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PubMed1970

Acidosis and hypercalciuria: renal mechanisms affecting calcium, magnesium and sodium excretion in the sheep.

1. Observations were made on the excretion of calcium and magnesium by the sheep's kidney following manipulation of the acid-base status.2. Intravascular administration of a synthetic solution resembling saliva abolished the naturally occurring acidosis in sheep during feeding, and it also prevented the normal onset of post-prandial hypercalciuria and hypermagnesiuria.3. Non-respiratory acidosis (induced by infusion of hydrochloric acid) and respiratory acidosis arising from inhalation of 6% (v/v) CO(2) in air both caused an acute increase in calcium excretion.4. Measurement of filtered loads showed that feeding exerted an effect on the functional characteristics of the sheep's kidney. The renal clearances of calcium and magnesium increased, whereas sodium clearance decreased.5. Experimental conditions were arranged so that variations in acid-base status could be imposed at a time when the filtered load of calcium was declining.6. With hydrochloric acid-acidosis the renal excretion of calcium increased, despite a steady fall in the filtered load. With sodium bicarbonate alkalosis, the filtered load and the renal excretion of calcium decreased in unison.7. These variations in calcium excretion were not accompanied by corresponding changes in the excretion of sodium.8. It is concluded that the renal tubules in the sheep are sensitive to acid-base status and that they respond to a lowering of the blood pH by decreasing the tubular reabsorption of filtered calcium.

Acid-Base Equilibrium↗
PubMed1989

Acid induced duodenal ulcer pain: the influence of symptom status and the effect of an antispasmodic.

The aims of this study were to determine whether the development of acid induced duodenal ulcer pain was influenced by the symptomatic status of the patient and whether the administration of an antispasmodic could abolish pain. One hundred millilitres of 0.1 N hydrochloric acid was infused onto the ulcer craters or scars of 143 duodenal ulcer patients on 168 occasions. Symptomatic patients were randomised to receive 40 mg of hyoscine intravenously before acid infusion, or to a control group. Typical ulcer pain developed in seven of 55 (13%) instances for non-symptomatic patients, 24/57 (42%) of control symptomatic patients, and 20/56 (36%) of symptomatic patients given hyoscine. (Asymptomatic group v control symptomatic group, p less than 0.005; control symptomatic group v hyoscine group, NS - 95% confidence limits 12% in favour of the control and 24% in favour of the hyoscine group). The results suggest that acid infusion seldom reproduces ulcer pain in non-symptomatic duodenal ulcer patients and that the pathogenesis of acid induced duodenal ulcer pain probably involves a mechanism other than spasm, as pain was not prevented by an anticholinergic.

Adolescent↗
PubMed1988

Studies of the oesophageal clearance responses to intraluminal acid.

Contraction of the upper oesophageal sphincter combined with secondary peristalsis clears the oesophagus of refluxed gastric contents and protects the trachea, but the nature of these reflex stimuli remains controversial. Secondary peristaltic and sphincteric responses were measured during intraluminal infusion of 0.1 N hydrochloric acid and equiosmolar saline solutions in seven normal volunteers. Responses to a single volume infused at varying sites in the oesophagus and to progressively increasing volumes of test solution were measured. In addition oesophageal responses to similar degrees of distension induced by inflation of an intraluminal balloon were also recorded. The sphincteric responses to both stimuli were similar, decreasing in value with distance from the sphincter from values of 70 (68-85) mmHg (median (range] for HCl; and 70 (55-85) mmHg for NaCl at 5 cm below the sphincter to 40 (30-60) mmHg for both HCl and NaCl at 20 cm. As the volume of the solution infused into the proximal oesophagus was increased, the sphincter pressure also rose from a median basal value of 30 (25-50) mmHg to 40 (30-50) mmHg for HCl and NaCl after 1 ml, while after 7 ml infusion, the responses were greater, 65 (45-85) mmHg for HCl, and 60 (45-80) mmHg for NaCl. In the more distal oesophagus, responses were qualitatively similar but quantitatively smaller than proximally, being 30 (25-40) mmHg for HCl and 30 (25-50) mmHg for NaCl following 1 ml and 45 (40-55) mmHg for HCl and NaCl after 7 ml. Secondary peristalsis was also induced equally by both solutions and varied with volumes infused and site of infusion in a manner similar to the sphincter responses. After a 7 ml/min acid infusion 14 (1- 40) secondary contractions/three min were recorded at 5 cm and eight (2 - 18)/three min were recorded at 20 cm. Values for saline were similar, 13 (1- 38)/three min at 5 cm and eight (4 - 25)/three min at 20 cm. Oesophageal distension by a balloon positioned 10 cm below the sphincter induced identical clearance responses to those seen after similar volumes of either acid or saline infused at the same site. These results suggest that the principal stimulus for upper oesophageal clearance is intraluminal distension and do not support the idea that the oesophagus is pH sensitive.

