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PubMed1995

Iatrogenic achalasia. A case series.

Between 1984 and 1992, 14 cases of "secondary" achalasia were diagnosed at our institution, five due to malignancy and nine as a result of esophageal or paraesophageal surgery. Preoperative manometry had excluded preexistent achalasia in eight of nine of the latter patients. Dysphagia developed immediately postoperatively in all. Esophagram and subsequent manometry were consistent with achalasia. All failed conventional dilation sessions and eight of nine underwent pneumatic dilation: Five were cured by this alone, two required surgery (one for iatrogenic perforation), and one was lost to follow-up. This achalasia-like picture appears to be the result of a tight antireflux repair that impairs the ability of the lower esophageal sphincter to completely relax, creating a functional obstruction with proximal dilation and stasis. Such secondary achalasia appears to be a distinct clinical entity and was more common than that associated with neoplasia in our institution. Therapeutically, pneumatic dilation was required and probably causes partial disruption of a tight surgical repair.

Adenocarcinoma↗
PubMed2005

D2 gastrectomy -- a safe operation in experienced hands.

In the contemporary practice, surgery is the only potentially curative treatment available for gastric cancer. However, there is no consensus on the extent of surgical resection. Advantages of D2 gastrectomy in terms of morbidity, mortality, local recurrence and survival are confirmed in Japanese as well as some European trials. In our hospital, all patients with operable gastric cancer are treated with D2 gastrectomy along with splenectomy and distal pancreatectomy followed by jejunal pouch reconstruction. The study was undertaken to evaluate our practice in terms of postoperative morbidity and mortality. All the patients who had total gastrectomy for gastric carcinoma from January 1995 to December 2000 were included in the study. During this 6-year period, 33 patients underwent potentially curative D2 gastrectomy. Postoperative morbidity and mortality were 18 and 9%, respectively. There were no anastomotic leaks. Three (9%) patients developed dysphasia, of which two (6%) had anastomotic stricture requiring dilatation. We feel D2 gastrectomy with splenectomy and distal pancreatectomy when performed electively is a safe procedure in experienced hands. Oesophago-jejunal anastomosis can be safely performed using circular stapler.

Aged↗
PubMed1991

[Protective effect of rebamipide (OPC-12759) on the gastric mucosa in rats and humans].

The protective effect of rebamipide against 0.15 N HCl solution containing 40% ethanol (HCl-ethanol)-induced mucosal lesion in the stomach was evaluated in rats and humans. In rat experiments: (1) rebamipide prevented development of mucosal damage induced by HCl-ethanol in a dose-dependent manner when tested at 10, 30, 100 and 300 mg/kg, i.p., and the prevention at 30-300 mg/kg was significant (P less than 0.05); (2) rebamipide significantly (P less than 0.05) increased mucosal blood flow by continuous i.v. dosing at 10 mg/kg/hr by the hydrogen gas clearance method; (3) rebamipide at 10 mg/kg, i.v., also significantly (P less than 0.05) inhibited reduction in gastric mucosal blood volume and tended to suppress oxygen saturation of hemoglobin following hemorrhagic shock by organ reflectance spectrophotometry. A double-blind crossover study was conducted to compare the gastric protective effect of rebamipide with an inactive placebo using 6 healthy male volunteers. Rebamipide was administered to them at a clinical dose of 300 mg/day orally for 7 days, and then HCl-ethanol was given once to induce mucosal damage. Rebamipide significantly (P less than 0.05) inhibited formation of mucosal lesion, decrease in the number of mucous granules and dilatation of intercellular space. These clinical findings indicate that rebamipide was protective against HCl-ethanol-induced gastric lesion at a clinical dose, and the mechanism of this gastric effect was considered to involve, in part, the improvement of mucosal microcirculation.

Adult↗
PubMed1997

Ultrastructural identification of the c-kit-expressing interstitial cells in the rat stomach: a comparison of control and Ws/Ws mutant rats.

