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Chronic pruritus can be a diagnostic sign of an underlying disease. In the intracutaneous histamine test, histamine (one of the best-known inducers of pruritus) may cause different reaction patterns depending on the underlying disease. The aim of this study was to determine if an intracutaneous injection of histamine can differentiate between the causes of chronic pruritus and thus be used as a diagnostic test in chronic pruritus of unknown aetiology. A total of 140 subjects with chronic pruritus with various dermatological, systemic or neurological diseases were included. The intracutaneous histamine test was performed once on each subject. Erythema, wheal and pruritus intensity were measured and analysed. Significantly greater wheal size was observed in patients with systemic or multifactorial causes. In general, there was a significant correlation between age and wheal size. Also, noticeable differences were found between males and females regarding pruritus and wheal size. In summary, the exact type of chronic pruritus could not be clearly determined based on the results of the intracutaneous histamine test. However, the results provide valuable insights into specific reaction patterns to experimental histamine-induced itch, e.g. sex-specific differences in the neurophysiology of pruritus, which should be considered in future studies.

Examinations of 83 patients and 13 healthy subjects with the augmented histamine test and gastric biopsy show that a maximal acid secretion lower than 10 mEq HCl/hour signifies a diffuse gastritic lesion, the type of which can be verified by a single gastric biopsy. Detailed investigations of the nature and clinical course of gastritis, however, require repeated tests of gastric function and multiple gastric biopsies.

The secretion of hydrochloric acid and of intrinsic factor was studied in 14 subjects with chronic duodenal ulcer before and during six 15 minutes periods of intravenous histamine infusion. The amount of infused histamine was increased with every 15 minutes period. The volume of gastric juice increased successively during the first four periods and was maximal and equal in the last three periods of increasing histamine stimulation. The secretion of hydrochloric acid increased steadily during the increasing rate of histamine infusion, reaching a maximal and equal output in the last two periods. The concentration of intrinsic factor, however, was maximal in the first period and decreased steadily in the following periods of histamine stimulation. The output of intrinsic factor was maximal during the first three periods and decreased during the following periods in spite of increasing rate of histamine infusion. Since the volume of gastric juice was maximal and equal during the last three periods the fall in intrinsic factor concentration was more marked than the decrease in its output. The concentration of intrinsic factor in the last period was lower than basally. These results indicate that histamine causes a ‘wash-out’ of stored intrinsic factor. The output of intrinsic factor was, however, still significantly higher than basally even 75–90 minutes after the histamine infusion had started. This could be due to a late ‘wash-out’ mechanism or to a stimulation of intrinsic factor production and secretion.

Although several different models have been proposed to explain force maintenance in vascular smooth muscle, the molecular mechanism responsible for this phase of contraction has yet to be elucidated. To investigate the molecular mechanism for force maintenance, force and stiffness were measured during (1 microM histamine) activation of single intact arterial smooth muscle cells. After histamine stimulation, the rise in quadrature stiffness preceded force (P0.05) and reached a steady state plateau before force (P0.05). These data suggest that the number of cycling cross-bridges increases during force activation and then remains constant during force maintenance. In-phase stiffness, on the other hand, continued to increase in amplitude after force had reached a steady state. The increase in the in-phase stiffness during force maintenance suggests that during force maintenance either a population of cross-bridges in an attached nonforce producing state develop or noncross-bridge force bearing structures are formed.

Epidermal growth factor (EGF) was measured in saliva and in gastric juice under basal conditions and after histamine stimulation (0.04 mg kg-1h-1). Sixty subjects studied comprised 20 normal volunteers, 20 patients with duodenal ulcer (DU), and 20 patients with non-ulcer dyspepsia (NUD). There was no difference in basal salivary EGF concentrations between control and DU or control and NUD subjects, but the EGF concentration in DU patients exceeded that in NUD patients (p > 0.05). After histamine stimulation, salivary and gastric EGF concentrations increased in all three groups: the increase was greater in gastric juice than saliva (p < 0.0001). There were no significant differences in the salivary EGF concentrations of controls and NUD patients, or controls and DU patients, but values were significantly higher when DU and NUD patients were compared (p = < 0.05). In the gastric juice, EGF increased more in DU patients than in controls or NUD patients (p < 0.05). This effect was not linked to the greater acid secretion in DU than in the other groups. There was no influence of gender or smoking on the EGF concentration. This evidence suggests that the stomach itself may be able to secrete large amounts of EGF and that histamine is a potent stimulus. It is more likely that the gastric EGF is responding to the presence of a duodenal ulcer than that lack of EGF is responsible for persistence of the ulcer.

