motility of 25 laryngectomized patients, 10 of them able to produce esophageal speech and 15 unable to produce esophageal speech, and 40 asymptomatic normal volunteers. The lower esophageal sphincter (LES) pressure was measured by the rapid pull-through method and the upper esophageal sphincter (UES) pressure by the station pull-through method. The contractions were measured at 5, 10, and 15 cm above the LES after the subjects performed 10 swallows with a 5-mL bolus of water. By comparing volunteers and laryngectomized patients, we found a lower UES pressure, lower amplitude of contractions, and increased percentage of simultaneous contractions in laryngectomized patients (p <0.05). There was no difference between patients able and unable to produce esophageal speech in LES and UES pressure, esophageal contraction duration and velocity, or in the percentage of failed and simultaneous contractions. The esophageal contraction amplitude was lower in patients who acquired esophageal speech than in patients who did not (p <0.05 at 10 cm from LES). We conclude that there are esophageal motility alterations in laryngectomized patients but only the decrease of esophageal contraction amplitude seems to be associated with the acquisition of esophageal speech.     

Alteration of esophageal peristalsis by pentagastrin in patients with diffuse esophageal spasm.

Although it has been shown that gastrin and gastric alkalinization affect the lower esophageal sphincter, in vivo studies have not demonstrated a measurable effect of pentagastrin on esophageal peristalsis. In 9 patients with diffuse esophageal spam and in 10 control subjects esophageal peristalsis was recorded before and after pentagastrin infections. Subcutaneous pentagastrin increased peak amplitude significantly more in patients, 31.2 +/- 8.1 mm Hg (mean +/- S.E.M.), than in controls, 12.1 +/- 5.1 mm Hg (P less than 0.02). Max. duration of contraction waves in patients showed a rise of 11.3 +/- 2.7 sec as compared to controls, 1.9 +/- 0.9 sec (P less than 0.01). The effect of pentagastrin on esophageal peristalsis in patients with diffuse esophageal spasm may be explained as denervation supersensitivity.     

Double-blind investigation of the effects of propranolol and placebo on the pressure of esophageal varices in patients with portal hypertension

This study was aimed at investigating the effects of propranolol on esophageal variceal pressure in patients with portal hypertension. Variceal pressure was measured at endoscopy using a miniature pressure-sensitive gauge in 20 patients with portal hypertension. Measurements were obtained under baseline conditions and 20 min after double-blind administration of propranolol (0.15 mg/kg; n = 10) or an identical amount of placebo (normal saline, 0.3 ml/kg; n = 10). Under baseline conditions, variceal pressure was similar in propranolol and placebo groups (14.1 +/- 5 mm Hg vs. 14.9 +/- 6.6 mm Hg, respectively; not significant). Placebo had no significant effect on variceal pressure (baseline = 14.9 +/- 6.6 mm Hg; placebo = 15.5 +/- 6.6 mm Hg; not significant), and values after placebo administration were closely correlated with baseline values (r = 0.98; y = 1.1 + 0.97 x; p less than 0.0001). In contrast, propranolol caused a significant decrease in the pressure of esophageal varices (from 14.1 +/- 5 mm Hg to 11.3 +/- 4.4 mm Hg; p less than 0.0002). No significant changes in the size of esophageal varices were observed after propranolol or placebo administration. This study shows (a) the endoscopic pressure-gauge technique has a low variability and may be used to assess acute drug-induced changes in variceal pressure; and (b) propranolol causes significant decreases in variceal pressure in patients with portal hypertension and esophageal varices.     

Metoclopramide response in patients with early diffuse systemic sclerosis. Effects on esophageal motility abnormalities