Interstitial cells in the circular muscle layer of the stomach of the Ws/Ws mutant rat, which lacks c-kit-expressing cells, and its siblings have been studied by electron microscopy. In the sibling control rats, two types of interstitial cells are found lying in close association with nerve bundles. Cells of the first type are characterized by electron-dense cytoplasm containing abundant mitochondria, granular endoplasmic reticulum, and Golgi apparatus. Intermediate filaments are richly distributed throughout the perinuclear region and the cell processes. Caveolae, subsurface cisterns, and indistinct basal lamina are observed along the cell membrane. The most conspicuous feature of this cell type is the existence of many large gap junctions that interconnect with the same type of cell, smooth muscle cells, or cells of the second type. Cells of the second type show an ultrastructure similar to fibroblasts, viz., a well-developed Golgi apparatus and granular endoplasmic reticulum whose cisterns often show a dilated form and contain flocculent material. Unlike typical fibroblasts, however, cells of this type also form many gap junctions with cells of the first type and smooth muscle cells. Both types of cells are observed in close apposition to nerve varicosities. Since cells of the first type are absent in the Ws/Ws mutant rat, we concluded that they correspond to c-kit-expressing cells and to interstitial cells of Cajal.

Animals↗
PubMed1998

Redefinition of dystrophin isoform distribution in mouse tissue by RT-PCR implies role in nonmuscle manifestations of duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is caused by a defect in a 427-kDa membrane-associated protein: dystrophin. The DMD gene also encodes several shorter isoforms which are believed to participate in nonmuscle manifestations of DMD, including abnormal retinal electrophysiology, dilated cardiomyopathy, mental retardation, and hearing defects. The purpose of this work was to determine the normal tissue expression of full-length dystrophin (Dp427) and the dystrophin isoforms Dp260, Dp140, Dp116, and Dp71, to aid in understanding what roles these isoforms might play in DMD nonmuscle manifestations. RT-PCR was performed on mRNA isolated from wild-type C57BL/6J mouse tissues, including brain, cardiac muscle, eye, intestine, kidney, liver, lung, skeletal muscle, spleen, stomach, testis, thymus, and uterus. RT-PCR amplification demonstrated that the isoforms were in a number of tissues which had not been revealed by previous Western and Northern blot analyses. Dp427 was expressed at equal levels in all tissues. Dp260 and Dp140 were present in all tissues tested, but the levels of expression varied. Dp116 was expressed in a subset of tissues and levels of expression varied. Dp71 was constitutively expressed in all tissues, suggesting that this isoform plays a basic role in normal tissue function. The expanded tissue distribution supports the hypothesis that dystrophin isoforms serve essential and unique functions, necessitating further investigation into their potential roles in DMD nonmuscle manifestations.

Actins↗
PubMed2000

EUS in cirrhotic patients with and without prior variceal hemorrhage in comparison with noncirrhotic control subjects.

BACKGROUND: Endoscopic ultrasound (EUS) was used to evaluate cirrhotic patients with and without prior variceal hemorrhage. The findings were compared with those of EUS in noncirrhotic control subjects to determine EUS features indicative of cirrhosis and of a risk for variceal hemorrhage. METHODS: Patients with cirrhosis undergoing indicated endoscopic screening for varices or surveillance after endoscopic therapy for variceal hemorrhage were studied and compared with healthy noncirrhotic control patients undergoing EUS for benign conditions. RESULTS: Sixty-six cirrhotic patients (31 with prior hemorrhage) and 32 control patients were studied. Nonhemorrhage cirrhotic patients had more severe liver disease by Child's class (p = 0.02) and less beta-adrenergic blocker usage (p < 0.0001). Paraesophageal varices were detected in 97% of cirrhotic patients and 3% of control patients (p < 0.001) and were a more sensitive predictor of cirrhosis than varices at endoscopy (74%, p < 0.0001). Azygos vein and thoracic duct diameters, and gastric mucosa and submucosa thickness were greater for cirrhotic than control patients (p < 0.001). More hemorrhage patients had large (5 mm or greater) paraesophageal varices (odds ratio 3.1: 95% CI [1.1, 8.3]; p < 0.05) and paragastric varices (odds ratio 3.7: 95% CI [1.3, 10.2]; p = 0.01). Paraesophageal varix size correlated with ascites (p = 0.03) and, for nonhemorrhage patients, with Child's class (p < 0.01). CONCLUSIONS: Paraesophageal and paragastric varices correlate with the presence and severity of liver disease and portal hypertension. These data support the hypothesis that large paraesophageal and paragastric varices (5 mm or greater) may be risk factors for variceal hemorrhage, an observation that merits further prospective study. Cirrhosis causes dilation of the azygos vein and thoracic duct and thickening of gastric mucosa and submucosa.

