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Large-scale mitochondrial DNA (mtDNA) deletions are associated with clinical conditions such as Kearns–Sayre syndrome and chronic progressive external ophthalmoplegia in adults and Pearson syndrome in children. Reported case series have suggested that deletions are not uncommon in the population, but their prevalence has not been documented.

To study the kinetics of glutaraldehyde fixation, fresh rabbit liver cubes were immersed in 3% buffered 3H-glutaraldehyde for various periods of time. Following weighing and a brief rinse in water, the tissues were solubilized, and the radioactivity was measured in a scintillation counter. Binding of the isotope was half-maximal after approximately 4 h and a plateau was reached after approximately 20 h. We also investigated the reversibility of glutaraldehyde fixation. Fixed liver cubes were weighed and immersed in water for various periods of time, and after solubilization, the radioactivity was determined. After rinsing for 48 h, approximately 95% of the radioactivity was lost from the tissue specimens, indicating that fixation with glutaraldehyde is largely reversible. Light and electron microscopy of specimens rinsed for 1 and 48 h showed essentially similar morphology. Rinsing for 48 h restored some of the immunoreactivity that was absent after rinsing for only 1 h.

Summary Pieces of rabbit gallbladders were incubated in vitro for 1 hr in Ringer's solution at 37° (“transporting epithelium”), or in Ringer's containing 1mm ouabain (“inhibited epithelium”). The tissues were fixed in 2% glutaraldehyde, postfixed in OsO4 and embedded in Epon. Stereological analysis was carried out on electron micrographs; with this type of analysis it is possible to obtain quantitative data for the three-dimensional structure of the tissue. The following data were obtained for crest transporting epithelium (crypt epithelium in parentheses): Epithelial height, 28 (18) μm; nucleus, 16.9 (18.7) % of cell volume; mitochondria, 18.7 (14.1) % of cytoplasmic volume; paracellular channels, 28.3 (11.0)% of epithelial volume; lateral plasma membrane, 4.1 (2.9) m2/cm3, and apical membrane, 0.5 (0.6) m2/cm3 of cell volume. The paracellular channels appeared as interconnected tissue sheets of a highly varying width. They were broader in the basal portion of the epithelium than in the apical portion; however, immediately above the basement membrane the channels became very narrow. The arithmetic mean width of the channels was 0.9 (0.2) μm and their length was in the range of 40–120 μm. Our stereological data seem compatible with the standing gradient model for water transport.

1. Female adult rats were subjected to sympathetic denervation of the parotid glands by bilateral removal of the superior cervical ganglion 10‐12 days before acute experiments. The sympathectomy was in some of the experimental groups combined with either bilateral adrenal medullectomy, treatment with the sensory neurotoxin capsaicin or parasympathetic denervation of the gland by cutting the auriculotemporal nerve. 2. Food but not water was withheld for 29‐32 h before acute experiments. All animals were given an intraperitoneal injection of phentolamine (2 mg kg‐1) and propranolol (1 mg kg‐1) and, when appropriate, also atropine (1 mg kg‐1). Then the experimental animals were fed their ordinary food of hard chow for 60‐90 min. Thereafter, these animals and their non‐fed controls were killed, and the parotid glands were removed and used for either morphometric assessment or measurement of amylase activity. 3. In the atropinized rats subjected to sympathectomy alone, eating reduced the numerical density of acinar secretory granules by 50% and the total activity of amylase by 55%; the corresponding figures were, when sympathectomy was combined with adrenal medullectomy, 51 and 63%. Also, in atropinized animals subjected to sympathectomy and capsaicin pretreatment, eating reduced the numerical density of acinar granules and the total amylase activity, in this case by 45 and 35%, respectively. 4. In the atropinized rats subjected to sympathectomy and parasympathectomy, eating caused no change in the numerical density of acinar granules but reduced the total amylase activity by 35%. 5. In the non‐atropinized rats subjected to sympathectomy alone, eating reduced the numerical density of acinar granules by 22%, while there was no change in the total amylase activity. 6. In conclusion, eating evoked a reflex activation of the sympathectomized parotid gland that engaged non‐adrenergic non‐cholinergic receptors of the acinar cells. The present results give weight to a physiological role for non‐adrenergic non‐cholinergic parasympathetic mechanisms in salivary secretion under reflex conditions.