OBJECTIVE: To assess the metoclopramide response in patients with early diffuse systemic sclerosis (dSSc) and the acute effects of intravenous (IV) metoclopramide on the lower esophageal sphincter (LES). METHODS: Twenty-one patients with early dSSc (mean age 41.4 +/- 9.8 yrs., mean disease duration 2.47 +/- 0.75 yrs.) were prospectively evaluated. Six patients with late dSSc (mean age 52.6 +/- 9.1 yrs., mean disease duration 9.5 +/- 2.5 yrs.) were used as control group. All underwent solid-state esophageal manometry at rest and 15 minutes later received 10 mg of metoclopramide in an intravenous single bolus. RESULTS: We found that the mean LES pressures measured by the station pull-through technique significantly increased in both early and late dSSc patients after metoclopramide administration (p < 0.05). While early dSSc patients did improve the mean residual pressures (p < 0.05), late dSSc patients did not (p > 0.05). In the esophageal body (EB), the mean contractions amplitude at 18, 13, 8, and 3 cm above the LES was < 20 mm Hg for both groups. However, peristaltic contraction velocitiy was significantly higher in early dSSc patients (< 0.05) than in that with late dSSc (p > 0.05). Our study did not show any major differences when comparing both groups. No side effects were seen. CONCLUSIONS: The results of our study show that metoclopramide may improve LES pressures in patients with early and late dSS. Metoclopramide improve the mean residual pressure in patients with early dSSc, but not in late dSSc patients. Although esophageal contractions amplitude were significantly improved, they did not achieve a pressure > 20 mm Hg. Because metoclopramide can be used orally, it may mitigate both dysphagia and heartburn.     

健康人食管测压及影响因素多中心研究

目的 建立不同年龄组食管动力参数正常值及测定方法.方法 应用气液压毛细灌注系统测定3个不同年龄组(Ⅰ组18～39岁,Ⅱ组40～59岁,Ⅲ组≥60岁)健康志愿者食管动力参数.同时观察本测定方法对下食管括约肌(LES)检测的重复性和稳定性.结果 实际入组162名,Ⅰ组62名,Ⅱ组73名,Ⅲ组27名.三组间下食管括约肌长度(LESL)、呼气末下食管括约肌压力(LESP)、LESP平均值、残余压、下食管括约肌松弛率(LESRR)差异无统计学意义(P＞0.05).Ⅰ组吸气末LESP为(28.98±1.11) mmHg,明显低于Ⅲ组[(34.35±1.96)mmHg,P＜0.05].Ⅰ组跨膈压为(9.55±0.62) mmHg,明显低于Ⅱ组[(13.05±0.76) mmHg,P＜0.05].三组食管体部远端和近端收缩波幅和时限差异无统计学意义(P＞0.05).Ⅲ组上食管括约肌压力( UESP)明显低于Ⅰ组、Ⅱ组(P＜0.05).重复性比较,Ⅰ组、Ⅱ组第2次呼气末LESP明显高于第1次(P＜0.05).远端食管蠕动收缩波幅女性明显高于男性(P＜0.05),近端食管蠕动收缩波幅女性与男性无明显差别(P＞0.05).结论 得到不同年龄组食管动力参数的正常值.LES的动力参数不随年龄的增长而变化.而食管体部蠕动收缩能力在40～59岁年龄组最强.老年人UESP明显下降.检测前让受试者有足够的适应时间,有利于得到准确、可靠的LES的动力参数.     

Abnormal Esophageal Pressures in Reflux Esophagitis: Cause or Effect?

Thirteen patients with gastroesophageal reflux disease underwent esophageal manometric evaluation during acute exacerbations and disease remission to evaluate lower esophageal sphincter and peristaltic pressure in response to treatment. No change was noted in lower esophageal sphincter pressure (15.2 +/- 2.6 mg versus 14.3 +/- 1.8 mm Hg) or peristaltic pressure (64.1 +/- 6.9 versus 62.1 +/- 7/8 mm Hg) with remission while both lower esophageal sphincter pressure and distal amplitude were lower in reflux patients than controls (p less than 0.05). Short-term treatment resulting in endoscopic and symptom improvement of gastroesophageal reflux disease does not appear to improve lower esophageal sphincter and peristaltic pressure.     

Augmentation of lower esophageal sphincter pressure and gastric yield pressure after radiofrequency energy delivery to the gastroesophageal junction: a porcine model