Azygos Vein↗
PubMed1985

The combined Collis gastroplasty-Nissen fundoplication: surgical procedure and radiographic evaluation.

The combined Collis gastroplasty-Nissen fundoplication consists of a combination of an esophagus-lengthening Collis gastroplasty with 360 degrees complete Nissen fundoplication operation. This report reviews the clinical and radiographic features of 60 consecutive patients who underwent this operation for the control of symptomatic gastroesophageal reflux. The surgical procedure, the technique of postoperative radiographic examination, normal radiographic anatomy, and abnormalities detectable radiographically are briefly described. All patients were examined on the seventh postoperative day initially with iodinated water-soluble contrast medium followed by barium to establish integrity of the gastroplasty tube, fundoplication wrap, and dilated esophageal stricture. Later in the postoperative period, elective barium esophagrams were prompted by complaints of dysphagia (three patients) and symptoms of gastroesophageal reflux (five patients).

Adult↗
PubMed1985

Chronic hypertrophic pyloric gastropathy as a cause of pyloric obstruction in the dog.

Six small-breed, middle-age dogs with a history of chronic intermittent vomiting had benign pyloric lesions causing gastric outlet obstruction. Marked similarities were found in clinical signs, pathologic changes, and treatment results. The condition was classified as a syndrome and was named chronic hypertrophic pyloric gastropathy. The appearance of the obstructive lesions at surgery were various forms of mucosal hypertrophy. Microscopically, the syndrome was characterized by mucosal foveolar and glandular hyperplasia, cystic glandular dilatation, superficial mucosal ulcerations, and various cellular infiltrates. The affected dogs were successfully treated by surgical correction of the gastric outlet obstruction.

Animals↗
PubMed1976

Identification and blockade of vascular H2 receptors.

Experiments were conducted in anesthetized dogs to determine the nature of receptors mediating vascular actions of histamine. In the perfused gracilis muscle histamine caused vasodilatation that was attenuated in part by mepyramine, an H1-receptor blocker. Metiamide, an H2 blocker, given alone had no effect on dilatation. However, the combination of mepyramine and metiamide resulted in a large attenuation of dilatation. Histamine caused constriction of the perfused saphenous vein that was totally blocked by mepyramine suggesting that venoconstriction by histamine involves only H1 receptors. Histamine infusion caused a fall in arterial pressure and a large reduction in peripheral resistance. Mepyramine attenuated the fall in pressure but not the reduction in resistance. Combined H1- and H2-receptor blockade largely eliminated the effects of histamine infusion further documenting the existence of H1 and H2 receptors. The effects of H1 and H2 antihistamines on a variety of physiological vasodilator responses were examined. Evidence was obtained to indicate that H1- and H2-histamine receptors are involved in the active component of baroreceptor-mediated reflex vasodilatation, poststimulation vasodilatation, sympathetic vasodilatation in the guanethidine-treated dog, and vasodilator responses following compound 48/80. No evidence for the participation of either H1- or H2-histamine receptors in reactive hyperemia or the dilatation accompanying exercise was found. It is concluded that in the dog both endogenously-released and exogenous histamine exert vascular effects by activation of both H1 and H2 receptors.

Animals↗
PubMed1996

Morphologic, histologic, and molecular similarities between adenocarcinomas arising in the gastric stump and the intact stomach.

BACKGROUND: Patients with gastric remnants resulting from partial resections have an increased risk for carcinoma. It is unclear whether adenocarcinoma arising in the gastric stump (GSca) differs from intact stomach carcinoma (Gca). The goal of this study was to examine the pathologic and molecular features of GSca and compare them with Gca. METHODS: Adjacent nonmalignant areas and tumors from 14 patients who were 19-55 years postgastrectomy (mean, 32.1 years) were compared with 14 Gca by pathologic and molecular analysis. Formalin fixed, paraffin embedded specimens were immunohistochemically stained for p53 followed by topographic genotyping. Exons 5-8 were amplified by the polymerase chain reaction and directly sequenced. RESULTS: No differences were noted between the two groups regarding gender, types of metaplasia, dysplasia, morphology, or histologic tumor type. However, a higher incidence of cystic dilatation and foveolar hyperplasia were present in GSca. p53 gene point mutations occurred in 5 of 14 (35.7%) GSca patients. GSca p53 mutations included missense point mutations (G:A transitions in four patients and G:C transversion in one patient) with allelic loss. In four of the five patients with p53 mutations, the same mutation was also observed in the adjacent area. p53 point mutations were present in 4 of 14 Gca (28.6%), in exons 5, 6, and 8. In one case, the same mutation was also detected in the adjacent nonmalignant mucosa. CONCLUSIONS: Similarities in clinical, pathologic, and molecular features between GSca and Gca suggest the possibility that they share similar mechanisms of carcinogenesis. p53 gene alterations in premalignant areas may denote a possible early role of this gene in gastric carcinoma.