Adult↗
PubMed2002

Acid aspiration induces bacterial pneumonia by enhanced bacterial adherence in mice.

The issue of whether acid aspiration facilitates bacterial pneumonia caused by Pseudomonas aeruginosa by enhanced bacterial adherence was examined in mice. Survival or the number of bacteria in lung tissues was evaluated after an intratracheal challenge of hydrochloric acid (HCl), a sublethal dose of P. aeruginosa, or both in mice. Bacterial adherence to the tracheal epithelium after acid aspiration was also examined by scanning electron microscopy. A simultaneous intratracheal challenge of 50 microl of 10(-1) N HCl, but not 10(-2) to 10(-4) N HCl, combined with a sublethal dose of P. aeruginosa significantly increased the number of bacteria in the lung tissues and decreased survival, while all mice that received either HCl or P. aeruginosa survived. Significantly higher numbers of adherent bacteria on the tracheal epithelium were found in mice that received 10(-1)N HCl, compared with mice that received HCl (10(-2) to 10(-4) N) or saline. These data indicate that acid aspiration induced airway epithelial injury and enhanced P. aeruginosa adherence to the epithelium, and led to the subsequent development of bacterial pneumonia in mice. Enhanced bacterial adherence on the acid-injured epithelium may explain fatal bacterial pneumonias in patients with respiratory aspiration of gastric contents.

Animals↗
PubMed1985

Regulation of acid-base equilibrium in chronic hypercapnia.

Previous studies from this laboratory have demonstrated that the decreased renal bicarbonate reabsorption prevailing during chronic hypocapnia is not mediated by the alkalemia that normally accompanies this acid-base disturbance but by some direct consequence of the change in PaCO2 itself. Based on the reasonable expectation that the mechanisms underlying the kidney's response to primary respiratory disturbances would be similar over the entire spectrum of physiologic carbon dioxide tensions, the present study was designed to assess whether an acidic change in systemic pH is a critical factor in the renal response to chronic hypercapnia. For this purpose, the plasma and renal responses to chronic respiratory acidosis in normal dogs were compared to those in dogs chronically fed a large hydrochloric acid (HCl) load (7 mmoles/kg/day). Exposure to 6% carbon dioxide for 7 days in a large environmental chamber induced a stable increment in PaCO2 which averaged 17 +/- 0.5 and 22 +/- 1.3 mm Hg in normal and HCl-fed animals, respectively. Steady-state plasma bicarbonate concentration rose from 22.0 +/- 0.4 to 27.1 +/- 0.5 mEq/liter in normals and from 14.7 +/- 0.7 to 24.2 +/- 0.8 mEq/liter in the HCl-fed group. As a result of these changes in PaCO2 and plasma bicarbonate, steady-state plasma hydrogen ion concentration rose in normals from 41 +/- 0.8 to 49 +/- 0.9 nEq/liter (pH 7.39 +/- 0.01 vs. 7.31 +/- 0.01) but did not change significantly in the HCl-fed group (55 +/- 1.4 vs. 56 +/- 1.4 nEq/liter; pH 7.26 +/- 0.01 vs. 7.25 +/- 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed2005

Acid and particulate-induced aspiration lung injury in mice: importance of MCP-1.