BACKGROUND: An endoscopic technique that eliminates gastroesophageal reflux disease would be of benefit to patients. The endoscopic delivery of radiofrequency energy to the porcine gastroesophageal junction was investigated and its effect on lower esophageal sphincter pressure, gastric yield pressure, and histology was assessed. METHODS: Twenty pigs underwent esophageal manometry and endoscopic injection of botulinum toxin (100 units) into the lower esophageal sphincter. After 1 week, animals were randomized to radiofrequency energy treatment of the gastroesophageal junction with a 4- needle catheter and thermocouple-controlled generator (n = 13) or no further intervention (control, n = 7). At 9 weeks, animals underwent esophagoscopy, manometry, gastric yield pressure determination, and sacrifice for histopathologic evaluation. RESULTS: Mean lower esophageal sphincter pressure declined by 3.7 +/- 2.6 mm Hg (control, p = 0.03) vs. 0.97 +/- 5.8 mm Hg (radiofrequency, p = 0.29) after 9 weeks. Mean gastric yield pressure was 24.9 +/- 8.2 mm Hg (control), compared with 43.4 +/- 10. 7 mm Hg (radiofrequency) (p = 0.0007). Histopathologic assessment demonstrated normal mucosa, mild fibrosis, and no inflammation. CONCLUSIONS: Radiofrequency energy delivery reversed much of the lower esophageal sphincter pressure reduction achieved with botulinum toxin injection and augmented gastric yield pressure by 75% compared with controls. Given the safety of radiofrequency energy delivery in this study and in other areas of medicine, human studies to assess the effect of radiofrequency energy on gastroesophageal reflux disease are warranted.     

Pulmonary artery pressure and left ventricular late diastolic pressure in rest and during dynamic load. Comparative studies on pressure transmission in the pulmonary circulation during simultaneous determination]

Left ventricular enddiastolic pressure (LVEDP), mean pulmonary artery pressure (PAPM) and enddiastolic pulmonary artery pressure (PADP) were simultaneously recorded in 19 subjects with normal left ventricular (LV) function, and in 109 patients with LV-dysfunction, 83 of whom were also studied during exercise. Patients with valvular heart disease or atrial fibrillation were excluded from this study. LVEDP and mean pulmonary capillary wedge (PCW) pressure were simultaneously recorded in 81 patients at rest, andin 16 patients also during exercise; the LV diastolic pressure prior to atrial contraction (LVPpreA) could accurately be identified in 45 patients at rest and in 23 patients with exercise. In contrast to the widely accepted opinion of others, the PADP (mean 8.2 +/- 2.2 mm Hg at rest and 12.3 +/- 3.4 mm Hg with exercise) showed a close approximation of LVEDP (10.0 +/- mm Hg at rest and 16.2 +/- 3.5 mm Hg with exercise) only in normal subjects at rest (p less than 0.05 and p less than 0.01 respectively). In patients with LV dysfunction there was no significant difference between PADP (11.7 +/- 4.5 mm Hg and 23.0 +/- 8.9 mm Hg), PCW (11.6 +/- 5.1 mm Hg and 24.1 +/- 11.9 mm Hg) and LVPpreA (12.5 +/- 5.5 and 21.5 +/- 7.7 mm Hg) at rest and during exercise. LVEDP could be estimated with sufficient accuracy only from the PAPM (18.9 +/- 6.5 and 35.7 +/- 10.8 mm Hg). The increase in LVEDP (14.7 +/- 7.7 mm Hg) with exercise was not significantly different from the increase in PAPM (16.8 +/- 7.1 mm Hg). There were highly significant correlations (p less than 0.001) between LVEDP and PADP (r = 0.85) as well as PAPM (r = 0.86) at rest and during exercise with the regressionline being closest to the line of identity for LVEDP and PAPM. The pressure gradient between LVEDP and PADP (LVEDP - PADP = 6.3 mm Hg with exercise) equaled the pressure increase in LV by atrial contraction (LVEDP - LVPpreA = 6.3 and 13.3 mm Hg). The pressure difference between PADP or PAPM and LVEDP remained constant despite marked variation of other hemodynamic parameters, e.g. stroke volume index (SVI), heart rate (HR) and cardiac index(CI). These data suggest that an elevated LVEDP is caused mainly by an augmented atrial contraction in patients with LV dysfunction at rest and with exercise. This mechanism precludes an enddiastolic pressure equilibrium between pulmonary artery and left ventricel. PAPM allows the best estimation of LVEDP independent from other hemodynamic variables.     