Conclusions1. Benadryl fails to alter the gastric secretory response to histamine stimulation in pouch dogs. 2. Benadryl (given in 100 mg doses in beeswax mixture intramuscularly) fails to protect against the histamine-provoked ulcer in dogs.

Titration to different pH end points was performed in all samples of gastric juice from 208 patients with gastro- instestinal diseases and healthy persons, examined with the augmented histamine test. Titration to pH 3.3 and to pH 7.0 revealed differences in hydrogen ion concentration, which were significantly negatively correlated to the maximal acid output, calculated from the acidity at pH 3.3. Differences between maximal acid outputs, calculated from the acidities at pH 3.3 and pH 7.0, varied only little in all examined groups with the exception of gastric juice contaminated by food. Titration to pH 7.0 or higher overestimates gastric hydrochloric acid, especially in gastric juice from patients with gastritis and gastric juice contaminated by food. The results of this study support previous investigations, which recommend titration of gastric juice to pH 3.5 with simultaneous measurement of pH. Achlorhydria corresponding to absence of parietal cells is hereby defined by a pH higher than 3.5 and a pH fall less than one pH unit from basal to maximally stimulated values.

To date three potential candidates for parietal cell basolateral Cl− entry have been described: the highly 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS)-sensitive \( {{\text{Cl}}^{{\text{ - }}} } \mathord{\left/ {\vphantom {{{\text{Cl}}^{{\text{ - }}} } {{\text{HCO}}_{{\text{3}}} ^{ - } }}} \right. \kern-\nulldelimiterspace} {{\text{HCO}}_{{\text{3}}} ^{ - } } \) exchanger AE2, the \( {\text{HCO}}_{{\text{3}}} ^{ - } \) and lowly DIDS-sensitive SLC26A7 protein, and the Na+-2Cl−K+ cotransporter (NKCC1). In this study we investigate the contribution of these pathways to secretagogue stimulated acid secretion. Individually hand-dissected rat gastric glands were microfluorimetrically monitored for Cl− influx and pHi changes. Transporter activity was determined by varying ion content and through the use of pharmacological inhibitors. Expression of SLC26A7 in rat parietal cells was shown by immunohistochemistry and Western blot. SLC26A7 was inhibited by 5-Nitro-2-(3-phenylpropyl-amino)benzoic acid (NPPB) (100 μM) in the Xenopus laevis oocyte expression system. Cl− influx in parietal cells was enhanced by histamine, depended partially on endogenous \( {\text{HCO}}_{{\text{3}}} ^{ - } \) synthesis and completely on extracellular Na+. Removal and subsequent readdition of Cl− revealed a low and a high DIDS-sensitive \( {\text{HCO}}_{{\text{3}}} ^{ - } \) extrusion system contributing to Cl− uptake. At acidic pHi, however, H+ extrusion via the H+,K+-ATPase depending on Cl− uptake was abolished only in the presence of 100 μM (NPPB) and at high (250 μM) DIDS concentration. There was no effect of the NKCC inhibitor bumetanide on stimulated H+ extrusion. These results would be compatible with SLC26A7 as a Cl− uptake system under histamine stimulation.

Gastric microcirculatory changes were studied by means of hydrogen clearance techniques in conscious cats during histamine stimulation. A considerable increase of corpus mucosa flow occurred, whereas a less substantial increase of antrum mucosa flow was observed during stimulation with histamine at 2 micrograms/kg/min, intravenously. Stepwise increase of infused histamine was accompanied by a gradual increase of corpus flow in the mucosa, which during supramaximal stimulation decreased slightly but still remained considerably elevated above control values. A similar decrease of antral mucosa flow occurred earlier during maximal stimulation, suggesting shunting of blood from the antrum to the corpus region. Total gastric flow measurements performed in anesthetized animals similarly showed decreased flow at a rate of histamine infusion which produced supramaximal stimulation in the conscious animals. However, total gastric flow remained elevated also during this stage compared with prestimulation values. A hypothesis of a dual effect of histamine on the gastric circulation is suggested, including regulation of flow through generalized vasodilatation and increased metabolic activity in the parietal cell mass.

