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Biomedical subjects

K L Schmidt

Publications and source records attributed to K L Schmidt.

At least 73 records · Page 4Linked to original sources
PubMed1987

The protective effects of a prostaglandin without antisecretory properties against ethanol-induced injury in the rat stomach: a histologic study.

This study examined the effect of 2-acetyl-2-decarboxy-15(S)-15 methyl PGF2 alpha (PGF2 alpha) on ethanol (EtOH) induced injury in the rat stomach to determine if a PG analogue devoid of antisecretory properties could confer full or partial gastric mucosal protection. Rats were orally administered saline or PGF2 alpha in a dose of 0.5 or 5.0 mg/Kg. Thirty minutes later animals received varying concentrations (i.e. 25%, 50%, and 100%) of EtOH orally. Five minutes following EtOH exposure, they were killed and samples taken from identical regions of the glandular mucosa for microscopic evaluation. All concentrations of EtOH tested damaged the gastric epithelium. The injury induced by 25% EtOH was almost exclusively confined to the surface epithelium and was not altered by either dose of PGF2 alpha pretreatment. In contrast, both 50% and 100% EtOH elicited comparable damage to the gastric mucosa involving both the deep and superficial mucosa of virtually the entire epithelium. The deep injury induced by these two EtOH concentrations was prevented by both the low and high dose of PGF2 alpha. Of particular importance the 5.0 mg dose of PGF2 alpha provided complete protection (i.e. both superficial and deep) to as much as 50% of the mucosa exposed to 50% or 100% ethanol. These findings indicate that PGF2 alpha possesses "cytoprotective" properties involving both the superficial and deep epithelium that are dose related.

Administration, Oral↗
PubMed1987

[Endocrine rhythms in patients with rheumatoid arthritis: possible neurohormonal influence on immunological reactions].

Recent studies are reporting on an influence of ACTH and prolactin in physiological dosages on the intensity of the immune response in the animal model of adjuvant arthritis. Therefore, we studied the circadian secretion patterns of ACTH, cortisol and prolactin by measurements throughout a 24-hour cycle in two-hour intervals in patients with rheumatoid arthritis with different inflammatory activity of the disease. We only investigated patients who never before were treated with corticosteroids and drugs like gold, d-penicillamine or immunosuppressive drugs. The circadian secretion patterns of cortisol and ACTH were disturbed in most patients. High inflammatory activity was accompanied by severe disturbance of the circadian rhythm, whereas patients with low inflammatory activity showed a nearly normal secretion pattern. Also the measurements of prolactin showed a tendency of loss of circadian rhythm in relation to the inflammatory activity of the disease. According to the found changes of endocrine regulation of ACTH, cortisol and prolactin, an influence of mediators of inflammation on hypothalamic centers, analogous to endogenous pyrogen in fever should be discussed.

Adrenocorticotropic Hormone↗
PubMed1986

Influence of prostaglandin on repair of rat stomach damaged by absolute ethanol.

This study was undertaken to determine the possible role that prostaglandins (PGs) may play in enhancing epithelial repair in ethanol-damaged gastric mucosa. Fasted rats were injected subcutaneously with 10 micrograms/kg of 16,16-dimethyl PGE2 or saline and 30 min later received an oral bolus of 1 ml of absolute ethanol or saline. At 5 min and 2, 8, and 24 hr after ethanol exposure tissues were prepared from identical regions of the glandular mucosa for microscopic evaluation. Normal, injured, and repairing tissues were differentiated and quantitated. The length of injured surface epithelium was the same in ethanol-treated tissues with and without PG pretreatment when evaluated 5 min after ethanol exposure, but the deeper epithelium was protected from injury in animals receiving PG pretreatment. Although the repair process itself was identical in the two experimental groups, in PG-treated tissues repair was initiated earlier, was more widespread, and was much more rapid than in tissues exposed to ethanol without such treatment. At the end of 24 hr of observation, only 5.5% of the surface epithelium was considered normal histologically in mucosa exposed to ethanol alone without PG pretreatment. This is in marked contrast to PG-treated tissues in which 82.7% of the gastric surface was normal at 24 hr. The mechanism responsible for our findings is unknown but may be related to PG's ability to spare the cellular pool in the gland isthmus from damage, enhancement of cellular migration from this pool to resurface the damaged epithelium, or a combination of both of these processes.