Laryngo-upper esophageal sphincter contractile reflex in humans deteriorates with age

BACKGROUND & AIMS: Recent studies have shown the existence of several reflex connections between the aerodigestive and upper gastrointestinal tracts. Our aim was to study the effect of laryngeal stimulation on upper esophageal sphincter (UES) pressure and to determine the reproducibility of this effect. METHODS: We studied 14 young and 10 elderly healthy nonsmoker volunteers and 7 patients with UES dysphagia using a concurrent manometric and video endoscopic technique. Three levels of laryngeal air stimulation were studied: 6 mm Hg/50 ms, 10 mm Hg/50 ms, and 6 mm Hg/2 s. Ten young subjects were studied twice. RESULTS: For 6-mm Hg/2-s and 6-mm Hg/50-ms duration stimuli, the frequency of UES response to air stimulation as evidenced by mucosal deflection (response/deflection ratio) in the elderly volunteers was significantly lower compared with that of young subjects (P < 0.05). The response/deflection ratio of the 6-mm Hg/2-s stimulus was significantly higher than those induced by stimuli of shorter duration (P < 0.01). Poststimulation UES pressure was significantly higher than prestimulation pressure (P < 0.05) in both groups. The magnitude of the increase in poststimulation UES pressure in the elderly volunteers was similar to that of the young subjects. Findings were similar in repeated studies. Four of 7 dysphagic patients exhibited an abnormal response. CONCLUSIONS: Afferent signals originating from the larynx reproducibly induce contraction of the UES: the laryngo-UES contractile reflex. This reflex is elicited most reliably by 6-mm Hg/2-s air stimulation. Frequency elicitation of this reflex decreases significantly with age while the magnitude of change in UES pressure remains unchanged, indicating a deleterious effect of aging on the afferent arm of this reflex. This reflex is altered in some dysphagic patients.     

Left ventricular function assessment using a floating catheter in dynamic and isometric (handgrip) stress in normal and heart infarct patients

Left ventricular function was examined in a control group of 8 healthy men (average age 26 +/- 6.2 years) and was compared to 40 post-MI patients (average age 50 +/- 8.2 years, 39 men, one woman). It was measured using the floating-catheter technique under isometric exercise (50% of maximal voluntary contraction using both hands) and also under dynamic exercise (progressive supine bicycle-ergometry). In the control group, there was a significant increase in heart rate, arterial blood-pressure and the average PCP from rest to isometric exercises. PCP was noted to stay within its normal range (less than 20 mm Hg) under both modes of exercise. There was no significant difference comparing the effects of dynamic and isometric exercise (isometric: PCP 13.3 +/- 3.3 mm Hg; dynamic: PCP 11.8 +/- 3.6 mm Hg). In Group I (20 post-MI-patients showing ischemia during exercise-ECG) PCP stayed normal under isometric exercise (PCP 18.8 +/- 10.2 mm Hg). Under dynamic exercise, their PCP increased up to a pathological level (PCP 24.9 +/- 10.1 mm Hg, p less than 0.01). In Group II (20 post-MI-patients with lacking proof of ischemia during exercise-ECG) there was no significant difference between the increase in PCP under isometric vs dynamic exercise (isometric: PCP 18.7 +/- 13.4 mm Hg; dynamic: PCP 18.5 +/- 10.0 mm Hg). Conclusion: The results lead to the conclusion that isometric exercise alone (50% of maximal voluntary contraction using both hands, handgrip) can replace dynamic exercise in the diagnosis of LV malfunction in post-MI patients who do not show ischemia during exercise-ECG.     

Esophageal motility differences among aged patients with achalasia: a Taiwan report

BACKGROUND AND AIM: There are limited reports on esophageal motility pressures in aged patients with achalasia and these are inconclusive. The aim of the present retrospective study was to understand the changes of esophageal motility in aged achalasia patients among the Taiwan population. METHODS: Manometric studies of 49 patients with achalasia had been performed through January 1998 to June 2005. The findings of lower esophageal sphincter (LES) basal and residual pressures and esophageal body contraction amplitudes were calculated and compared between the older and younger patient groups at different age cut-offs. RESULTS: Higher basal LES pressure increased significantly from the cut-off age of 65 years (i.e. patients over 65 had significantly higher basal LES pressure than younger patients: 37.0 +/- 4.19 mmHg vs 30.0 +/- 1.32 mmHg, P = 0.045). With patients > or =70 years old, it was more obvious (46.0 +/- 3.7 mmHg vs 29.6 +/- 1.2 mmHg, P = 0.001). Beginning at the cut-off age of 55, the LES residual pressure was significantly higher in older patients than those who were younger (14.0 +/- 11.06 mmHg vs 11.1 +/- 0.6 mmHg, P = 0.017). LES residual pressure is more significant in the older groups. A linear correlation between age and residual LES pressures (r = 0.383) was found. No differences were found in esophageal contraction pressure. CONCLUSIONS: Older achalasia patients in Taiwan have higher basal LES pressures, with a linear correlation between age and residual LES pressures. Age has no influence on esophageal contraction pressure.     