Histamine stimulates prostaglandin E (PGE) production by cultures of adherent rheumatoid synovial cells and human articular chondrocytes. When subcultured synovial fibroblasts or human articular chondrocytes were "primed" by preincubation with conditioned media from primary adherent rheumatoid synovial cell cultures (synovial factor), each produced even higher PGE levels upon histamine exposure. This histamine stimulation was prevented by histamine H1, but not H2, antagonists and was more marked if serum was absent from the culture media. Thus, histamine-induced PGE production by these cells is mediated via H1 receptor activation and subsequent arachidonic acid liberation.

The onset of burimamide inhibition of histamine stimulation of rabbit atria is rapid, and a near steady-state blockade occurs at approximately 15 min ( larger than or equal to 90% complete). The blockade is reversible but requires several washings suggesting the disassociation is slow. The administration of histamine may accelerate the decay of the burimamide effect. Reciprocal plots (rate response versus histamine concentration) of dose-response curves are linear for both rabbit and guinea pig atria. In the presence of low concentrations of burimamide; (2.4 times 10-5 M), the displacement of curves suggests a competitive type of inhibition both for rabbit and guinea guinea pig atria. The apparent association constants calculated from these curves are: K1 (rabbit) 3.7 times 10-6M and K-1 (guinea pig) 6.7 times 10-6M. These results for guinea pig atria are in satisfactory agreement with the value obtained in another laboratory (2). At higher concentrations of burimamide, inhibition curves showed distinct evidence of departure from competitive character for both guinea pig and rabbit atria.

Gastric mucosal blood flow as measured by the hydrogen gas clearance method was compared with total gastric blood flow as determined by venous outflow in an isolated segment of canine stomach. During rest and histamine stimulation, hydrogen gas clearance correlated lineally with total gastric blood flow (p less than 0.001). Correlation analysis revealed a slope of 1.21 and a correlation coefficient of 0.97. The slope of 1.21 indicates that the ratio of mucosal to total gastric blood flow was approximately 82 percent. This fractional distribution of blood flow is in agreement with that previously reported by microsphere technique. In the intact stomach of anesthetized rats and dogs, antral mucosal blood flow was significantly higher than that of the corpus. This finding may, in part, contribute to the observation that acute stress erosion occurs predominantly in the corpus of the stomach. Histamine stimulation selectively increased the mucosal blood flow of the corpus, whereas antral mucosal blood flow remained unchanged. As a result, there was no significant difference in mucosal blood flow between the antrum and the corpus during histamine stimulation.

The gastric mucosal cAMP time course following i.p. injections of carbachol, insulin, 2-deoxy-D-glucose (2-DG) and histamine was investigated in rats. Cholinergic stimulation by either carbachol, insulin or 2-DG caused a double peak in rat gastric mucosal cAMP. A first peak was reached within 15 min, a second after 75 min post injection. The first cAMP rise preceded, the second outlasted, acid secretion of chronic fistula rats stimulated with insulin and 2-DG. After histamine cAMP was elevated within 15 min for about 30 min and then dropped to control values. The rise in gastric mucosal cAMP following cholinergic stimulation suggests: the first peak may be involved in initiating acid secretion, the second has to be related to other functions.

Conclusions1. Gastric secretion obtained by histamine stimulation (0.01 mg. per kilo) under standard conditions, seems to be quite constant for the same individual, both as to volume and height of free acidity. 2. Histamine tests repeated in succession and on succeeding days give practically identical results. 3. Atropine, in doses of 1 mg., decreases the volume of gastric secretion obtained by histamine stimulation in man, approximately SO%, but does not affect the free acid content appreciably.

Hirschowitz, B. I. & Hutchison, G. A. A working hypothesis for urecholine effects on histamine stimulation of gastric secretion. Scand. J. Gastroent, 1973, 8, 569-576Gastric juice volume, H and Cl ...

Glucagon suppresses gastric acid secretion in normal subjects and in ulcer patients. It has no inhibitory effect while the stomach is under maximal histamine stimulation. The mechanism of action is discussed, and experiments are described which indicate that glucagon is unlikely to be of value in the treatment of peptic ulcer.

1. Although the gastric secretory curve in response to histamine is, in a given individual, quite constant as a rule, remarkable unexplained variations do occur. 2. “Histamine-proved” achlorhydria is not necessarily true anacidity. Great care is needed to exclude technical errors such as an incorrect location of the tip of the tube, excessive regurgitation of duodenal content, or the swallowing of saliva. 3. “Histamine-proved” achlorhydria is not necessarilypermanent anacidity, for transient refractoriness to histamine does occur. The cause of this phenomenon is not known.

