HCl Instillation Research Articles

Aerosolized Versus Instilled Exogenous Surfactant in a Nonuniform Pattern of Lung Injury

Previous studies have shown that the underlying patterns of lung injury influence subsequent responses to aerosolized exogenous surfactant. The purpose of this study was to compare aerosolized versus tracheally instilled surfactant in a nonuniform lung injury. Adult sheep underwent whole lung lavage with subsequent HCl instillation into the right middle lobe (RML) and lingula (LING) to create a nonuniform injury. Animals were treated with either nebulized surfactant (Neb.Surf.), tracheally instilled surfactant (Inst.Surf.), or nebulized saline (Neb. Saline). PaO2, alveolar-arterial O2 gradient (PAO2-PaO2), PaCO2, and peak inspiratory pressure (PIP) values all significantly improved during 180 min of continuous aerosolization for Neb.Surf. animals compared with pretreatment values (p < 0.01) and with the other two treatment groups (p < 0.01). Although PaO2 and (PAO2-PaO2) values improved for the Inst.Surf. group by 180 min after treatment (p < 0.05), PaCO2 and PIP values were significantly increased 30 min after surfactant instillation (p < 0.05). Neb. Saline animals had no significant changes in physiologic parameters over 180 min. Approximately 8% of the total aerosolized surfactant deposited in lung tissue was recovered from the more severely damaged RML and LING, compared with approximately 50% of the total instilled surfactant recovered from these lobes. This resulted in significantly greater percentages of the total aerosolized surfactant deposited in each of the remaining lobes compared with the percent deposition of instilled surfactant (p < 0.05). Both the underlying pattern of lung injury and the exogenous surfactant delivery technique may influence clinical responses to surfactant therapy in patients with the adult respiratory distress syndrome (ARDS).

Simultaneous measurements of gastric motility and acid-bicarbonate secretions in the anaesthetized cat.

Chloralosed cats were acutely vagotomized, their splanchnic nerves cut and the adrenal glands ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was monitored as changes in hydrostatic pressure within the perfusion circuit. Gastric secretion of H+ and HCO3- were calculated from continuous measurements of pH and PCO2. Methodological tests ex vivo showed good accuracy of the estimations. Recovery of H+ after HCl instillation into the stomach in vivo was almost complete, while HCO3- recovery after NaHCO3 instillations was 85-95%. Pentagastrin (10 micrograms kg-1 h-1 i.v.) stimulated gastric contractile activity and increased gastric H+ secretion 30-fold, while HCO3- secretion decreased somewhat. Carbachol (4 micrograms kg-1 h-1) induced gastric contractions and increased H+ secretion by 400% and HCO3- output by 100-130%. Electrical stimulation of the cut vagal nerves (10 Hz for 10 min) induced well known gastric motor responses and increased gastric H+ secretion 20-fold preceded by a transient doubling of HCO3- secretion. Omeprazole, a selective inhibitor of gastric H+ secretion, decreased the vagally induced H+ secretion, while recorded gastric HCO3- secretion was clearly enhanced. In conclusion, the technique permits simultaneous recordings of rapid alterations of gastric motility and H+ and HCO3- secretions. However, HCO3- secretion was modestly underestimated, probably due to mucosal CO2 absorption.

Exocrine secretion of canine pancreas perfused extracorporeally.

A canine gastroduodenopancreatic block was isolated and perfused extracorporeally with homologous blood. This preparation was used for studying stimulated exocrine secretion of the pancreas. Stimulants were infused intra-arterially. Both vagi were stimulated electrically. Hydrochloric acid or L-phenylalanine were instilled intragastrically. Pancreatic secretion induced by secretin and during HCl instillation was rich in bicarbonate and poor in total protein. Pancreatic secretion obtained during the infusion of normal saline, cholecystokinin, bethanechol chloride or acetylcholine chloride and during instillation of amino acid as well as during electrical stimulation of vagi, contained less bicarbonate and more protein than secretin-induced secretion.

Effects of glycine and other instillates on concentration of gastric acid

Instillation of isosmotic glycine solution on the mucosal surface of the histamine-stimulated canine stomach increases the concentration of HCl beyond its value in gastric juice. This was found to be primarily due to a reduction in the rate of water flow toward the lumen. Other instillates, including isosmotic sucrose, mannitol, and NaCl also produced an increase in the measured acidity. The effect is therefore not exclusively a result of the buffering of H ions by glycine. Instillation of urea did not significantly change the secreted acidity, and HCl instillation was accompanied by a decrease in acidity. The results can be most easily explained by assuming that the water component of gastric acid flows in response to an osmotic gradient due to secreted HCl. Instillation of the more impermeable solutes (sucrose, mannitol, NaCl) presumably reduces this gradient by dilution, while glycine acts in addition to reduce the gradient by buffering H ions.

Effect of duodenal freezing on the secretin mechanism.

1. Experience with 17 dogs subjected to duodenal freezing for 10 minutes suggests that secretin release to acid stimulation of the duodenum is significantly impaired for at least 3 months. Average total response to HCl instillation in the post-freeze duodenum is 28.2% of control mean response. More prolonged periods of freezing do not result in greater depression. 2. No evidence of significant pancreatic derangement has been found to result from duodenal freezing. 3. If the duodenum is exposed to air during the freezing process, there is a significant incidence of duodenal necrosis, which was not observed with intraperitoneal freezing for 10 minutes.