16,16-Dimethylprostaglandin E2↗
PubMed1986

N-acetyl-cysteine and prostaglandin. Comparable protection against experimental ethanol injury in the stomach independent of mucus thickness.

The role of barrier mucus in mediating the protective effects of 16,16 dimethyl PGE2 (dm PGE2) against ethanol-induced gastric injury, with and without concomitant treatment with N-acetyl-cysteine (NAC), a potent mucolytic agent, was evaluated. Fasted rats were orally administered either saline, 10 micrograms/kg dm PGE2, 20% NAC, or 10 micrograms/kg dm PGE2 plus 20% NAC. In the first study, the rats were killed 15 minutes later and their stomachs were removed and assayed for barrier mucus adherent to the gastric wall using the Alcian blue technique. In the second study, the rats were orally given 2 mL of absolute ethanol (EtOH) after receiving one of these pretreatment regimens, and 5 minutes later they were killed and their stomachs were evaluated histologically by light microscopy for the magnitude of EtOH injury. Although NAC significantly reduced the thickness of barrier mucus by 76% when compared with control animals, it did not adversely affect the ability of dm PGE2 to spare the deep epithelium from injury by EtOH. In fact, NAC was as effective a protective agent as dm PGE2. Neither agent prevented damage to the surface epithelium by EtOH, verifying previous studies regarding the protective effects of prostaglandins. These results indicate that both dm PGE2 and NAC prevent EtOH-induced damage to the deeper layers of the gastric mucosa independent of mucus gel layer thickness, suggesting that other mechanisms than mucus are involved in mediating this protection.

Acetylcysteine↗
PubMed1986

Intrauterine device (IUD) associated pathology: a review of pathogenic mechanisms.

This paper summarizes our studies of IUD-related disease with those previously published by others. Our data are based upon 51 IUDs and 42 index cases of IUD-related disease demonstrating specific processes. Gross, dissecting microscope, scanning electron microscope and X-ray microanalysis examinations were made of selected IUDs and associated tissues. Tissue associated with the IUDs revealed inflammation in 59.4%, calcific material in 6.3% and no abnormality in 34.4%. IUD-associated tissue responses were accompanied by changes of the IUD; these changes involved deposition of substances upon the IUD surface and degradation of the IUD itself. Disintegration of the IUD, its string or both, has been repeatedly observed. The material deposited upon the surface of the IUD included proteins and calcium salts. The changes which involve the IUD and the host appear to be operative in the genesis of IUD-related disease. Inflammatory changes and infections are the most common IUD-related disease processes and are also the mechanisms commonly associated with the most serious complications of IUD use, reproductive failure and death. We propose that serious IUD-related disease is caused by or is a direct consequence of processes which alter the IUD and which potentiate inflammation and infection. A model amenable to testing is proposed.

Electron Probe Microanalysis↗
PubMed1985

Comparison of specific red-cell adherence and immunoperoxidase staining techniques for ABO(H) blood-group cell-surface antigens on superficial transitional cell carcinoma of the bladder.

The presence or absence of blood-group antigens have been used to predict the clinical course of patients with superficial transitional cell carcinoma of the bladder. Antigen loss has been associated with neoplastic change. The red-cell adherence test has been the most widely accepted method of antigen determination, but this technique has inherent weaknesses. Recently, the immunoperoxidase assay has been used to detect antigens on tumor cells. We compared 30 patients using the red-cell adherence and immunoperoxidase methods on adjacent microtome cut sections. The red-cell adherence and immunoperoxidase methods performed similarly (86%) when assessing antigen presence or absence. However, the immunoperoxidase method was clearly superior in: 1) specificity for antigens on tumor cells and normal internal controls; 2) localization of antigen; 3) demonstration of cellular morphology; 4) increased objectivity of analysis; 5) ease of reproducibility; and 6) cost effectiveness.