Rodbro, P. & Christiansen, P. M. Quantitative Determination of Gastric Intrinsic Factor after Large Histamine Doses in Healthy Persons. Scand. J. din. Lab. Invest. 19, 186-189, 1967. In 30 healthy persons the average secretion of gastric intrinsic factor after augmented histamine stimulation was 15400±6650 ng vitamin B12 units/hour.A modification of the protein-coated charcoal assay for intrinsic factor-using a variable ratio between amounts of gastric juice and vitamin B12-is described in detail.

Over the past few years there has been an apparent increase in interest in various methods of gastric analysis. The diagnostic and therapeutic implications of the results of the various types of gastric analyses have recently been re-examined by several authors [l-8]. The augmented histamine stimulation test has gained increasingly wide acceptance by clinicians. Growing experience with this method of gastric analysis has indicated it to be reliable and reproducible. This method of gastric analysis is currently the standard procedure at the Veterans Administration Hospital, Charleston, South Carolina. In the interest of simplifying the methodology of the augmented histamine stimulation test while retaining its reliability, a modification suggested by Stavney et al. [9] and others [JO,111 has been adopted. It consists primarily of intragastric titration of acid monitored by the Heidelberg pH telemetering capsule. Results obtained from the augmented histamine stimulation test utilizing the Heidelberg pH capsule have been compared to those results obtained by the standard nasogastric tube aspiration technic. The method and comparative results are presented herein.

Summary Heidenhain pouches were exposed to 4876 to 4977 rad by means of intracavitary P 32 , with or without concomitant histamine stimulation. Depression of secretory capacity in response to intravenous histamine occurred in all eight animals, but was somewhat (not significantly) less in the four radiated during stimulation. Maximal effect occurred at 3 weeks, after which there was partial recovery to 13 to 66 per cent of preradiation secretion, little change between 2 months and 1 year. After radiation there was often some bleeding from pouches during histamine stimulation. Histologic evidence of damage was more severe on prominent parts of rugae.

Summary A patient who presented with the clinical manifestations of hypoproteinemia and in whom gastric hyperrugosity was associated with excessive gastric protein loss and acid hypersecretion is reported. Atropine sulfate markedly reduced both the hypersecretion and gastric protein loss. It is suggested that anticholinergic therapy be considered in any patient with a protein-losing gastropathy of nonmalignant etiology in whom high, normal, and perhaps even subnormal acid secretion is found following maximal histamine stimulation.

The secretory patterns and hourly outputs of volume, acid, and intrinsic factor secretion after augmented histamine stimulation were studied in 18 children without gastrointestinal disorders, 9–30 months of age.The stimulated outputs of acid and intrinsic factor were correlated to age, body-weight, and body surface area. The results indicate that the secretion of intrinsic factor in this age group is more mature than the secretion of acid.

The effect of injury on the gastric mucosal response to histamine stimulation has been investigated in dogs by 2 technics. (1) Exposing the intact surface of the stomach to several kinds of trauma, e.g., friction, heat, salt, alcohol, and formalin. It was found that the surface of the traumatized area, in each instance, was coated with an alkaline surface of pH 7–9. This alkalinization of the surface after trauma was not affected by submucosal infiltration of local anesthetic. (2) Total gastric pouches in stimulated and unstimulated dogs were filled with ethanol (50% and 70%). In stimulated animals, the gastric secretory output of volume and acid were considerably reduced. In nonstimulated animals, there was a transient rise in the volume of gastric juice after ethanol instillation followed by a reduced output. However, the concentration of acid was low after ethanol administration. It is suggested that part of the explanation for these findings lies in the effect of injury on the secreting epithelium, this effect being physiologic and not associated with gross structural damage to the secreting cells.

Helander, H. F. 1970. Gastric Acidity in Young and Adult Mice. Scand. J. Gastroent. 5, 221-224.Gastric acid secretion in response to histamine stimulation was studied in young and adult mice. In th...

Summary The continuous administration of histamine intravenously in every instance in human subjects stimulated the secretion of pepsin. This effect reached a plateau within 1 hour and was maintained at that level as long as the histamine was administered; viz. , up to 2 hours in 16 studies, to 3 1/2 hours in 11 studies and 5 1/2 hours in 2 studies.

Summary The results of feeding urea, using the preparation in this study, were so universally unpleasant as to render this agent unfit for clinical trial. There is an apparent diminution in output of gastric secretion to histamine stimulation (i.e., volume and actual HCl output) in normal subjects whose BUN levels are elevated by oral administration of urea, but the concentration of acid is apparently unchanged.

