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Hydrochloric acid was instilled into the bronchial tree in anaesthetized dogs. A severe respiratory acidosis resulted. The metabolic component of acid-base balance was little affected.
Human adult and umbilical cord-derived leukocytes were shown to be capable of generating tissue factor activity on exposure to endotoxin and to reduced pH. Blood for leukocyte separation was collected from normal adults and from newly delivered sections of umbilical cord and mixed leukocyte preparations were obtained by separation over methyl cellulose Hypaque. The coagulant activity of the cell suspension was assayed using a one-stage or two-stage method. Cord-derived leukocytes were shown to develop greater coagulant activity than adult-derived leukocytes when stimulated by endotoxin in vitro at 2,000 cells/mm-3. This response to endotoxin was partially inhibited by prior exposure of the cells to prostaglandin (PG) E1 an to L-epinephrine. Acetylcholine stimulated the production of coagulant activity in the absence of endotoxin. Both cord and adult-derived leukocytes (20,000/mm-3) developed coagulant activity when exposed to pH reduction by lactic or hydrochloric acids and this activity was shown to be tissue factor.
Systemic hypotension during sepsis is thought to be due to nitric oxide (NO) overproduction, but it may also be due to acidosis. We evaluated in healthy rats the consequences of acid infusion on NO and blood pressure. Sprague-Dawley rats were anesthetized, and ventilated with room air. The animals were randomized into four groups. Group 1 (C, n = 10) received only normal saline at rates comparable to the other groups. Group 2 (A1, n = 10) received hydrochloric acid at 0.162 mmol in the first 15 to 30 min, followed by a continuous infusion of 0.058 mmol/h for 5 h. Group 3 (AG+A1, n = 6) was pretreated with aminoguanidine (AG, 50 mg/kg), and HCl was infused as above. Group 4 (A2, n = 7) received HCl at twice the rate used in A1. Nitric oxide concentration in the exhaled gas (ENO), blood gases, and mean arterial pressure were measured every 30 min. Acid infusion in A1 caused the pH to fall gradually from 7.43 +/- 0. 01 to 7.13 +/- 0.05. This moderate decrease in pH was associated with a marked increase in ENO (1.6 +/- 0.3 to 114.2 +/- 22.3 ppb), an increase in plasma nitrite/nitrate (17.3 +/- 3.7 to 35.2 +/- 4.3 microM), and a significant decrease in blood pressure (110.5 +/- 6.3 to 63.3 +/- 15.0 mm Hg). Furthermore, acidosis caused lung inflammation, as suggested by the increase in lung myeloperoxidase activity (282.2 +/- 24.7 to 679.3 +/- 57.3 U/min/g) and lung injury score (1.7 +/- 0.2 to 3.5 +/- 0.6). Acidosis after AG pretreatment was associated with a similar change in pH, but the increase in ENO, nitrite/nitrate, and systemic hypotension were prevented. Furthermore, lung injury was attenuated by AG, as suggested by a lower myeloperoxidase activity, though lung injury score was not altered. In this model, moderate acidosis causes increases in NO, hypotension, and lung inflammation. Lung inflammation and injury are due in part to acidosis and NO production. This is the first report to show a direct effect of chronic acidosis on NO production and lung injury. These results have profound implications on the role of acidosis on NO production and lung injury during sepsis.
The newly developed fluoride-releasing sealant (F + sealant) used in this experiment is expected to have the combined cariostatic effects of a sealant and fluoride. The purpose of this study was to investigate F + sealant's effects on the enamel in regard to the uptake of fluoride and resistance to acid. F + sealant's effect was compared to that of acid phosphate fluoride (APF) which has effect as topical fluoride applicant. Bovine teeth applied with F + sealant or APF were immersed for 4 weeks in a pH 7.0 phosphate buffer at 37 degrees C. After 4 weeks of immersion, each tooth was biopsied with pH 1.0 sodium acetate-hydrochloric acid buffer. The fluoride and calcium in the biopsy samples were analyzed by means of fluoride ion electrode and atomic absorption spectroscopy, respectively. The following results were obtained: (1) The fluoride in the enamel was significantly increased by the incorporation of fluoride from the F + sealant. Almost all fluoride in the surface enamel was found to be fluorapatite by the method of alkaline extraction. (2) The amount of fluoride increased by APF application was about 50% of that of F + sealant application. (3) The calcium released from the enamel treated with F + sealant or APF decreased by 13% and 9%, respectively, compared to that without treatment.