Adenocarcinoma↗
PubMed1989

The diagnostic value of endoscopic ultrasonography in pancreatic disorders.

The introduction of endoscopic ultrasonography (EUS) makes it possible to demonstrate the pancreas in detail by intraluminal scanning. To assess the clinical usefulness of EUS in the diagnosis of pancreatic disorders, 33 patients with various pancreatic disorders were examined by conventional ultrasonography (US) and EUS concomitantly. There were 16 patients with pancreatic carcinomas: 7 chronic pancreatitis, 5 pseudocysts, 2 mucinous cystadenocarcinomas, one each serous cystadenoma, Von-Hippel-Lindau disease, and simple cyst of the pancreas. An Olympus EUS (Japan) radial type machine with a 7.5 MHz transducer with the balloon inflation method was used. The overall diagnostic sensitivity of conventional US (90.9%, 30/33) was as high as that of EUS (93.9%, 31/33), but the latter demonstrated pancreatic parenchyma more clearly. Three patients were misdiagnosed by conventional US. One patient with chronic calcifying pancreatitis, which was initially diagnosed as dilatation of the main pancreatic duct without evidence of calcifications by conventional US, was confirmed to have a trace of calcification by EUS and computed tomography. Two other patients, whose initial diagnosis was pseudocyst, were proved to have mucinous cystadenocarcinoma and serous cystadenoma respectively by EUS, as a result of improved image resolution. Two patients were misdiagnosed by EUS. One patient with carcinoma of the pancreatic head was missed by EUS because of a partially gastrectomized stomach which precluded successful observation. The other patient with cystadenocarcinoma of the pancreatic tail was misdiagnosed as pseudocyst by EUS due to non-visualization of a papillary crescent within a cystic tumor. We conclude that EUS and conventional US were complementary.(ABSTRACT TRUNCATED AT 250 WORDS)

Endoscopy↗
PubMed1990

Indications for esophagectomy in nonmalignant Barrett's esophagus: a 10-year experience.

Between 1978 and 1988, 88 patients were referred for the surgical treatment of nonmalignant Barrett's esophagus. Nineteen patients required esophageal resection. Male/female ratio was 13:6; age range was 13 to 84 years (mean age, 49.8 years; median age, 40 years). Preoperative studies demonstrated strictures in 11 patients and ulcers in 7. Penetrating Barrett's ulcer resistant to treatment was the indication for resection in 5 patients. Ulcers penetrated to the pericardium (1 patient), pulmonary vein (1), lung (1), and mediastinum (2). Other indications for resection included undilatable strictures (2), previous operations (4), high-grade dysplasia (3), parietal cells lining the esophagus (1), patient's refusal of long-term surveillance (2), and the inability to exclude adenocarcinoma preoperatively (2). Reconstruction was achieved by colon interposition (15) or esophagogastrostomy (4), with one postoperative death. Mean follow-up was 41 months and was 100% complete. Of the 18 patients, 3 have occasional regurgitation but none have any dysphagia or weight loss. Esophageal resection is indicated in a select group of patients with Barrett's esophagus. Absolute indications include a deep penetrating ulcer confirmed intraoperatively, high-grade dysplasia, strong suspicion of cancer, and multiple previous operations. Relative indications include strictures not responding to dilation and young patients refusing long-term surveillance.

Adolescent↗
PubMed2001

Corrosive injury-induced gastric outlet obstruction: a changing spectrum of agents and treatment.