This review examines recent concepts of gastric mucosal cell biology in relation to acid inhibition. Powerful acid-inhibitory drugs have been associated with the production of enterochromaffin-like (ECL) cell proliferation and the induction of ECL-cell carcinoids in rats. The ECL-cell lineage and its renewal is discussed, and the factors that regulate ECL-cell proliferation are reviewed. Current methods in use for assessing genotoxicity in gastric mucosa are scrutinized; the much discussed claim that antisecretory drugs induce unscheduled DNA synthesis is examined, and the methodology that is the basis for these claims is found defective and wanting. The nature of ECL-cell proliferation in rats receiving lifelong treatment with H2-receptor antagonists or acid pump inhibitors is explored, and their relationship to ECL-cell proliferation and ECL-cell carcinoids discussed. It is concluded that aged rats are very prone to developing endocrine proliferations, and this may be related to the multiple endocrine neoplasia syndrome found in humans. There is no evidence at present that long-term antisecretory therapy causes significant ECL-cell proliferation in humans.

The efficacy of and tolerance to omeprazole, 40mg/day, was studied in an open-label study in 18 patients with endoscopically verified duodenal ulcers. The effects of the drug on the oxyntic mucosa and pentagastrin-stimulated acid secretion during and after treatment were also studied. Fifteen patients completed the final endoscopy. The ulcers were healed in all after 4 weeks' treatment. Both basal and peak acid output were significantly reduced during omeprazole treatment, whereas 4 weeks after the cessation of treatment neither basal nor peak acid output differed from the pretreatment levels. Fasting serum gastrin levels rose by 56% during treatment but had returned to pretreatment values when tested again 4 weeks after the end of the treatment period. Histological examination of the biopsy specimens taken before and after treatment showed that omeprazole had no significant effect on the volume densities of either parietal or endocrine cells. We conclude that omeprazole is of value in the treatment of duodenal ulcer and that the effects of the drug on acid output and serum gastrin levels are fully reversible.

Biopsy specimens from the oxyntic mucosa were obtained on 210 occasions from 76 patients with the Zollinger-Ellison syndrome (ZES) before and during omeprazole treatment. One-micrometer sections were examined by light microscopy, and in 5% linear hyperplasia of endocrine cells was observed. Morphometry was carried out in 91 of the specimens and showed a significant increase of the mean endocrine cell density in comparison with both young, healthy subjects and patients suffering from active peptic ulcer disease (PUD). No metaplasia, dysplasia, or neoplasia was detected in patients with ZES, and the mean mucosal thickness and parietal cell density remained normal. The parietal cells often displayed endosome-like structures, and occasionally there were Ungulate cytoplasmic projections into the gland lumen. Electron microscopic morphometry was carried out in specimens from nine patients with ZES and did not show any significant differences in the parietal cells in comparison with healthy subjects.

For 2 weeks four groups of adult female rats were given daily peroral doses of 400 μmol/kg of one of the following inhibitors of gastric acid secretion: omeprazole, SCH 28080, SCH 32651, or ranitidine; additional control rats were given vehicle only. Six rats in each group were killed 2 h after the last dose and another six in each group at 48 h. Samples of the gastric corpus wall were processed for light and electron microscopy. The maximal reduction of stimulated acid secretion in parallel gastric fistula rats was 100%, 90%, 40%, and 85%, respectively. Forty-eight hours after the last dose only SCH 28080 produced significant inhibition of acid secretion. 'Vacuolation' of parietal cells was occasionally observed in paraffin sections. Such 'vacuoles', which were not found in plastic sections, probably represent dilated secretory canaliculi. A small number of lucid parietal cells - presumably in the process of desquamation - were seen in all groups of rats; their proportion was significantly higher 2h after the last dose of ranitidine, SCH 28080, or SCH 32651 than in the controls. Forty-eight hours after the last dose the proportion of such degenerating parietal cells was about the same in all groups.

Background: This study aimed at determining the turnover rate of parietal cells after inhibition of acid secretion. Methods: Rats were given omeprazole (80 μmol/kg) by gavage once daily or ranitidine (1200 μmol/kg) by osmotic minipump for 5 days. Control rats received saline only. All rats were also given 3H-thymidine by osmotic minipumps. The animals were killed, 5,14,28, or 56 days after the start of the 3H-thymidine infusion. After formaldehyde fixation by perfusion through the aorta, light microscopic autoradiography was carried out on plastic sections of the oxyntic mucosa to determine the labeling index of the parietal cells. Results: The average turnover rate in the control rats was calculated to be 0.61% per day, corresponding to a mean turnover time of 164 days. In the rats given inhibitors of acid secretion, the turnover rates did not differ significantly from those of the control group. Conclusion: Inhibition of gastric acid secretion did not significantly change the turnover rate of the parietal cells.