The corrosion layer on steel surfaces that formed after exposure to waste isolation pilot plant (WIPP) brines under anoxic conditions was characterized for chemical composition, thickness and phase composition. The chemical composition of the corrosion layer was determined both by X-ray photoelectron spectroscopy (XPS) and by chemical analysis of acid solutions used to remove the corrosion layer. Atomic force microscopic (AFM) images indicated that the brine-corroded surface layer shows extensive granulation along the contours of the steel surface that is characteristic of sharp polishing marks. The corrosion layer seemed to be porous and could be dissolved and detached in dilute hydrochloric acid. The corrosion layer appears to be composed of iron oxides with some ionic substitutions from the brines. The 77 K Mössbauer spectrum recorded for iron powder leached under similar conditions indicated the corrosion layer was comprised principally of green rust.
OBJECTIVE: Extensive corrosive injury involving the structures beyond the pylorus caused by ingestion of strong acid has a poor prognosis. We reviewed six cases of patients who underwent total upper gastrointestinal tract ablation to see the effect of this extensive procedure for such an injury. DESIGN: Case series. SETTING: Tertiary care center. PATIENTS: Six patients who ingested more than 250 mL of 20N hydrochloric acid were treated in the Department of Surgery, Chang Gung Memorial Hospital, Taipei, Taiwan, Republic of China, from 1986 to 1992. RESULTS: Three patients with preoperative metabolic acidosis and renal failure died of multiple organ failure within the first postoperative month. The other three patients survived the acute stage. While being readied for a late reconstructive procedure, sepsis developed in one patient due to cholecystostomy leakage about 1 year postoperatively. Another patient died of respiratory failure after development of aspiration pneumonia due to poor drainage of a spit fistula, after surviving for 6 months. Only one patient had a good recovery following a full reconstruction procedure and restoration of the continuity of the gastrointestinal tract. CONCLUSIONS: Three of six patients died in the hospital. The risk factors were preoperative metabolic acidosis, renal failure, and an upper jejunal resection greater than 100 cm in length. Early and aggressive approaches to resect all the necrotic tissue certainly provide good chances to survive the acute stage and later reconstruction.
1. Incorporation of [(14)C]leucine into protein by isolated rat liver mitochondria was examined by using incubation media similar to those used by Sandell, Löw & Decken (1967) (medium A) and Roodyn, Reis & Work (1961) (medium B). The incorporation process was found to be almost completely inhibited in medium A. 2. By decreasing the amount of sucrose and omitting tris-hydrochloric acid from medium A, incorporation proceeded at a rate higher than that found in medium B. It was found that the inhibitory action of medium A was due to its high osmolarity. 3. Oxidative phosphorylation and RNA synthesis by the isolated mitochondria proceeded at the same rate in media essentially the same as media A and B. 4. There was a partial inhibitory action of medium A on leucine uptake by the mitochondria and also on the formation of leucyl-transfer-RNA. The major block of inhibition by the hyperosmolarity of medium A seemed to be located at a later step of protein synthesis involving mitochondrial ribosomes. 5. Protein synthesis by Escherichia coli B was only slightly inhibited, if at all, in hyperosmotic media in which protein synthesis by isolated mitochondria was completely stopped.
The number and severity of gastric stress ulcers (= ulcer index) in rats caused by the restraint technique can be reduced by instilling water, hydrochloric acid or Ringer solution intraduodenally during the stress period. This effect is not caused by lower gastric acid, lower blood gastrin and glucagon and most likely not by an improved gastric mucosal microcirculation.
Mottling of teeth can have significant psychological impact on patients--particularly on adolescents, who may be subjected to much unkind teasing. A number of procedures have been suggested for removal of mottling and stains. The authors describe a simple and quick technique using a paste of hydrochloric acid and pumice, and on the basis of their clinical and laboratory experience suggest it as a treatment of first choice.
1. A radio-immunoassay for gastrin has been developed using partially purified porcine gastrin to raise antibodies and highly purified natural porcine gastrin I for radio-iodination with (125)I. The separation of antibody-bound from free hormone was performed by a double-antibody method.2. In this assay highly purified natural porcine gastrin I, synthetic human gastrin I, radio-iodinated porcine gastrin I, gastrin in the plasma of a healthy volunteer, a patient with pernicious anaemia and another patient with the Zollinger-Ellison syndrome were immunologically identical.3. The fasting plasma gastrin concentration of fourteen gastric ulcer patients was significantly higher than that of the 113 hospital controls with no history of gastro-intestinal disease, while twenty-seven duodenal ulcer patients had gastrin levels within the normal range.4. Plasma gastrin concentration was significantly elevated in pernicious anaemia (fifty-one patients), achlorhydria (thirty-three patients), hypochlorhydria (eleven patients) and in nine patients with histologically proven Zollinger-Ellison syndrome.5. In human volunteers a protein meal stimulated endogenous gastrin release while a carbohydrate meal did not. Atropine sulphate I.M., and hydrochloric acid orally, produced a significant fall in the level of circulating gastrin.