Effect of spinal microinjections of an antagonist to substance P or somatostatin on the exercise pressor reflex.

The purpose of this study was to determine the heart rate and arterial blood pressure changes to isometric skeletal muscle contraction and muscle stretch before and after microinjecting an antagonist to substance P (SP) or somatostatin (SOM) into the L-7 dorsal horn region of the spinal cord of anesthetized cats. Anesthesia was induced by administering an anesthetic gas mixture and was subsequently maintained with alpha-chloralose. Triceps surae contraction was induced by electrically stimulating the L-7 ventral root. Three muscle manipulations (all 1 minute in duration) were performed: 1) continuous tetanic contraction, 2) intermittent tetanic contractions (1 second of contraction, 1 second of relaxation), and 3) passive muscle stretch. Saline microinjections had no effect on the cardiovascular responses to these muscle manipulations. However, both peptide antagonists blunted the pressor response to a continuous tetanic contraction as mean arterial pressure increased 47 +/- 4 and 44 +/- 4 mm Hg before and 28 +/- 3 and 28 +/- 4 mm Hg after microinjecting the SP or SOM antagonist, respectively. In contrast, neither antagonist influenced the increase in mean arterial pressure produced by passive stretch; values were 43 +/- 6 versus 41 +/- 6 mm Hg (SP antagonist) and 39 +/- 7 versus 42 +/- 7 mm Hg (SOM antagonist) before and after injections, respectively. Microinjecting the SOM antagonist attenuated the pressor response to intermittent tetanic contractions (44 +/- 4 mm Hg before SOM antagonist versus 26 +/- 4 mm Hg after SOM antagonist), whereas the SP antagonist had no effect (35 +/- 3 mm Hg before SP antagonist versus 32 +/- 4 mm Hg after SP antagonist).(ABSTRACT TRUNCATED AT 250 WORDS)     

Total volume paracentesis decreases variceal pressure,size, and variceal wall tension in cirrhotic patients

It has been suggested that ascites is a risk factor for variceal bleeding in cirrhotic patients. However, no data of total volume paracentesis (TVP) effects on variceal hemodynamics has yet been published. The aim of this study was to investigate the effects of TVP on variceal pressure, size, and tension in cirrhotic patients. Before sclerotherapy, 18 cirrhotic patients with grade II esophageal varices were studied. The following measurements were performed on 12 patients at basal condition and after TVP: inferior vena cava pressure, esophageal pressure (EP), and intravariceal pressure (IVP) by direct punction and variceal size at endoscopy. The same measurements were performed at basal condition and 1 hour later without TVP on the other 6 patients used as a control group. Variceal pressure gradient (VPG) and variceal wall tension (WT) were calculated. Paracentesis and intra- abdominal pressure were obtained with a direct punction. No demographic differences were observed between both groups. Paracentesis produced a significant reduction of IVP (from 25.6 +/- 2.4 to 17.9 +/- 2.1 mm Hg, means +/- SEM, -30%, P < .05), VPG (from 16.6 +/- 2.4 to 10.8 +/- 1.4 mm Hg, -35%, P < .05). TVP also reduced variceal size (from 9 +/- 0.3 to 5.6 + 0.4 mm, -38%, P < .05) and WT (from 75.3 +/- 11.6 to 30 +/- 4.7 mm Hg. mm, -60%, P < .05). Intra-abdominal pressure decreased from 18 +/- 2.2 to 4 +/- 0.9 mm Hg (P < .05), and IVC decreased from 15.5 +/- 2.4 to 5.7 +/- 1.5 mm Hg (P < .05). No significant differences were observed in mean arterial pressure and heart rate. The mean ascitic fluid removed was 8 +/- 0.71 L. No significant difference between measurements was observed in the control group. Our results show that TVP significantly decreases variceal pressure and tension. These results suggest that ascites removal can be useful in the treatment of variceal bleeding in cirrhotic patients.(Hepatology 1997 Jan;25(1):59-62)