ABO Blood-Group System↗
PubMed1985

Prostaglandin cytoprotection against ethanol-induced gastric injury in the rat. A histologic and cytologic study.

Using macroscopic criteria for injury, prostaglandins have been alleged to possess potent antiulcer properties despite meager histologic evidence for this cytoprotective action. This time-sequence study used light, scanning, and transmission electron microscopy to evaluate the effects of 16,16-dimethyl prostaglandin E2 on gastric mucosal integrity after exposure to 100% ethanol. Macroscopically, virtually complete protection against injury to the glandular mucosa of the in vivo rat stomach was noted in animals receiving 10 micrograms/kg body wt of prostaglandin subcutaneously before oral ethanol administration when killed at 5, 20, and 60 min after ethanol exposure compared with oral ethanol after saline injection. On light microscopy the length of injured epithelium in prostaglandin/ethanol- and saline/ethanol-treated tissues was not significantly different at all time periods studied. Although the depth of injury extended into gastric glands in both groups killed at 5 min, the deep pit surface mucus cells in prostaglandin/ethanol mucosa were less damaged and necrotic lesions were virtually absent when compared with saline/ethanol mucosa. At 20 and 60 min, cellular injury could still be identified in prostaglandin/ethanol-treated mucosa but the depth of injury became even less pronounced over time in contrast to mucosa exposed to ethanol without prostaglandin. Scanning electron microscopy and transmission electron microscopy confirmed these differences. Despite the macroscopic findings, these results indicate that prostaglandin does not prevent superficial surface mucus cell necrosis in ethanol-exposed mucosa even though it does spare cells in the pit base. The reduction in damaged cells over time in prostaglandin/ethanol-treated mucosa, in contrast to saline/ethanol-treated mucosa, supports the hypothesis that the reepithelialization of the lamina propria is initiated by spared deep-lying pit cells.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Nonprotein sulfhydryl compounds in canine gastric mucosa: effects of PGE2 and ethanol.

By use of an in vivo canine chambered stomach preparation in which the gastric mucosa was partitioned into two equal halves, the effect of topical 16,16-dimethyl PGE2 (DMPGE2) (1 microgram/ml of perfusate) and 8% and 40% ethanol on tissue levels of nonprotein sulfhydryl compounds was assessed. Both DMPGE2 and 8% ethanol significantly increased (P less than 0.005) mucosal levels of nonprotein sulfhydryls when compared with corresponding mucosa bathed with saline alone. In contrast, mucosa bathed with 40% ethanol showed significantly decreased levels. If mucosa was bathed with DMPGE2 or 8% ethanol prior to exposing the stomach to 40% ethanol, this depletion in sulfhydryl compounds was not observed. Since other experimental observations have shown that exogenously administered prostaglandins and mild irritants (such as low-dose alcohol) can prevent gastric mucosal damage by necrotizing agents (such as high-dose alcohol), our findings are consistent with the hypothesis that nonprotein sulfhydryls may play a role in mediating gastric mucosal protection.

16,16-Dimethylprostaglandin E2↗
PubMed1984

Ultrastructure of trypan blue-induced ocular defects II. Cornea and mesenchyme.