A model of aspiration lung injury was developed in WT C57BL/6 mice to exploit genetically modified animals on this background, i.e., MCP-1(-/-) mice. Mice were given intratracheal hydrochloric acid (ACID, pH 1.25), small nonacidified gastric particles (SNAP), or combined acid plus small gastric particles (CASP). As reported previously in rats, lung injury in WT mice was most severe for "two-hit" aspiration from CASP (40 mg/ml particulates) based on the levels of albumin, leukocytes, TNF-alpha, IL-1beta, IL-6, MCP-1, KC, and MIP-2 in bronchoalveolar lavage (BAL) at 5, 24, and 48 h. MCP-1(-/-) mice given 40 mg/ml CASP had significantly decreased survival compared with WT mice (32% vs. 80% survival at 24 h and 0% vs. 72% survival at 48 h). MCP-1(-/-) mice also had decreased survival compared with WT mice for CASP aspirates containing reduced particulate doses of 10-20 mg/ml. MCP-1(-/-) mice given 5 mg/ml CASP had survival similar to WT mice given 40 mg/ml CASP. MCP-1(-/-) mice also had differing responses from WT mice for several inflammatory mediators in BAL (KC or IL-6 depending on the particle dose of CASP and time of injury). Histopathology of WT mice with CASP (40 mg particles/ml) showed microscopic areas of compartmentalization with prominent granuloma formation by 24 h, whereas lung tissue from MCP-1(-/-) mice had severe diffuse pneumonia without granulomas. These results indicate that MCP-1 is important for survival in murine aspiration pneumonitis and appears to act partly to protect uninjured lung regions by promoting isolation and compartmentalization of tissue with active inflammation.

Animals↗
PubMed2005

The effect of chemical stimulation of esophageal mucosa on citric acid induced cough and specific airway resistance in guinea pig.

BACKGROUND: Gastroesophageal reflux disease is one of the most common causes of chronic cough. The mechanism of the cough initiation in these patients remains unresolved. OBJECTIVES: This study was designed to investigate the effect of intraesophageal (IE) administration of capsaicin on cough and specific airway resistance (Saw) in guinea pigs. METHODS: Male TRIK strain guinea pigs were used. In the first experiment 12 controls received IE saline, 9 animals (group 1) received IE capsaicin (400 microM, 0.2 ml) and 12 guinea pigs (group 2) received IE capsaicin (400 microM, 0.2 ml) 24 hours after IE administration of hydrochloric acid (3 M, 0.2 ml). Cough induced by inhalation of citric acid (CA) and Saw was determined after IE administration of saline in controls and capsaicin in groups 1 a 2. In the second experiment, CA induced cough was determined in guinea pigs (n=13) in the beginning of the study (control response), after NaOH (1 M, 0.2 ml) was administered IE. One week later in conditions of corrosive esophagitis CA induced cough was determined after IE administration of capsaicin (cough during esophageal stimulation). RESULTS: There was no difference in CA induced cough between controls, group 1 and 2 (p=0.98). Saw was hot affected by IE capsaicin stimulation and CA inhalation in group 1 and group 2. There was no difference found between control cough response and those induced after IE capsaicin in animals with corrosive esophagitis (p=0.75). CONCLUSION: Esophageal stimulation with capsaicin did not trigger and/or modulate CA induced cough and Saw in guinea pigs models. (Fig. 5, Ref. 22.)

Airway Resistance↗
PubMedDate not supplied

Interference in the quantitation of methylated arsenic species in human urine.