Information on compatibility of nutrients and drugs with parenteral nutrient (PN) solutions is reviewed and evaluated. Precipitation of calcium phosphate when calcium and phosphate salts are added can be affected by pH, amino acid concentration, amino acid product, temperature, sequence of additives, specific salt used, and time since admixture; precipitate formation can occur gradually over 24 hours. Insulin is chemically stable in PN solutions, but adsorption to the infusion system can cause decreased availability. Poor delivery of vitamin A via PN solutions has been reported. The sodium bisulfite content of amino acid injections may cause degradation of thiamine, but studies simulating clinical use are needed. Folic acid stability in PN solutions has been demonstrated, and phytonadione appears to be stable. Drug administration via PN solutions may be advantageous when fluid intake is restricted or peripheral vein access is limited and in home PN therapy. Summarized are results of studies involving heparin, cimetidine hydrochloride, aminophylline, amphotericin B, iron dextran, hydrochloric acid, corticosteroids, narcotics, metoclopramide, digoxin, and fluorouracil. Many antibiotics are probably stable, especially when administered by co-infusion rather than by direct mixture in the PN solution container. When lipids are mixed in the same container with amino acid-dextrose solutions, compatibility and stability of electrolytes, vitamins, and trace elements must be reassessed. Practical research is needed, and availability of additives should be studied in specific patient populations and for specific PN formulations. Valid conclusions are dependent on careful study design.
OBJECTIVES: To examine the role of complement in the development of acid aspiration-induced lung injury in the rat. It was postulated that inhibition or depletion of complement attenuates aspiration-induced lung injury. DESIGN: Controlled animal trial. SETTING: Animal Laboratory, Jefferson Medical College, Philadelphia, PA. SUBJECTS: Anesthetized rats. INTERVENTIONS: Aspiration was induced by the intratracheal administration of 0.2 mL of 0.1 N hydrochloric acid (n = 7) and lung injury was evaluated by determining water content, myeloperoxidase activity, protein concentration, and leukocyte count in bronchoalveolar lavage fluid. Muscle PO2 was directly measured using a thin-film chamber oxygen sensor and serum tumor necrosis factor-alpha was assayed by enzyme-linked immunosorbent assay. The effect of complement inhibition by recombinant human soluble complement receptor type 1 (n = 8) or complement depletion by cobra venom factor (n = 7) on lung injury was evaluated. MEASUREMENTS AND MAIN RESULTS: Acid aspiration induced pulmonary leukosequestration, edema, and a microvascular permeability defect, along with tissue hypoxia. Pretreatment with soluble complement receptor type 1 (complement inhibition) or cobra venom factor (complement depletion) significantly reduced lung edema (-61 +/- 7%; p < .05), eliminated protein accumulation in bronchoalveolar lavage fluid (p < .01), and improved (p < .05) tissue oxygenation. In contrast, there was no effect of soluble complement receptor type 1 or of cobra venom factor on leukosequestration. CONCLUSIONS: Acid aspiration induces lung injury through a complement-dependent mechanism that leads to microvascular permeability defects. Therefore, the possibility that complement inhibitors may have a salutary effect in humans with aspiration-induced lung injury should be investigated.
Insulin is stored in pancreatic islets as a zinc-insulin complex, and stimulating the islets results in the release of insulin and zinc. Simulant pancreatic islet beads have been developed using agarose beads (50-250 micro m diameter) derivatized with iminodiacetic acid that have been loaded with zinc. A qualitative comparison of the simulant beads with pancreatic islets has been made by staining with dithizone and a zinc-binding fluorescent dye, TSQ. The binding capacity of simulant beads was determined to be 34 micro mol Zn(2+)/g of dried beads using anodic stripping voltammetry. Hydrochloric acid was used to release zinc from beads to mimic the secretion of insulin from pancreatic islets and a release profile was established. The simulant beads can be used to optimize the islet isolation process and reduce the use of real islets in method development.