The appearance of the enzyme H+,K+-ATPase was studied in the gastric mucosa of rats during the perinatal period. By means of monoclonal antibodies against the enzyme, immunoreactivity was regularly detected in parietal cells 1 day before birth. The intensity of the staining and the frequency of stained cells increased up to 10-12 days after birth, when adult levels were approached. Electron microscopy showed that the initial staining occurred at the apical surface of the parietal cells, with only faint or no staining at the secretory canaliculi. From 5 days after birth immunoreactivity was observed also at the tubulovesicular membranes.

Abstract:  In some species, including man and mouse, bile salt-stimulated lipase (BSSL) in milk catalyzes the hydrolysis of triacylglycerides into glycerol and free fatty acids, a reaction that is of particular importance during suckling. The enzyme is also secreted by the pancreas (referred to as carboxyl-ester hydrolase, CEH). We wished to localize sources and storage sites for BSSL/CEH in rats, in wild-type mice, and in transgenic mice producing recombinant human BSSL in milk. Immunoreactivity against several BSSL fragments was strong in the pancreatic acinar cells and moderate in the absorptive cells of the small intestine and in salivary duct cells of the mice, as well as in rats. Sections from lactating mammary glands of mouse, but not rat, also showed immunoreactivity for BSSL; the signal was strongest in the transgenic mice. Radioactive riboprobes for BSSL mRNA hybridized on sections of rat and mouse pancreatic acinar cells, and mouse mammary glands (both wild-type and transgenic). Using RT-PCR, it was possible to amplify BSSL mRNA from wild-type mouse pancreas and mammary gland, from rat submandibular glands, and, in a few cases, from rat liver. In transgenic mice, the BSSL mRNA was highly expressed only in lactating mammary gland, but could be detected in a few other organs as well.

1. A method has been developed whereby gastric glands can be obtained from biopsies taken from the human gastric mucosa. 2. Minced pieces of the mucosa incubated with collagenase (1 mg/ml) for 2 h yielded a fraction rich in isolated glands. Shorter incubation with collagenase produced larger chunks of tissue, whereas longer incubation resulted in many free cells which were less responsive to dibutyryl-cAMP and histamine; electron microscopy revealed the presence of mucous neck cells, parietal cells, zymogen cells and endocrine cells in the glands. Most of the cells appeared normal, but some of them were vacuolized. Acid secretion in these human glands was determined by the [14C]aminopyrine accumulation technique. 3. Owing to the limited amount of starting material, only a few determinations could be made from each set of biopsies by using the regular macro-method, which normally requires approximately 15 mg dry weight of glands per incubation. To overcome this problem a micro-method was developed which permitted the sample size to be scaled down to approximately 0.1 mg dry weight; in comparison with the previously used macro-method, the glands assayed by the micro-method seemed less sensitive to the method of shaking during incubation. In the micro-method the glands also seemed more responsive to secretagogues, i.e. histamine or dibutyryl-cAMP produced a two- to three-fold increase in [14C]aminopyrine accumulation. The histamine-induced secretion in human glands was effectively inhibited by the histamine H2-receptor antagonist, cimetidine, and that of dibutyryl-cAMP by the substituted benzimidazole, timoprazole. Cholinergic stimulation in the form of carbacholine led to a small and transient response. 4. Thus human gastric glands, as studied by this micro-method, seem to reveal normal secretory properties. The method may be used to study acid secretory function of gastric glands when human gastric material is restricted, as in the case of gastroscopic biopsies.

Morphometric (strictly stereologic) methods, based on simple mathematical formulae and elementary statistical principles, permit the synthesis of quantitative models having the coordinates of three-dimensional space, of organelle, cell, and tissue structures. This provides a sounder basis than has previously been available for the detailed comparison of the results of structural investigations with those obtained by other techniques, e.g., physiology or biochemistry. After a brief outline of the methods of determining volume and area, the estimation of numbers of objects is considered in more detail. The influence of fixatives upon results and the use of correction factors for various systematic errors are discussed. A summary of the available data on various differentiated organs in steadystate is provided, with emphasis on the liver. A description of the changes of cellularity in liver during the life cycle and in response to various stimuli (e.g., hormones, nutrition pharmaceuticals, etc.) is followed by sections on cellular and organelle organization. Other organs are given a comparable treatment as far as available results permit. A comparison of models of selected phenomena (e.g., mitochondrial changes and ER biosynthesis) derived from morphometric investigations are made with equivalent models derived from other techniques, illustrating some of the advantages and difficulties of this comparative approach and emphasizing the importance of an integrated viewpoint for the understanding of cellular reaction patterns.