Using scanning and transmission electron microscopy, the histological and cytological alterations induced in the developing eye by trypan blue were examined. Microphthalmic and anophthalmic eyes were analyzed from 16-day rat fetuses whose dams had received a teratogenic dose of trypan blue. Cell and tissue damage within cornea and mesenchyme were assessed. Corneas from the treated groups were undulating and uneven owing to abnormal lens placement and corneal cell injury. Extensive extracellular spacing, few cell-to-cell contacts, patchy glycocalyces, and abnormal surface morphology characterized the corneal cells of treated tissues. Mesenchyme of severely malformed eyes typically filled the eye field in regions normally occupied by retina and lens. As a tissue, mesenchyme lacked organization and those surface features normally present in component cells were altered. Mesenchymal cells were packed so closely that extracellular spaces were nearly obliterated. Microvilli, filopodia, and lamellipodia, cell processes observed in normal mesenchyme, were altered in both number and structure. The cytoplasm of mesenchymal cells was condensed and decreased in volume. These data suggested that 1) in this trypan blue ocular model, virtually all major tissue types were morphologically altered; 2) because healthy mesenchyme and cornea are required for normal development of lens, optic vesicle and ocular adnexa it follows that abnormal cornea and mesenchyme also will compromise these tissues; and 3) since necrotic reminants were not present, this trypan blue model probably causes developmental arrest. The most likely teratogenic pathway is presented with emphasis on the cell surface as a probable site of dye action.

Abnormalities, Drug-Induced↗
PubMed1984

Prevention of the inhibitory effects of aspirin on sodium transport in canine gastric mucosa by prostaglandin. Correlation with mucosal morphology.

Using an in vitro canine gastric mucosal preparation, this study evaluated the effects of 1 mM aspirin in a buffered Ringer solution (pH = 7.4), with and without concomitant prostaglandin (PG) treatment, on net sodium transport (mucosa to serosa) across gastric epithelium. Administration of aspirin to the mucosal bathing solution for 2 hr significantly decreased the potential difference (PD), short circuit current (Isc), and net sodium transport (net J-Na+) when compared with untreated control mucosa. In mucosa treated with 16,16-dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution 40 min after aspirin exposure and for 80 min thereafter, the initial inhibitory effects on PD, Isc, and net J-Na+ induced by aspirin were completely reversed within 40 min of PG treatment, having returned to control values. Histologically, mucosa exposed to aspirin alone showed evidence of diffuse cellular injury involving 50-60% of the surface epithelium. In contrast, mucosa treated with prostaglandin in conjunction with aspirin exposure demonstrated damage involving only 20-30% of the epithelium. These findings suggest that stimulation of sodium transport by PG may play a role in mediating the cytoprotective effects of PGs against aspirin-induced gastric mucosal injury.

Animals↗
PubMed1984

Characterization of long-term monolayer cultures of human granulosa cells from follicles of different size and exposed in vivo to clomiphene citrate and hCG.

To determine the effects of prolonged hCG treatment in vitro upon granulosa cells from follicles of various sizes previously exposed to clomiphene citrate and hCG in vivo, progesterone and relaxin concentrations of spent media were correlated with light microscopic and ultrastructural characteristics. Intact, freshly dispersed cells were characterized by numerous lipid droplets, elliptical mitochondria with tubular or lamellar cristae, moderate rough-surfaced endoplasmic reticulum (RER), sparse smooth-surfaced endoplasmic reticulum (SER), and few Golgi. After 10-24 days in culture, 2 morphologically distinct cell types, 'granulosa-type' and 'luteal-type', were noted at the light microscopic level. Ultrastructurally, lipid droplets decreased in number, mitochondria became pleomorphic, RER became more prominent and dilated, and Golgi became more widely dispersed. Tubular SER became abundant and annular nexuses became more numerous after hCG treatment in vitro. Granulosa cells generated from all follicles responded to hCG treatment with significantly increased progesterone secretion after 4 days in culture. Relaxin was not detectable in any sample of medium. This study shows that human granulosa cells from 15-25-mm follicles retain their differentiated function of progesterone secretion in long-term culture and recover responsiveness to hCG in vitro, as demonstrated by enhanced progesterone secretion and development of prominent SER and increased annular nexuses.

Cells, Cultured↗
PubMed1983

Ultrastructure of trypan blue induced ocular defects: I. Retina and lens.

