Brian A. Hills

Effect of 16,16-Dimethyl Prostaglandin E2 on the Surface Hydrophobicity of Aspirin-Treated Canine Gastric Mucosa

The canine gastric mucosa has a uniquely hydrophobic or nonwettable surface that is rapidly disrupted by damaging agents such as aspirin. In this study we investigated the effects of acidified aspirin on the wettability of the luminal surface of gastric mucosae mounted in Ussing chambers in the presence of varying concentrations of 16,16-dimethyl prostaglandin E2. It was determined that surface hydrophobicity of the stomach, as measured by contact angle measurements, could be reduced by 50% with an aspirin concentration of 5 mM in the mucosal bath and that this change could be completely and significantly reversed by the addition of 16,16-dimethyl prostaglandin E2 (1 microgram/ml) to the nutrient compartment. 16,16-Dimethyl prostaglandin E2 at this dose was less effective in restoring the surface hydrophobicity in response to a higher concentration of aspirin (20 mM) that abolished the nonwettable property of the tissue. The reduced surface hydrophobicity in the presence of 5 mM aspirin could be increased in a dose response relationship to the nutrient 16,16-dimethyl prostaglandin E2 concentration, with an effect being seen at doses as low as 1 ng/ml. These results support the concept that prostaglandins may protect the stomach by the maintenance of a nonwettable hydrophobic lining between damaging agents in the lumen and the gastric epithelium.

Phospholipids identified on the pericardium and their ability to impart boundary lubrication

Phospholipids have been identified by thin-layer chromatography in appreciable quantities in pericardial fluid taken from 12 dogs and found to include sphingomyelin and phosphatidylcholines,-ethanolamines,-inositols and-serines—the cholines predominating. The extracts, the synthetic surfactants and a mixture of synthetics simulating the extracts were all found to be good lubricants when tested by a standard method. The phosphatidylcholines were capable of reducing friction between two otherwise hydrophilic surfaces by as much as 100- to 200-fold when deposited as an oriented monolayer. A goniometer was used to measure an average contact angle of 33° for a drop of saline placed upon the internal wall of the pericardium, indicating an appreciably hydrophobic surface anticipated if surfactant were directly adsorbed. The results are consistent with the classical theory of “boundary” lubrication (17) as modified (21) to reflect the almost ideal molecular structure of the identified surfactants for adsorption, film cohesion and interaction of fatty-acid chains during sliding. This model is proposed as an alternative to hydrodynamic lubrication in the pericardium and one compatible with several practical aspects such as pericardial rub and the maintenance of normal heart action after pericardectomy.

Premature rupture of membranes and surface energy: Possible role of surfactant

Thirty-one human placental membranes of various gestational ages (24 1/2 to 42 weeks) have been studied for their surface properties by use of a goniometer to observe drops of saline and olive oil applied at regular intervals to the amniotic and chorionic surfaces as they dried in air. Results show that the epithelial surfaces of the chorion and amnion and their interface are all appreciably hydrophobic. Surface energy decreased on the amniotic surface with fetal maturity while the surface energy of the chorion was significantly (137%) higher in those displaying premature rupture of the membranes than in others of comparable gestational age. This is explained on the basis that low-energy surfaces (for instance, Teflon) do not stick and provide boundary lubrication which facilitates movement. These properties are needed to avoid the buildup of local mechanical stress which could initiate rupture. It is speculated that the release agent-lubricant is surfactant derived from amniotic fluid and directly adsorbed onto the epithelial walls. On other tissues, the same surfactants have been shown to reduce surface energy, rendering them hydrophobic and imparting many desirable properties such as release, lubrication, and resistance to erosion.

Surface hydrophobicity and water transport of the toad urinary bladder: effects of vasopressin.

SummaryThe present study investigated whether the hydrophobic properties (wettability) of the luminal surface of the toad urinary bladder might play a role in modulating water transport across this epithelium. In the absence of vasopressin (ADH), water transport across the tissue was low, while luminal surface hydrophobicity (water contact angle) was relatively high. Following stimulation by ADH, water transport increased and surface hydrophobicity decreased. The addition of indomethacin to inhibit ADH-induced prostaglandin synthesis did not reduce these actions of ADH. In an attempt to alter water transport in this tissue, a liposomal suspension of surface-active phospholipids was administered to the luminal surface. This addition had no detectable influence on the low basal rates of water transport, but blocked the ADH-induced stimulation of water transport. We suggest that surface-active phospholipids on the toad bladder luminal membrane may contribute to the hydrophobic characteristics of this tissue. ADH may act to decrease surface hydrophobicity, facilitating the movement of water molecules across an otherwise impermeable epithelium. This surface alteration may be associated with the appearance of water channels in the apical membrane.

Effect of bronchial blood flow on pulmonary artery wedge pressure with pulmonary embolism

Discrepancies between pulmonary artery wedge pressure (WP) and left atrial pressure (LAP) occur with pulmonary embolism. Theoretically, this discrepancy could be affected by the bronchial circulation or by the type of embolus. To test this in dogs, we determined the effects of embolism induced by glass beads and by air upon the WP with intact vs. ligated bronchial blood flow to the left lower lobe. For those animals receiving pulmonary air infusions, the pulmonary artery pressure, WP, and pulmonary vascular resistance showed significant (p < .05) elevations with no change in LAP. There were no changes in these values when the bronchial blood flow was interrupted. When glass beads (120 ±) were injected into the left lower lobe, the pulmonary artery pressure and pulmonary vascular resistance rose as in the air emboli groups (p < .05); however, WP remained at control values and approximated LAP. Obstructing the bronchial blood flow did not change this response. We conclude that the discrepancy between WP and LAP depends upon the type of embolus and is not affected by bronchial blood flow.