The aim of this paper is to report on the presence of chemical interferences in the quantitation of methylated arsenic species in human urine when using a method based on selective volatile arsine species generation, chromatographic separation, and hydride generation atomic absorption spectrometry (HGAAS) detection. An abnormal profile of methylated arsenic species characterized by the absence of the peak corresponding to dimethylarsinic acid (DMA) was observed in urine from some individuals exposed to arsenic via drinking water and living in rural communities of northwestern Argentina. The absence of this peak persisted even after the addition of known amounts of DMA to the samples. However, the DMA peak appeared after urine digestion with hydrochloric acid (2M). Samples showing interferences were provided by individuals who had mate consumption and coca-leaf chewing habits. Because the relative proportions of methylated arsenic species present in urine have been used to evaluate the efficiency of the methylation process, interferences in the formation or detection of methylarsines may cause underestimation of As exposure and also lead to erroneous conclusions about relative biomethylation efficiencies. Therefore, we recommend that urine samples should be digested with 2M HCl before performing speciation analysis using HGAA techniques. Further studies on the impact of this type of interferences on other arsenic speciation methods are also required.

Adolescent↗
PubMed1985

Oesophageal stimulation lowers exertional angina threshold.

The effect of oesophageal stimulation with acid on the exertional angina threshold was examined in 12 subjects. Each walked until the angina threshold was reached on four successive occasions; during two tests the oesophagus was instilled with 0.1 mol/l hydrochloric acid and during the other two with physiological saline. Oesophageal instillation was carried out for 20 min at rest before each walk. In 10 patients the angina point was reached after walking a significantly shorter distance on the treadmill when acid was instilled than when the saline was instilled. ST-segment changes and rate-pressure product were not significantly different during the acid and saline tests. The mechanism responsible for the reduction of angina threshold is not known. However, the effect was more pronounced in the 6 patients who had experienced regular oesophageal symptoms than in those who had not. Ischaemic heart disease and gastro-oesophageal reflux are both common, and the possibility that acid reflux may aggravate angina should be borne in mind, particularly when oesophageal symptoms are present.

Adult↗
PubMed1981

Studies on the hygiene of drinking water for laboratory animals. 1. The effect of various treatments on bacterial contamination.

Daily autoclaving of drinking-water bottles or daily replacement of their contents resulted in drinking water hygienically acceptable for laboratory rats. However, daily autoclaving of the bottles imposes an additional workload which many institutions cannot afford. The daily replacement of the drinking water is not desirable, since with the usual routines it is virtually impossible to guarantee a bottle is returned to the same cage. A reliable method of preventing bacterial growth for more then 1-2 days in the drinking water of conventional laboratory rats is its acidification with hydrochloric acid to pH 2.3-2.5.

Animals↗
PubMed2006

Hyperchloremic acidosis increases circulating inflammatory molecules in experimental sepsis.

RATIONALE: Hyperchloremic acidosis is common in the critically ill and is often iatrogenic. We have previously shown that hyperchloremic acidosis increases nuclear factor-kappaB DNA binding in lipopolysaccharide-stimulated RAW 264.7 cells. However, evidence that hyperchloremic acidosis leads to increased inflammation in vivo has been limited to nitric oxide. OBJECTIVES: To determine if acidosis, induced by dilute hydrochloric acid (HCl) infusion, will increase circulating inflammatory mediator levels in an experimental model of severe sepsis in rats. METHODS: Eighteen hours after inducing lethal sepsis by cecal ligation and puncture in 20 adult, male, Sprague-Dawley rats, we randomized animals into three groups. In groups 2 and 3, we began an IV infusion of 0.1 N HCl to reduce the standard base excess (SBE) by 5 to 10 mEq/L and 10 to 15 mEq/L, respectively. In group 1, we infused a similar volume of lactated Ringer solution. In all groups infusion continued 8 h or until the animal died. MEASUREMENTS AND MAIN RESULTS: We measured arterial blood gases, whole-blood lactate, and chloride, tumor necrosis factor (TNF), interleukin (IL)-6, and IL-10 levels at 0 h, 4 h, and 8 h. All measured cytokines increased over time. Compared to group 1, animals in groups 2 and 3 exhibited greater increase in all three cytokines, with the greatest increases seen with severe acidosis. CONCLUSION: Moderate (SBE, - 5 to - 10) and severe (SBE, - 10 to - 15) acidosis, induced by HCl infusion, increases circulating levels of IL-6, IL-10, and TNF in normotensive septic rats.

