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Biomedical subjects

R R Pfister

Publications and source records attributed to R R Pfister.

90 records · Page 5Linked to original sources
PubMed1975

Management of non-penetrating distal urethral trauma.

Two cases of non-penetrating distal urethral trauma are reported to illustrate the potential routes of urinary extravasation. The nature and management of such injuries are discussed to emphasize that the typically incomplete rupture of the distal urethra responds satisfactorily to catheter diversion of the urinary stream, antibiotic coverage, drainage of extravasated urine and delayed debridement of necrotic tissue. Primary surgical repair of the urethra is rarely indicated in this injury.

Administration, Oral↗
PubMed1975

The healing of corneal epithelial abrasions in the rabbit: a scanning electron microscope study.

The morphologic appearance and time course of regenerating rabbit corneal epithelium was studied after 6.0 mm. corneal abrasions. The immediate response to injury was separation and thickening of basal and squamous epithelial cells at and near the wound margin. A variable number and distribution of polymorphonuclear leukocytes appeared on the basal lamina and regenerating epithelial edge at 3 hours, persisting up to 38 hours after abrasion. Most of the epithelial cells at the wound margin were extensively flattened after 15 hours. These flattened epithelial cells showed a wide variety of surface ruffling near their free edges. This ruffling activity often was associated with long fingerlike processes (filopodia) extending out on to the basal lamina. The method of epithelial cell movement on the basal lamina appeared to depend mainly on the ruffling and filopodial activity of squamous epithelial cells. Ruffles and filopodia projected out ahead of the cell edge, contacted the basal lamina, and appeared capable of drawing the cells forward into the area of the defect. Normal corneal re-epithelization proceeded with two or three cell layers moving as an orderly sheet over the basal lamina until the defect was closed. The corneal surface showed no defect at 55 hours and was returned to normal at 114 hours.

Animals↗
PubMed1975

The normal surface of conjunctiva epithelium. A scanning electron microscopic study.

Scanning electron microscopy (SEM) of the cellular surface of the rabbit conjunctiva show the monotonous appearance of fine, finger-like cytoplasmic protrusions (microvilli) covering the polygonal cells. Many of these surface cells contained a variety of intracytoplasmic vesicles, unroofed vesicles, and full-thickness holes of different sizes. These surface changes were interpreted as occuring in a sequential pattern leading to cell destruction and exfoliation. Interspersed among these light and dark polygonal cells were goblet cells representing various stages in their maturation. Specialized filopodia were found between epithelial cells only in the area just proximal to the tarsi. Duct openings of many glands were shown to enter onto the conjunctival surface. The relation of these finding to the tear film is discussed.

Animals↗
PubMed1975

Prostaglandin-like activity in the aqueous humor following alkali burns.

Following application of 20 mul of 2 N sodium hydroxide to the rabbit cornea, the prostaglandin-like activity in the aqueous humor increased from undetectable levels to around 30 ng, per milliliter, a level which was sustained for up to 24 hours. This increase correlated with the previously reported sustained elevation of intraocular pressure following a 20 mul alkali burn. Pretreatment with aspirin or indomethacin virtually abolished the increase in intraocular pressure and elevation of prostaglandin-like activity in the aqueous humor following a 20 mul burn. Marked ocular hypotension following 50 mul and 100 mul sodium hydroxide burns correlated with very low prostaglandin-like activity in the aqueous humor. The low prostaglandin-like activity probably resulted from alkaline hydrolysis of aqueous prostaglandins and massive cellular death in iris and ciliary body tissues.

Alkalies↗
PubMedDate not supplied

The effects of citrate on fMLP-induced polymorphonuclear leukocyte stimulation and locomotion.

Citrate reduces the incidence of corneal ulceration and perforation in alkali burned eyes and prevents polymorphonuclear leukocyte (PMN) accumulation in certain inflamed ocular tissues. Chelation of Ca2+ and Mg2+ by citrate appears to be the mechanism causing strong inhibition of in vitro PMN stimulation by opsonized zymosan. It is important to know if other activating agents of PMNs, with differing sensitivity to divalent cations, are inhibited by citrate. Citrate (12 mM) partially inhibits fMLP stimulation of the respiratory burst (50%) and degranulation (65%) of PMNs in a divalent cation free media, while having no effect or only a small effect in the presence of 1 mm Ca2+. Citrate also caused significant inhibition of fMLP (12 mM = 50%) induced locomotion of PMN when incubated in media containing 500 microM Ca2+ and 600 microM Mg2+ in a modified Boyden chamber. When used together, Ca2+ (6 mM) and Mg2+ (6 mM) reduced this inhibition to only 20%. Citrate apparently inhibits fMLP-induced stimulation in cation free media by chelating CA2+ effluxed from intracellular storage sites. In the chemotactic studies, citrate probably chelates extracellular Ca2+ and Mg2+. The divalent cation requirements of the activating agents and/or the PMN function may determine the degree of inhibition by citrate. It is therefore important to identify the mediators in alkali burned corneas as well as other inflammatory conditions.

Calcium↗
PubMedDate not supplied

The effect of citrate and other compounds on PMN incubated in vitro: further studies on the site and mechanism of action of citrate.

Polymorphonuclear leukocytes (PMN) are important in corneal disease because of their role as effector cells in inflammation and ulceration. The favorable effect of citrate on corneal ulceration appears to result from inhibition of the PMN. Citrate does not enter the cells but chelates Ca2+ in the extracellular fluid and may promote a loss of some intracellular Ca2+. Isocitrate is the only tricarboxylic acid cycle intermediate that inhibits PMN, also by Ca2+ chelation. When isobutylcyanoacrylate is polymerized, a substance, probably formaldehyde, inhibitory to PMN, continuously leeches from the plastic. Although acetylcysteine has been reported to inhibit collagenase in vitro it has a direct effect of enhancing the respiratory burst and possibly degranulation of PMN stimulated by opsonized zymosan. Dexamethasone had no effect on PMN stimulation while prednisolone was partially inhibitory at high concentrations. Indomethacin exerts an inhibitory effect on all parameters of PMN stimulation. These studies clarify the site and mechanism of citrate action as well as show the importance of knowing the effect of drugs on the PMN.

Acetylcysteine↗