Omeprazole is a substituted benzimidazole which blocks gastric acid secretion by inhibiting H+K+ATPase. Radioactive omeprazole was given intravenously or orally to mice, and the distribution of the drug was investigated at various intervals by scintillation counting and by autoradiography. The half-life for radioactivity in the stomach was 14 hours versus 30-36 hours in the liver, kidneys and blood. At 16 hours after the drug was given, the radioactivity in the stomach was ten times higher than that in the liver and kidneys, and 100 times that in the blood. Whole-body autoradiography showed sustained high levels of radioactivity only in the gastric mucosa. Light microscopic autoradiographic investigations of the gastric mucosa from mice killed 1 or 16 hours after the drug was given revealed radioactivity in the parietal cells. By electron microscopy of gastric mucosa from the mouse killed 16 hours after omeprazole injection the isotope label was found mainly over the secretory surface and the tubulo-vesicles. At these locations H+K+ATPase has previously been demonstrated, and it is suggested that omeprazole - or its metabolites - binds to this enzyme.

This review examines recent concepts of gastric mucosal cell biology in relation to acid inhibition. Powerful acid-inhibitory drugs have been associated with the production of enterochromaffin-like (ECL) cell proliferation and the induction of ECL cell carcinoids in rats. The ECL cell lineage and its renewal is discussed, and the factors that regulate ECL-cell proliferation are reviewed. Current methods in use for assessing genotoxicity in gastric mucosa are scrutinized; the much discussed claim that antisecretory drugs induce unscheduled DNA synthesis is examined, and the methodology that is the basis for these claims is found defective and wanting. The nature of ECL cell proliferation in rats receiving lifelong treatment with H2-receptor antagonists or acid pump inhibitors is explored, and their relationship to ECL cell proliferation and ECL cell carcinoids discussed. It is concluded that aged rats are very prone to developing endocrine proliferations, and this may be related to the multiple endocrine neoplasia syndrome found in humans. There is no evidence at present that long-term antisecretory therapy causes significant ECL cell proliferation in humans.

Background: Helicobacter pylori is associated with peptic ulcer disease. In the present study, the influence of VacA and CagA- H. pylori on gastric ulcer healing was studied in the rat. Methods: Twenty-four rats with acetic-acid-induced gastric ulcer were divided into two groups and given either vehicle (Brucella broth) or H. pylori suspension by gavage every 12 h for 7 days. The animals were killed 1 and 8 days after the last H. pylori gavage (i.e. 10 and 17 days after the induction of the ulcer). One hour before death, 3H-thymidine was given intraperitoneally. Tissue samples from the stomach (including the ulcer area) and the duodenum were processed for determination of labelling index and apoptotic cells. Results: Compared with the vehicle-treated controls, the ulcer area in H. pylori-inoculated rats was significantly larger, the epithelial apoptotic cells in the ulcer margin and intact corpus were more numerous, while the cell proliferation of gastroduodcnal epithelium was slightly, but not significantly, increased by H. pylori gavage. Conclusion: Gastric ulcer healing was delayed after the inoculation of VacA- and CagA H. pylori in the rat, possibly as a result of excess cell loss by apoptosis.

Gastrin/CCK‐B receptors are involved in the regulation of several types of cells of the gastric mucosa, including the parietal cells, the ECL cells and the D cells. In this study, we aimed at localizing such receptors in the gastric mucosa. For this purpose, we prepared monospecific antibodies against two sequences of the canine gastrin/CCK‐B receptor. Sections of formalin‐fixed, paraffin‐embedded corpus and antrum from dog and guinea‐pig were immunostained with these antibodies. In parallel, sections were stained with antibodies against somatostatin. Staining with gastrin/CCK‐B receptor antibodies was observed in a few, small epithelial cells in the bottom part of the corpus mucosa. Immunoreactive cells of the antral mucosa were structurally similar, but more frequent. The same cells also stained with somatostatin antibodies. In addition, one of the gastrin/CCK‐B antibodies reacted with canine submucosal smooth muscle cells. No staining was observed in sections exposed to antibodies that were pre‐absorbed with the corresponding antigen. We conclude that gastrin/CCK‐B receptors are present in D cells of the gastric mucosa and in submucosal smooth muscle cells.