Acid-Base Equilibrium↗
PubMed2003

Barrett's esophagus evokes a quantitatively and qualitatively altered response to both acid and hypertonic solutions.

OBJECTIVE: The stomach contents become hypertonic after a meal and provide esophageal refluxate that is both acidic and hypertonic. This study examined the symptomatic response to esophageal exposure to hypertonic and acidic solutions in patients with gastroesophageal reflux disease (GERD) and Barrett's esophagus. METHODS: Symptom intensity and character were measured in double-blind fashion during esophageal instillation of water, hypertonic saline (osmolality 1030 mOsm/kg), hydrochloric acid (pH 1 and 2.5), and acidified hypertonic saline (pH 1 and 2.5). The studies were performed in healthy controls and GERD patients with and without Barrett's esophagus. RESULTS: The GERD patients with Barrett's differed from the non-Barrett's GERD patients in being less sensitive to acid (mean intensity score, 2.3 vs 4.8, p < 0.05), more sensitive to hypertonic saline (1.3 vs 0.4, p < 0.05) and by showing an additive effect when the acid and hypertonic solutions were combined, resulting in similar scores in the two patient groups to the combination (4.4 vs 4.3). The frequency of nausea was higher in the Barrett's group compared to the other GERD patients after hypertonic saline (21% vs 0%, p < 0.05), acid (50% vs 21%, p < 0.05) and the acid hypertonic combination (71% vs 29%, p < 0.05). CONCLUSIONS: Barrett's mucosa is associated with reduced symptomatic response to acid, increased response to hypertonic solutions, and a higher incidence of nausea in response to either stimulus.

Adult↗
PubMed1986

Pulmonary and systemic consequences of localized acid aspiration.

Acid aspiration may recruit a generalized inflammatory reaction that can potentiate the local injury. After surgical isolation of bronchi in a group of 15 dogs, 1 milliliter per kilogram of 0.37 normal hydrochloric acid was instilled into either side. After five minutes, platelet and white blood cell counts fell to 10,000 and 1,000 per cubic millimeter (p less than 0.05). Platelet aggregates were noted in blood smears. 111Indium-platelet activity doubled over both the aspirated and nonaspirated lung (p less than 0.05). Physiologic dead space rose from 18 to 67 per cent and to 46 per cent in the aspirated and nonaspirated lung (p less than 0.05). Physiologic shunt increased from 12 to 47 per cent and to 43 per cent (p less than 0.05) on the two sides. Plasma thromboxane B2 levels at 30 minutes rose from 0.28 to 0.93 nanograms per milliliter (p less than 0.05). Edema fluid from the aspirated lung had thromboxane B2 values of 2.87 nanograms per milliliter, indicating pulmonary synthesis. Within five minutes of aspiration, systemic effects were prominent; mean arterial pressure fell from 114 to 46 milliliters of mercury (p less than 0.05), and the cardiac index fell 24 per cent from 106 to 81 milliliters per kilogram per minute (p less than 0.05) along with an 18 per cent decrease in contractility of a rat papillary muscle bathed in plasma from the aspirated dog. Mean pulmonary arterial pressure rose from 12 to 18 millimeters of mercury (p less than 0.05). Despite fluid infusion at 36 milliliters per kilogram per hour to keep wedge pressure constant at 5.5 millimeters of mercury, and sampling of one-third the blood volume, hemoglobin concentration rose 0.9 grams per cent (p less than 0.05) indicating increased microvascular permeability. At autopsy, the aspirated and nonaspirated lung were indistinguishable with congestion, interstitial hemorrhage, and white blood cell infiltrates. Systemic organs showed vascular congestion and edema. These data demonstrate that local aspiration leads to generalized inflammatory sequelae with cardiopulmonary failure.

