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The present study was carried out to determine the effect of cyclooxygenase-2 (COX-2) inhibitor on acid aspiration-induced lung injury in rats. Rats were allocated into one of four groups. Group H received intratracheal instillation of HCl. Group S received saline intratracheally. Group HC received COX-2 inhibitor (celecoxib) 10 mg/kg intravenously 30 min before intratracheal instillation of HCl. Group C underwent bronchoalveolar lavage (BAL) only. All rats were mechanically ventilated for 30 min before BAL. Arterial blood gas analysis was done immediately before BAL. Groups H, S, and HC were subdivided to each two groups. Groups H-1, S-1, and HC-1 underwent BAL 1 h after instillation, whereas groups H-8, S-8, and HC-8 underwent BAL 8 h after instillation. The BAL fluid was used to measure the prostaglandin E2 (PGE2) concentration. Intratracheal HCl resulted in impaired oxygenation. COX-2 inhibitor attenuated the impairment of oxygenation 8 h after instillation but not after 1 h. Intratracheal HCl caused an increase in PGE2 concentration. COX-2 inhibitor attenuated an increase in PGE2 concentration 8 h after instillation but not after 1 h. The results show that COX-2 inhibitor attenuates the oxygenation impairment and the increase in alveolar PGE2 concentration during the inflammatory phase of acid aspiration-induced lung injury in rats.
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The purpose of this in vitro study was to compare the protective effect of TiF4, SnF2 and NaF (all 0.5 M F) on the development of erosion-like lesions in human dental enamel. Four enamel specimens from each of 6 extracted molars were polished and embedded in epoxy resin. The enamel surfaces of 3 specimens from each tooth were treated with the different fluoride solutions for 2 min. Following fluoride treatments, the specimens were immersed in 0.01 M HCl (pH 2.0), for 2, 4 and 6 min in order to mimic a gastric reflux situation. One specimen from each tooth was used as a control and was only exposed to acid. The etching depths (in micrometres) after 6 min were: TiF4 0.8 (SD 0.8), SnF2 3.5 (SD 0.7), NaF 5.3 (SD 0.4), and 7.0 (SD 0.3) for the control specimens. Compared to the control, TiF(4) protected the enamel surface from acid attack almost completely (88%), while SnF2 reduced the etch depth after 6 min by 50% and NaF by 25%.
Pepsin secretion is stimulated by the back-diffusion of acid across the mucosa of the vagally denervated canine pouch. If back-diffusion is enhanced by damage, pepsin secretion increases. The current study investigates whether this mechanism exists in man. The stomach of normal human volunteers were irrigated for 1 hour with either buffer of 0.01 N HCl, 1 hour with 0.2 N HCl, and a final hour with buffer or 0.01 N HCl. During the middle hour both the concentration and output of pepsin increased three- or fourfold. From these studies it appears that the human gastric mucosa contains a mechanism similar to the dog's which results in the stimulation of pepsin secretion when exposed to acid. This mechanism could be of etiologic significance in gastric ulcer disease, which has been shown to be associated with increased gastric-mucosal permeability.
The chorda tympani nerve response of the rat to HCl was obtained with the lingual receptive field under voltage clamp. Unlike NaCl responses, HCl responses were not affected by inside positive voltage perturbations. However, HCl responses under negative voltage clamp were suppressed in contrast to NaCl responses, which were enhanced. Unlike NaCl responses, HCl responses were amiloride insensitive. HCl rinsing from the tongue produced a large off-response. At zero current clamp the off-response coincided with an anomalous increased positive potential. The paracellular resistance was also higher for HCl relative to the same concentration of NaCl. This is evidence that H+ binds to the normally fixed anionic sites of the paracellular pathway rendering it anion selective. It is postulated that release of bound H+ from surface buffer sites is responsible for the second burst of neural activity upon rising HCl. Acids stimulate primarily through the paracellular pathway, which also furnishes buffering sites that regulate H+ concentration, thereby protecting the sensory apparatus from hyperacidic conditions.
A case of intentional ingestion of concentrated acid, in which both disseminated intravascular coagulation and acute respiratory insufficiency complicated initial resuscitation, is reported. The assessment and the acute management of this unusual problem are reviewed, with emphasis on early endoscopy and laparotomy.
Investigations were carried-out on corneas of rabbit eyes burned with 1N HCl and then treated with low temperature. It was found that cryotherapy has advantageous influence on collagenase activity. In early period after burn cryotherapy could prevent collagenolysis and later inhibited collagenase activity.
A simple, rapid, and reliable method was developed for determination of inorganic As in biological samples such as fish fillet. Inorganic AS was distilled from the sample as AsCl3 with HCl. The separated inorganic AS was determined by flow-injection hydride-generation atomic absorption spectrometry after prereduction with KI and HCl. The influences of various concentrations of KI, ascorbic acid, and HCl in the prereduction stage; NaBH4 as the reductant; and HCl as the carrier solution on analytical results were studied. Digestion was performed in a Kjeldahl digestion system for 75 min with 4 mL nitric acid and 1 mL sulfuric acid at 380 degrees C. The concentrations of inorganic As in samples were less than 0.1 mg/kg dry weight for fish fillet and somewhat higher for crustaceans and bivalve molluscs. The total and inorganic As contents of various marine biological samples and certified reference materials were determined.
Severe metabolic alkalosis is often treated by infusion of arginine-HCl. Since we know that this substance leads to a supplemental increase of intracellular pH and fails to reduce intracellular bicarbonate concentration we use HCl for correction of this disturbance of acid-base equilibrium. 18 intensive-care patients with severe metabolic alkalosis were treated with an infusion of 0.2 m HCl. While base excess and sodium decreased significantly, chloride increased slightly. Arterial plasma pH, potassium, Hb, Hk, pCO2, pO2, and SO2 remained unchanged. Instructions for preparing different HCl solutions and advice on dosage are given.
Human saliva seeded with H. pylori was incubated in urea-HCl and then cultured on nonselective media. Pretreatment with 0.06 N HCl-0.08 M urea for 5 min at 37 degrees C resulted in reproducible isolation of H. pylori, even at low inocula (< or =10(2) CFU/ml of saliva), despite the presence of large numbers of contaminating organisms.
The ingestion of a caustic acid resulted in retractile fibrosis of 2/3 of the stomach with a secondary duodenal fistula. The antro-pyloro-duodenal circuit was re-established at around the 3rd after ingestion. However, the duodenal fistula caused the formation of encysted pelvic abscesses which were difficult to drain and satisfactorily treat. The clinical course stretched over a period of 4 years.