A synthetic pentapeptide (pentagastrin, 'I.C.I. 50, 123') in a dosage of 6 μg. per kg. produces a similar gastric acid response to augmented histamine stimulation. In 15 patients, 7 of whom were achlorhydric, preliminary results suggest that these drugs also produce similar amounts of intrinsic factor.

Augmented histamine tests and gastric mucosal biopsies were performed on 97 patients. The amount of acid secreted was closely correlated with the histological appearances of the gastric mucosa. There was a striking difference between the acid secretion of patients with normal biopsies and patients with superficial gastritis. Achlorhydria was not present in patients with normal biopsies. An occasional patient with gastric atrophy will be found to secrete small amounts of acid.

Changes in parietal cell membranous structures that accompany the onset of acid secretion were studied with electron microscopy using isolated gastric glands from rabbit. A stereological analysis was performed to quantitate the morphological changes occurring within 5 min following histamine stimulation. These changes were compared to the changes resulting from osmotic expansion of parietal cell components following addition of 1mm aminopyrine (AP) to glands incubated in medium containing 108mm K+ (high-K+). Morphometric analyses, together with measurements of glandular water content, indicated that parietal cells swell in high-K+ medium. Addition of 1mm AP to glands incubated in high-K+ medium resulted in massive distention of the secretory canaliculus but no difference was observed in the amount of tubulovesicular membrane or the relative size of these cytoplasmic structures. In the histamine-treated glands the parietal cells displayed a rapid loss of tubulovesicular membrane and a reciprocal increase in canalicular membrane. These morphological changes were complete long before a maximum level of acid formation was achieved. Taken together, these results indicate that; (i) the morphological change accompanying stimulation does not require acid formationper se; (ii) the site of acid secretion is the intracellular canaliculus and not the tubulovesicles; (iii) there is no preexisting actual or potential continuity between the tubulovesicular space and the canalicular space; and (iv) the AP-induced expansion of the canaliculus in high-K+ medium, while yielding some valuable information, is not an appropriate model for studying the normal stimulus-induced morphological transition, despite a superficial similarity of appearance.

The bronchoconstriction induced by repeated histamine inhalation tests was studied in eight mild stable asthmatic subjects to determine whether histamine tachyphylaxis occurs in asthmatics. We also studied the specificity of histamine tachyphylaxis by examining for tachyphylaxis in response to inhaled acetylcholine in these subjects. We subsequently investigated whether indomethacin pretreatment inhibited histamine tachyphylaxis. Tachyphylaxis in response to inhaled histamine occurred in all subjects. The mean histamine provocative concentration causing a 20% fall in the forced expiratory volume in 1 s (PC20) increased from 3.04 +/- 1.9 (%SD), to 4.88 +/- 1.9, and to 6.53 +/- 2.2 mg/ml (P less than 0.0005) with successive inhalation tests. Tachyphylaxis was still present at 3 h (P less than 0.01), but not in all subjects at 6 h (P greater than 0.05). Tachyphylaxis, however, did not occur in response to inhaled acetylcholine. In addition, indomethacin pretreatment prevented histamine tachyphylaxis. Thus this study demonstrates that there is a histamine-specific mechanism that can partially protect the airways against repeated bronchoconstriction caused by histamine. This effect may occur through the release of inhibitory prostaglandins in the airway after histamine stimulation. Also when histamine inhalation tests are repeated on the same day, the tests should be separated by greater than 6 h to avoid tachyphylaxis.

Salivary secretions on mechanical stimulation with forced spitting method and on chemical simulation with 10% citric acid and gastric acid secretions on maximal histamine stimulation were studied in 20 adults with tropical sprue and 20 adult control subjects. It was observed that the chemical method provided a better stimulus than the mechanical one in both groups. The salivary flow rates as well as salivary amylase, pH, sodium and potassium were similar in both groups. Tropical sprue patients, however, had significantly lower maximal acid output as compared to normals. It was concluded that, although tropical sprue patients are known to have widespread damage to alimentary tract mucosa, salivary glands do not seem to be involved.