Animals↗
PubMed1997

Inhibition of CD18 or CD11b attenuates acute lung injury after acid instillation in rabbits.

Acid-induced lung injury is mediated primarily by activated neutrophils. Although a prior study demonstrated that acid-induced neutrophil influx into the air spaces was not CD18 dependent, we hypothesized that either a neutralizing anti-CD18 monoclonal antibody (MHM23) or a neutrophil inhibitory factor (NIF), NIF (CD11b,18), might attenuate acid-induced lung injury in rabbits by interfering with neutrophil activation. This hypothesis derived from in vitro stu ies that reported that anti-CD18 therapy prevented tumor necrosis factor-alpha-induced neutrophil activation. Hydrochloric acid (pH = 1.5 in one-third normal saline) or one-third normal saline (4 ml/kg) was instilled into the lungs of ventilated, anesthetized rabbits. The rabbits were studied for 6 h. In acid-instilled rabbits without the anti-CD18 monoclonal antibody or NIF (CD11b,18), severe lung injury developed. In acid-instilled rabbits, pretreatment (5 min before acid) with the anti-CD18 monoclonal antibody (2 mg/kg i.v.) or pretreatment with the NIF (anti-CD11b,18, 10 mg/kg i.v.) prevented 50-70% of acid-induced abnormalities in oxygenation, the increase in extravascular lung water, and extravascular protein accumulation. The anti-CD18 monoclonal antibody was associated with a significant increase in air space neutrophils by bronchoalveolar lavage, suggesting that the neutrophils respond normally to chemotactic stimuli but that the neutrophils did not injure the lung even though they accumulated in the air spaces. In summary, neutralization of CD18 attenuates the acute lung injury after acid instillation without reducing the number of neutrophils in the air spaces, suggesting that anti-CD18 therapy may be beneficial because of its capacity to reduce neutrophil activation.

Acute Disease↗
PubMed1996

[Genes for gastric proton pump and their transcriptional regulation].

The highly differentiated gastric parietal cell has a characteristic morphology and plays a specialized role in the hydrochloric acid secretion into the stomach lumen. The major enzyme in this system is an ATP-driven proton pump, the H+/K(+)-ATPase, which is responsible for proton translocation across the apical plasma membrane. The primary structures of the catalytic alpha and glycosylated beta subunits, and their transmembrane topology are similar to those of the corresponding subunits of Na+/K(+)-ATPase, suggesting that the reaction mechanism of both ATPases would be essentially the same if not identical. Most of the positions of introns in the H+/K(+)-ATPase subunit gene. These findings suggest that the alpha and beta subunit genes, respectively, of the two ATPases were derived from the common ancestors. We found that a DNA sequence motif, (G/C)PuPu(G/C)NGAT(A/T)PuPy, was located in the upstream regions of both alpha and beta subunit genes from human and rat. This motif may be a binding site for a positive transcriptional regulator that functions specifically in the parietal cells. cDNA cloning and in situ hybridization demonstrated that novel zinc finger proteins (GATA-GT1 and GATA-GT2) are present in the gastric parietal cells. These proteins bind to the (G/C)PuPu(G/C)NGAT(A/T)PuPy motif. Furthermore, they activate the transcription of the reporter gene with the 5'-upstream region of the alpha or beta subunit gene. These results suggest that gastric GATA DNA-binding proteins play important roles in transcriptional activation of H+/K(+)-ATPase genes in the parietal cells.

Amino Acid Sequence↗
PubMed2004

Nociceptin inhibits airway microvascular leakage induced by HCl intra-oesophageal instillation.