METHODS: During the last 5 years, 61 children were admitted to the authors' hospital because of corrosive substance ingestion, and among them 6 patients were seen with gastric outlet obstruction. Two of them had ingested acid substances, and the other 4 had ingested alkali corrosives. The mean age was 2.9 years (range, 1.5 to 3). Their common complaint was postprandial vomiting, which had begun 3 weeks after the event (range, 1 week to 10 weeks). Endoscopic evaluation and barium contrast radiographies were performed at admission. Four patients had a pyloric stricture, 1 had an antral stricture, and another had an antropyloric stricture. Balloon dilatation of the pylorus (in 1 patient), pyloroplasty (in 3 patients), and Billroth I procedures (in 2 patients) were performed. The mean follow-up period was 22 months (range, 6 weeks to 48 months). One patient, who had undergone a Billroth I procedure, underwent reoperation because of intestinal obstruction 3 months later. On follow-up they are all free of symptoms. CONCLUSIONS: The treatment of gastric outlet obstruction caused by corrosive ingestion should be treated surgically. Although endoscopic and radiologic evaluation helps to determine the time and necessity, once the diagnosis is confirmed, early definitive surgical intervention should be performed, and the type of the surgery depends mostly on the findings of the surgeon at laparotomy. Endoscopic balloon dilatation of the pylorus maybe attempted in suitable cases. Special care should be given to prevent children from accidental corrosive ingestion.

Burns, Chemical↗
PubMed1991

Wischnevsky's gastric lesions in accidental hypothermia.

We examine the pathogenesis of Wischnevsky's lesions. These gastric lesions were found in 15 of 17 deaths due to accidental hypothermia. Deaths occurred at various minimum temperatures (-2.4-20.4 degrees C); gastric lesions did not always reflect exposure temperatures. However, all victims exposed to temperatures greater than 10 degrees C had severe lesions. At temperatures less than 5 degrees C, on the other hand, severe gastric lesions were seen in victims younger (43.2 years old) than those with mild lesions (61.0 years old). These findings suggest that gastric lesions develop by exposure to temperatures at which the body's response to cold stress continues, or as result of a strong response to short-term stress. Histopathologic examination demonstrated a characteristic finding of cystic dilatation of the capillaries, presumably due to massive reperfusion after functional collapse of the microcirculation in the gastric mucosa.

Accidents↗
PubMed1976

[Indications and technics for esophagoduodenostomy].

From 1961 to 1974 19 esophagoduodenostomies have been performed after total gastrectomy. One patient died postoperatively because of pulmonary embolism. The mean survival rate was 16,4 months. In far advanced gastric carcinomas an elongation and dilatation of the duodenum favours this kind of anastomosis. In low risk patients, in the aged and for palliative gastrectomy we suggest to prove the possibility for performing an esophagoduodenostomy.

Adenocarcinoma↗
PubMed1991

Ciliated gastric cells among Japanese living in Hawaii.

A total of 129 consecutive gastrectomy specimens from Japanese (99), Philippinos (11), Hawaiians (8), Koreans (5), Chinese (4) and Caucasians born in Hawaii (2) were examined under high-power light microscopy (1000 x) for the presence of ciliated gastric cells. Fifty-two of the 129 gastrectomy specimens (40.3%) contained ciliated cells. Ciliated cells were found in the basal segments of antral glands (usually cystically dilated) whose superficial segments had undergone intestinal metaplasia. The presence of ciliated cells in the gastric mucosa was influenced by the age of the patient and by the degree of intestinal metaplasia: the older the patient, the greater the degree of intestinal metaplasia and the greater the frequency of specimens with ciliated cells. The presence of ciliated cells was also influenced by the type of lesion in the specimen. Although the highest frequency (47.2%) was found in stomachs removed for adenocarcinoma, a substantial number of stomachs removed for gastric ulcer also showed that change (36%). The data suggest that increasing age and advanced atrophic gastritis, especially of the antrum, provide the necessary conditions that lead to the development of cilia, not only in Japanese subjects, but in other Hawaiian ethnic groups as well.

Adult↗
PubMed1993

Transhiatal esophagectomy for benign and malignant disease.