Summary The effects of varying intensities of histamine stimulation on cells of the western newt fundic stomach epithelium have been studied. Oxyntic, mucous neck and surface mucous cells all secrete. In the oxyntic cell, the main effects are a movement of zymogen granules toward the apex, the discharge of their contents into the lumen and, eventually, their disappearance from the cytoplasm. Additionally, the tubular membrane elements (tubulo- vesicles) fuse with the apical plasma membrane with a corresponding reduction in their numbers and an increase in microvilli, which eventually are so numerous as to virtually occlude the lumina of gastric glands. Total histamine stimulation results in apparent damage to the oxyntic cells. Mucous neck and surface mucous cells release their mucigen droplets by exocytosis and are grossly changed in appearance also. Zusammenfassung Feinstruktur des Epithels des Magenfundus beim “Western” Molch (Triturus torosus) 2. Nach Histaminstimulierung Als Folge unterschiedlich starker Histaminstimulierung sezernieren alle Zellen (Belegzellen, mukose Halszellen und mukose Oberflachenzellen) des Magenfundus von Triturus torosus. Bei den Belegzellen ist besonders auffallig: eine Apikalstromung von Zymogengranula, ihre Entleerung ins Drusenlumen und, zuweilen, deren volliger Schwund aus dem Zytoplasma. Auserdem vereinigt sich die Membran der Tubuli (Tubulovesikel) mit dem apikalen Zytolemm, wobei die Tubuli zahlenmasig abnehmen, die Mikrovilli jedoch derart zunehmen, das sie praktisch das Drusenlumen verlegen. Starkste Histaminstimulierung schodigt die Belegzellen offensichtlich. Mukose Hals- und Oberflachenzellen schleusen ihre Mucigen-Tropfchen durch Exozytose aus; auch ihr Erscheinungsbild ist stark verandert. Resume La structure de l'epithelium fundique de l'estomac du triton (Triturus torosus) 2. Apres stimulation avec Histamine On a etudie les effets de stimulations d'intensites differentes par l'histamine sur les cellules de la muqueuse fundique de l'estomac du triton Triturus torosus. Les cellules oxyntiques, les cellules a mucus des cols glandulaires et les cellules a mucus de la surface sont toutes secretantes. Dans les cellules oxyntiques, les effets principaux consistent en un mouvement des granules de zymogene vers l'apex, la decharge de leur contenu dans la lumiere et eventuellement leur disparition du cytophsme. En outre, les elements de la membrane rubulaire (tubulo-vesicules) fusionnent avec la membrane plasmatique apicale, en meme temps que se reduit leur nombre et que les microvillosites augmentent; ces dernieres sont parfois si nombreuses qu'elles ferment virtuellement la lumiere des glandes gastriques. La stimulation histaminique totale semble provoquer une degradation des cellules oxyntiques. Les cellules a mucus des cols glandulaires et de la surface dechargent leurs gouttelettes de mucigene par exocytose et sont egalement tres modifiees dans leur apparence. Resumen Ultraestructura del epitelio en el fondo gastrico de la salamandra “del oeste” (Triturus torosus) 2. Despues de estimulacion con histamina Como consecuencia a una estimulacion variable con histamina, todas las celulas (celulas de revestimiento, celulas mucosas del cuello y celulas mucosas de la superficie) en el fondo gastrico de Triturus torosus muestran secrecion. En las celulas de revestimiento se observa especialmente un flujo apical de los granulos cimogenos, su vaciamiento hacia la luz de las glandulas y a veces su desaparicion completa en el citoplasma. Ademas, la membrana de los tubulos (tubolovesiculas) se une con el citolema apical, reduciendose el numero de los tubulos y aumentando el de las microvellosidades, de tal manera que pueden obstruir la luz de las glandulas. Estimulacion maxima con histamina produce danos en las celulas de revestimiento, aparentenemente. Las celulas mucosas del cuello y de la superficie segregan las gotitas de mucigeno mediante exocitosis; tambien estas celulas cambian su aspecto fundamentalmente.

Ten minute samples of gastric juice were collected by naso-gastric aspiration during maximal histamine stimulation in 14 subjects (6 normal, 8 with duodenal ulceration). In eight of these studies, a simultaneous intravenous infusion of Indocyanine green (ICG) was used to label the bile. A single intravenous injection of Boots secretin was given during the maximal plateaux, and further samples collected. The volume, titratable acidity, electrolyte concentrations and ICG concentrations were measured. Changes in volume and in electrolyte concentrations after secretin were consistent with the hypothesis that secretin stimulated duodenogastric reflux, and that duodenogastric reflux was the major determinant of spontaneous variations in electrolyte concentrations in gastric aspirate. Duodenogastric reflux was calculated by a previously described formula based on the sodium content of the aspirate, and this was found to correlate well with the concentration of the ICG label in the aspirate.

A patient is presented who had heavyStrongyloides infection, manifesting gastrointestinal abnormalities, including achlorhydria to maximal histamine stimulation and malabsorption. Successful cure of strongyloidiasis, in this man