1. Gastro-oesophageal acid reflux may cause airway responses such as cough, bronchoconstriction and inflammation in asthmatic patients. Our previous results suggest that microvascular leakage induced, in the guinea-pig airways, by intra-oesophageal hydrochloric acid (HCl) infusion was mainly dependent on the release of tachykinins. Nociceptin, an endogenous ligand of the opioid receptor NOP, has been shown to inhibit bronchoconstriction and cough in guinea-pig or cat by inhibiting tachykinin release. 2. The purpose of this study was to investigate the effects of nociceptin on the intra-oesophageal HCl-induced airway microvascular leakage evaluated by Evans blue dye extravasation measurement in anaesthetised guinea-pigs pretreated with propranolol, atropine and phosphoramidon. 3. Infusion of intra-oesophageal HCl led to a significant increase in plasma extravasation in the main bronchi and trachea. This increase was abolished when animals underwent a bilateral vagotomy. 4. Airway microvascular leakage was inhibited by nociceptin (3-30 microg x kg(-1) i.v.) in a dose-dependent manner (maximal inhibition at the dose of 30 microg x kg(-1): 19.76+/-1.13 vs 90.92+/-14.00 ng x mg(-1) tissue for nociceptin and HCl infusion, respectively, in the main bronchi, P<0.01). The NOP receptor agonist [Arg(14),Lys(15)]N/OFQ mimicked the inhibitory effect of nociceptin, but at a 10-fold lower dose (3 microg x kg(-1) i.v). The NOP receptor antagonist J-113397 had no effect on plasma protein extravasation by itself, but was able to block the inhibitory effect of nociceptin. 5. Morphine (1 mg x kg(-1)) had a similar inhibitory effect as that of nociceptin. Naloxone pretreatment abolished the effect of morphine, but was enable to block the inhibitory effect of nociceptin. 6. Under similar conditions, nociceptin, in the previous range of concentration, was unable to counteract the airway microvascular leakage induced by substance P (SP). 7. These results suggest that airway plasma extravasation induced by intra-oesophageal HCl instillation might be inhibited by specific stimulation of the NOP receptor with nociceptin. Nociceptin is likely to act at a pre-junctional level, by inhibiting tachykinin release, since it was unable to prevent SP-induced airway plasma extravasation.

Animals↗
PubMed1978

The endogenous release of pancreatic polypeptide by acid and meal in dogs. Effect of somatostatin.

The response of pancreatic polypeptide (PP) to testmeal (5 ml/kg) and intraduodenal acid (4 mEq HCl/5min) and its reaction to somatostatin (3.5 microgram/kg/h following bolus injection of 3.5 microgram/kg) was studied in dogs with chronic duodenal and gastric fistulae. In addition the influence of atropin (0.5 mg/kg/h) on acid-induced PP response was examined. PP was measured by radioimmunoassay pancreatic secretion by determinating volume, bicarbonate, protein, and enzyme in duodenal contents and pancreatic juice. Plasma PP increased significantly following intraduodenal application of testmeal and hydrochloric acid. Its release was completely suppressed by SST. Furthermore, PP response to intraduodenal acid was blocked by atropin. Exocrine pancreatic secretion of bicarbonate and protein was inhibited by somatostatin as well as atropin. Since PP was released following administration of testmeal and acid, both potent stimulators of pancreatotropic duodenal hormones, it may play an important role in the control of the entero-pancreatic axis. The effect of atropin indicates a cholinergic nervous component of PP release.

Amylases↗
PubMed1991

Timed acid bath effects on kidney podocytes prepared for scanning electron microscopy.

In perfusion fixation of dog kidney glomeruli, observation of tear fractured surfaces by scanning electron microscopy reveals the deposition of "debris" on the surface of glomerular visceral epithelium (podocytes) that is not deposited on other kidney tissue surfaces. It is of concern to remove this debris without damage to tissue surfaces. A 5 minute bath in 8N HCl (hydrochloric acid) following postfixation in 1% OsO4 (osmium tetroxide) removes only some of the debris. A 10 minute acid bath removes this debris without visible damage to podocyte surface structures such as cilia, plicae or blebs. A 20 minute acid bath is destructive to these surface features.

Animals↗