Helander HF. Quantitative morphological methods in intestinal research. Scand J Gastroenterol 1985, 20(suppl 112), 1-5.Measurements of intestinal length suffer from considerable errors, because of variable degrees of contraction in the longitudinal muscles. in vitro organ bath techniques may solve these problems. Villi and microvilli amplify the internal surface area; measurements of the amplification factors should be based on stereological methods. Villus height and crypt length provide information on mucosal net growth; such data might be useful when studying hypertrophic and hypotrophic conditions. More precise knowledge on cell turn-over requires autoradiographic studies of 3H-thymidine incorporation into nuclei cell. Ultimately, stereological analyses of mucosal components and cell structures will supply detailed information needed for cell biological research.

Parietal cells from rabbit gastric mucosa, enriched to >90% purity, were used to study the effect of the H+K+-ATPase inhibitor omeprazole on DNA in vitro. In this preparation, omeprazole undergoes acid-catalyzed conversion to its active form, the sulfenamide, which subsequently binds to luminal SH groups of the H+K+-ATPase and thereby inhibits acid secretion. In the parietal cell fraction the S-phase inhibitor hydroxyurea (HU) decreased [3H]thymidine uptake by 40% as measured by liquid scintillation counting (LSC), presumably due to inhibition of scheduled DNA synthesis in contaminating stem cells. In the presence of HU, irradiation with ultraviolet light (UV) or treatment with the gastric carcinogen, l-methyl-3-nitro-l-nitrosoguanidine (MNNG) increased [3H]thymidine uptake by a factor of 5. Autoradiography of isolated, stimulated parietal cells showed that UV irradiation and MNNG treatment increased the average number of silver grains over the nuclei 18-fold and 4-fold, respectively. In contrast, treatment of histamine-stimulated parietal cells with omeprazole or ranitidine in concentrations 100 times the IC50 value for inhibition of acid secretion in the parietal cells did not increase [3H]thymidine incorporation above the control levels, measured either by LSC or by autoradiography. Extracted DNA from stimulated parietal cells treated with [3H]omeprazole or [3H]MNNG showed no binding of [3H]-omeprazole but considerable binding of [3H]MNNG. It is concluded that parietal cells can undergo DNA repair, but there is no indication that omeprazole, or its acid-derived metabolites, should cause any damage to DNA, nor does it bind to DNA in its target cell, where the highest concentrations of omeprazole and its acid-derived products are found.

We report the isolation and characterization of cDNA clones for a novel isoform of lysyl hydroxylase (lysyl hydroxylase 2), a posttranslational enzyme of collagen biosynthesis. The open reading frame predicted a protein of 737 amino acids, including an amino-terminal signal peptide. The amino acid sequence has overall similarity of over 75% to the lysyl hydroxylase (lysyl hydroxylase 1) characterized earlier. This similarity is even higher in the carboxyl-terminal end of the molecules. Lysyl hydroxylase 2 contains nine cysteine residues, which are conserved in lysyl hydroxylase 1. Furthermore, the conserved histidines and aspartate residues required for lysyl hydroxylase activity are present in the sequence. Northern analysis identified a transcript of 4.2 kilobases, which was highly expressed in pancreas and muscle tissues. Expression of cDNA in insect cells using a baculovirus vector yielded proteins with lysyl hydroxylase activity and an antiserum against a synthetic peptide of the deduced amino acid sequence recognized proteins with molecular weights of 88 and 97 kDa in homogenates of the transfected cells.

Gastric mucosal homogenates from hog were fractionated by differential and density gradient centrifugation and free-flow electrophoresis. The two major membrane fractions (FI and FII) thus obtained are distinct both enzymically and in terms of transport reactivity. This heterogenicity extends to their antigenic activity. Purified antibodies which were raised against the K+-ATPase-containing H+ transport fraction FI were of two types: inhibitory and non-inhibitory. Inhibitory antibodies reduced the K+-ATPase activity by approximately 80% and the K+-p-nitro-phenylphosphatase activity by approximately 40% in a concentration-dependent manner, while the small Mg++-dependent component of the enzyme activity was unaffected. Antibodies inhibiting the K+-ATPase also inhibited H+ transport. These antibodies did not cross-react with the other major membrane fraction isolated by free-flow electrophoresis, FII, and gave a single band on rocket immunoelectrophoresis. Antibodies against this FII fraction also did not react with the K+-ATPase and were heterogeneous, giving at least four bands with rocket immunoelectrophoresis and inhibiting both the 5'-nucleotidase and Mg++-ATPase of this fraction. Immunofluorescent staining of tissue sections showed that the FI was derived from the parietal cell of gastric tissue and was localized to the supranuclear area of the cell. Staining of isolated rat gastric cell suspensions by FI antibodies confirmed the selectivity of the antibody and showed a polar, plasma membrane localization. FII antibodies also largely stained the parietal cells in tissue sections. In the 16 hog tissues tested, FI antibodies cross-reacted only with gastric fundus, thyroid and weakly with thymus. Immunoelectronmicroscopy showed that FI antibodies reacted strongly with the secretory membrane at the apical cell surface of the parietal cells and at the secretory canaliculi, weakly with the apical surface of the zymogen cell, and not with the basal-lateral surface of the cells. Thus, the protontranslocating ATPase is localized in the parietal cells and in the region postulated to be the site of acid secretion.