A major aim of the present study was to investigate whether exposing the jejunal mucosa to a noxious stimulus induces a net fluid secretion by activating the enteric nervous system (ENS) and, if so, to what extent an axon reflex was involved. Net fluid transport was measured in vivo with a gravimetric method. The intestinal mucosa was exposed to an isotonic solution with an unphysiologically low pH (1.0). This evoked a fluid secretion, which was markedly attenuated by giving hexamethonium (nicotinic receptor antagonist) i.v. or exposing the intestinal serosa to lidocaine (local anaesthetic). Atropine (muscarinic receptor antagonist) had no effect. Luminal acid evoked a fluid secretion of the same magnitude in acutely denervated segments and in segments denervated about 3 weeks prior to the experiments. Luminal capsaicin (1.6-16 mM) did not influence jejunal net fluid transport. A second aim of the study is to investigate the effect of nifedipine (Ca channel blocker of L-type) on the acid-induced fluid secretion. Nifedipine markedly attenuated acid-induced fluid secretion. In contrast to cholera toxin-evoked secretion, the nifedipine effect was not mediated via 5 hydroxytryptamine (5-HT) as judged by measurements of 5-HT release into the intestinal lumen and the lack of effect of granisetron (5-HT3 receptor antagonist). It is concluded that the net fluid secretion evoked by hydrochloric acid in the small intestine is mainly mediated via an intramural reflex in the ENS. No experimental evidence was obtained for the involvement of an axon reflex. The site of action of the calcium channel blocker is tentatively discussed.
Decreased acid clearance and increased exposure to acid of the duodenum have been reported in a subset of functional dyspepsia patients. However, the mechanism by which increased duodenal acid exposure may affect symptoms is unclear. The aim of the present study was to investigate the effects of duodenal acidification on proximal gastric tone and mechanosensitivity in humans. An infusion tube with a pH electrode attached was positioned in the second part of the duodenum, and a barostat bag was located in the gastric fundus. In 12 healthy subjects, fundic tone and sensitivity to distensions were assessed before and during duodenal infusion of 0.1 N hydrochloric acid or saline in a randomized, double-blind design. In 10 healthy subjects, meal-induced accommodation was measured during duodenal infusion of acid or saline. Acid infusion in the duodenum significantly increased fundic compliance and decreased fasting fundic tone. This was accompanied by a significant decrease in the pressures and the corresponding wall tensions at the thresholds for discomfort. During infusion of acid, significantly higher perception and symptom scores were obtained for the same distending pressures. The meal-induced fundic relaxation was significantly smaller during acid infusion compared with saline infusion. In conclusion, duodenal acidification induces proximal gastric relaxation, increases sensitivity to gastric distension, and inhibits gastric accommodation to a meal. Through these mechanisms, increased duodenal acid exposure may be involved in the pathogenesis of dyspeptic symptoms.
Significant progress has been made in recent years in the development of new bone resorption markers, based principally on the urinary excretion of pyridinoline (Pyd) and deoxypyridinoline (Dpd) crosslinks. For their measurement, in spite of the recent development of immunoassays, HPLC remains the method of reference. However, the lack of an appropriate internal standard requires large amounts of pure crosslinks for external standardisation. Herein, we describe an efficient method for the isolation of both crosslinks from bone of adult turkey by isocratic semi-preparative HPLC. Demineralized bone is hydrolysed in hydrochloric acid, 9 M. A first liquid extraction step in butanol allowed to eliminate less polar compounds. The aqueous phase was concentrated and separated by gel filtration on Biogel P2 and eluted by acetic acid solution (10%). Fractions containing pyridinoline were pooled, concentrated, and purified on a CF1 cellulose column. Pyd and Dpd crosslinks were then separated isocratically by HPLC on a C18 reversed phase column (Vydac 218 TP 1010, 250x10 mm) and eluted with HFBA as the ion-pairing agent. Retention times of Pyd and DPD were 23.6 and 28.7 min, respectively. Both crosslinks prepared by HPLC were then transformed as hydrochloride to cellulose phosphate and desalted on Sephadex G-10 columns. These two further steps yielded highly purified compounds (the purity was greater than 98% evaluated by aminoacid analysis). In conclusion, the efficiency of this method allows to obtain rapidly Pyd and Dpd without interfering compounds as proven by spectral studies (NMR and mass spectroscopy).
Treatment of the secoiridoids oleuropein (4), ligstroside (5) and methyloleoside (6) by beta-D-glucosidase in the presence of ammonium chloride led exclusively to monomeric pyridine alkaloids 7, 1, and 8. Dimeric 3,4,5-trisubstituted pyridines were obtained from methyloleoside (6) when ammonium chloride was generated in the reaction mixture by successive additions of ammonia and hydrochloric acid. The use of ammonium acetate permitted conversion of secoiridoids 4 and 5 into the naphthyridine alkaloid jasminine (3).
1. An increase in motor activity of transplanted fundic pouches can be produced repeatedly by an alkaline buffer solution in the duodenum.2. The response can be abolished by small doses of a cholecystokinin-pancreozymin extract.3. The secretagogues, olive oil and peptone will inhibit the response when introduced into the duodenum.4. Acetylcholine in the duodenum will also inhibit the effect.5. Hydrochloric acid will inhibit the motor activity produced by alkaline buffer in the duodenum and also resting activity of the pouches.