Transhiatal esophagectomy has been performed in 583 patients with diseases of the intrathoracic esophagus: 166 (28%) benign and 417 (72%) malignant (6% upper, 28% middle, and 66% lower third and cardia). The benign esophageal diseases included strictures (40%); neuromotor dysfunction-achalasia (24%), esophageal spasm (8%); recurrent gastroesophageal reflux (16%); acute perforation (5%); acute caustic injury (2%); and others (3%). Among the patients with benign disease, 60% had undergone at least one prior esophageal operation. Transhiatal esophagectomy was possible in 97% of patients in whom it was attempted, 19 patients (13 with benign disease and 6 with carcinoma) requiring addition of a thoracotomy for esophageal resection. Esophageal resection and reconstruction were performed in a single operation in all but 5 patients. The esophageal substitute was positioned in the posterior mediastinum in the original esophageal bed in 96%. Stomach was used to replace the esophagus in 553 patients (95%) and colon in 28 (5%) who had undergone prior gastric resections. Overall hospital mortality was 5% in patients with benign disease and 5% in those with carcinoma. There was 1 intraoperative death caused by uncontrollable hemorrhage. Complications included intraoperative entry into a pleural cavity necessitating a chest tube (74%), anastomotic leak (9%), recurrent laryngeal nerve paralysis (3%), and chylothorax and tracheal laceration (< 1% each). Three patients required reoperation for mediastinal bleeding. Average intraoperative blood loss was 875 ml (1023 ml for benign disease and 817 ml for carcinoma). Of the surviving patients, 88% were discharged able to swallow within 3 weeks of operation and 78% within 2 weeks. The actuarial survival of the patients with carcinoma is similar to that reported after more traditional transthoracic esophagectomy. Among patients with benign disease, good or excellent functional results have been achieved in nearly 70% after a cervical esophagogastric anastomosis. Although approximately 44% have required one or more anastomotic dilations within 1 to 3 months of operation, true anastomotic strictures have developed in 10%. Clinically troublesome nocturnal reflux has occurred in 3%. Transhiatal esophagectomy is feasible in most patients requiring esophageal resection for either benign or malignant disease and is a safe, well-tolerated operation if performed with care and for the proper indications.

Adenocarcinoma↗
PubMed1996

Tachykinin inhibition of acid-induced gastric hyperaemia in the rat.

1. Primary afferent neurones releasing the vasodilator, calcitonin gene-related peptide, mediate the gastric hyperaemic response to acid back-diffusion. The tachykinins neurokinin A (NKA) and substance P (SP) are located in the same neurones and are co-released with calcitonin gene-related peptide. In this study we investigated the effect and possible role of tachykinins in the acid-evoked gastric vasodilatation in urethane-anaesthetized rats. 2. Gastric acid back-diffusion, induced by perfusing the stomach with 15% ethanol in the presence of 0.05 M HCl, increased gastric mucosal blood flow by 60-90%, as determined by the hydrogen clearance technique. NKA and SP (0.14-3.78 nmol min-1 kg-1, infused intra-aortically) inhibited the gastric mucosal hyperaemic response to acid back-diffusion in a dose-dependent manner, an effect that was accompanied by aggravation of ethanol/acid-induced macroscopic haemorrhagic lesions. 3. The inhibitory effect of NKA (1.26 nmol min-1 kg-1) on the acid-induced gastric mucosal vasodilatation was prevented by the tachykinin NK2 receptor antagonists, MEN 10,627 (200 nmol kg-1) but left unaltered by the NK1 receptor antagonist, SR 140,333 (300 nmol kg-1) and the mast-cell stabilizer, ketotifen (4.6 mumol kg-1). 4. Under basal conditions, with 0.05 M HCl being perfused through the stomach, NKA (1.26 nmol min-1 kg-1) reduced gastric mucosal blood flow by about 25%, an effect that was abolished by SR 140,333 but not MEN 10,627 or ketotifen. 5. SR 140,333, MEN 10,627 or ketotifen had no significant effect on basal gastric mucosal blood flow nor did they modify the gastric mucosal hyperaemic reaction to acid back-diffusion. 6. The effect of NKA (1.26 nmol min-1 kg-1) in causing vasoconstriction and inhibiting the vasodilator response to acid back-diffusion was also seen when blood flow in the left gastric artery was measured with the ultrasonic transit time shift technique. 7. Arginine vasopressin (AVP, 0.1 nmol min-1 kg-1) induced gastric mucosal vasoconstriction under basal conditions but was unable to inhibit the dilator response to acid back-diffusion. 8. These data show that NKA has two fundamentally different effects on the gastric circulation. Firstly, NKA reduces gastric blood flow by activation of NK1 receptors. Secondly, NKA inhibits the gastric hyperaemic response to acid back-diffusion through an NK2 receptor-mediated mechanism. These two tachykinin effects appear to take place independently of each other since they are mediated by different receptors. This concept is further supported by the inability of AVP to mimic tachykinin inhibition of the gastric vasodilator response to acid back-diffusion.

Animals↗