Parietal cell regeneration in cauterized gastric wounds was studied in rats after antrectomy (Billroth I), pyloroplasty, and truncal vagotomy with pyloroplasty. Six to eight animals in each group were killed 90 or 130 days after operation, and in each rat stereological data were obtained from electron micrographs of 15 to 20 parietal cells from the wound area, from the normal mucosa beside the wounds, and from the mucosa in unoperated controls. Antrectomy reduced parietal cell size and mucosal thickness in normal mucosa and retarded parietal cell maturation and reduced mucosal thickness in the healing wounds. Pyloroplasty slightly reduced parietal cell size in normal mucosa and retarded maturation of the parietal cells in the wounds. If truncal vagotomy was added, the reduction in parietal cell size induced by the pyloroplasty was prevented in normal mucosa.

The parietal cell occupies a unique niche among eukaryotic cells in that it develops a proton gradient of more than 4 million-fold across the membrane of the secretory canaliculus. At rest, the cell is still able to develop a proton gradient across intracellular membranes, such that the acid compartment has a pH of less than 4. Acidification depends on the simultaneous presence of ATP, K+ and Cl− as demonstrated in permeabilized cells. With acidification of the luminal side of the proton pump, there is a corresponding alkalinization of the cytosolic face as revealed by carboxyfluorescein fluorescence enhancement. Disposal of the resultant alkali depends on carbonic anhydrase activity and the functioning of a coupled Na+:H+ and Cl−: OH − antiport across the basal lateral membrane. Accordingly, with secretion there is an increased cellular Cl− level, which is exported across the apical membrane in association with K+. The Na+ pump dependent secretion of KCl across this membrane is one of the major sites of regulation of acid secretion since K+ is required at the luminal face of the gastric ATPase. Membranes isolated from secreting tissue contain a KC1 permeation pathway largely absent from membranes isolated from resting tissue. The pump itself acts as an H+ for K+ exchange ATPase which is most probably composed of at least two peptides of 100000Mr. That catalytic cycle consists of formation and breakdown of a covalent aspartyl phosphate. Formation of the intermediate depends on loss of K+ from cytosolic binding sites, and breakdown of the intermediate depends on K+ binding to the luminal face of the enzyme. During breakdown, an acid labile E P is formed, and, at high ATP concentrations, loss of this form of the enzyme is probably the rate limiting step.

Mouse thyroids were preserved for electron microscopy by means of freeze-drying. The tissue specimens were frozen in liquid isopentane, dried at a temperature of -79° C to a pressure of 4×10-5 mm Hg, stained in vacuo with osmium tetroxide vapour at room temperature, and embedded in vacuo in Epon or Vestopal W.

Radioactively labeled lipids were administered intragastrically to 10-day-old rats. To prevent further passage of the lipids, the pylorus was ligated. A decrease in the radioactivity in gastric contents gastric walls with time, or an appearance of radioactive carbon dioxide in the expiratory air was taken as proof of net absorption of the lipids. The results show that medium-chain fatty acids are readily absorbed through the gastric mucosa of suckling rats and are utilized in the body. The net absorption of long-chain fatty acids is much less. Triglycerides, partial glycerides, cholesterol, and cholesterol esters are poorly absorbed. The uptake of medium-chain fatty acids probably occurs by diffusion.

Antral exclusion was performed in seven adult male Sprague-Dawley rats, which were killed 10 weeks later. Fasting serum gastrin concentrations were almost four times higher than in unoperated controls. There was a slight increase in the thickness of the gastric mucosa, but quantitative electron microscopy showed no significant changes in parietal cells.

Following surgery newborn rats are often eaten by their mothers. This can be avoided if the wound is closed carefully, the blood removed from the skin, and the wound area covered by a plastic film.