The histological and cytological basis of trypan blue-induced ocular defects were studied using scanning and transmission electron microscopy. Microphthalmic and anophthalmic eyes of 16-day rat fetuses were utilized from dams exposed to a teratogenic dose of trypan blue. Retinal and lenticular anlagen were specifically examined for architectural and cellular changes. Nearly all severely abnormal eyes showed no evidence of retina development: Of 41 such eyes, only two retinal rudiments were observed. Those eyes with mild microphthalmia always demonstrated retinae although architectural changes were present. In every abnormal eye, some degree of lenticular morphogenesis was always present. Lenses were small, displaced in the eye field, and arrested at the lens vesicle stage. Lens cells were markedly undifferentiated and thus lacked most of the cytological features normally present at this developmental stage. Neither retinal nor lenticular rudiments were necrotic despite major architectural and cytological disturbances. The data offer three conclusions: First, the absence of necrosis suggests that trypan blue causes developmental arrest in this eye model; second, absence of retinae is most likely due to primary failure of optic vesicle development; third, lack of lens differentiation is attributed to absence of the retina, the primary lens inducer.

Abnormalities, Drug-Induced↗
PubMed1983

Klebsiella-induced LIF response in Klebsiella infection and ankylosing spondylitis.

Lymphocyte transformation and leucocyte migration inhibition was studied in Klebsiella-sensitized patients, ankylosing spondylitis patients and healthy controls. The results show that mononuclear cells from ankylosing spondylitis patients respond more vigorously to Klebsiella, one of the 'trigger' bacteria, than do mononuclear cells from healthy persons, either with or without HLA-B27.

Adult↗
PubMed1983

Glucose absorption by in vitro perfused colon of the fetal rat.

The anatomic configuration of fetal rat colon resembles that of the small bowel. Accordingly, glucose and amino acid absorption were measured in order to see whether the fetal rat colon resembled the small bowel functionally. In vitro luminal perfusion of the fetal rat colon at 20 days of gestation was employed to measure the rate of glucose and L-alanine absorption and the unidirectional flux rates of 3-O-methylglucose (3-O-MG). The colon was mounted between pipettes in a heated oxygenated bath and perfused with the solute to be studied dissolved in buffered physiological solution and polyethylene glycol with average molecular weight of 4,000 (PEG) as a nonabsorbable marker substance. The PEG was not transported and did not diffuse across fetal colon. Scanning and transmission electron microscopy of perfused and control colon showed the presence of villi and the preservation of mucosal anatomy during perfusion. Glucose was absorbed at 173 +/- 16 mumol . h-1 . g-1 (8) and absorption was abolished in Na-free solution. 3-O-MG flux was 40 +/- 7 mumol . h-1 . g-1 (8) from lumen to bath and 7 +/- 1 mumol . h-1 . g-1 (8) from bath to lumen. L-Alanine flux was 130 +/- 15 mumol . h-1 . g-1 (8) from lumen to bath and 18 +/- 4 mumol . h-1 . g-1 (5) from bath to lumen, and the lumen-to-bath flux was only partially abolished by Na-free solutions.

Alanine↗
PubMed1983

Rheumatoid factor-negative arthritis, especially ankylosing spondylitis, and infections of the male urogenital tract.

146 men with rheumatoid factor-negative (sero-negative) arthritis, i.e., 97 patients with ankylosing spondylitis, 36 patients with Reiter's syndrome, and 13 patients with reactive arthritis, were examined for infections of the urogenital tract by following recently established criteria. 74 patients (50.7%) had infections of the male adnexes: 3 patients suffered from balanitis, 14 patients from urethritis, 49 patients from prostatitis, 1 patient from epididymitis, and 7 patients from urinary tract infection. Balanitis and urethritis were almost exclusively associated with Reiter's syndrome. In 37 of 97 patients with ankylosing spondylitis, a urogenital tract infection, mainly a prostatitis (31 patients), was detected. The microorganisms isolated most frequently from patients suffering from urethritis and prostatitis, were Chlamydia trachomatis and Ureaplasma urealyticum.

Arthritis↗