PubMed Health⌕ Search

Biomedical subjects

R L Swarm

Publications and source records attributed to R L Swarm.

15 recordsLinked to original sources
PubMed1981

Ultrastructural study of rat liver and liver neoplasms after long-term treatment with phenobarbital.

The purpose of this investigation is to study the ultrastructure of liver and liver neoplasms after long-term administration of phenobarbital. Liver from female Charles River rats treated with 0.1% sodium phenobarbital by dietary admix for 60, 180, or 113 weeks was examined; liver neoplasms present at 108 or 113 weeks were also examined. At 60 weeks, an outstanding feature of most hepatocytes was the extensive proliferation of smooth endoplasmic reticulum, increase in autophage vacuoles, lysosomes, blebbing, and Kupffer cells containing phagosomes. At 108 or 113 weeks, additional changes in liver included an abundance of myelin figures in vacuoles, sinusoids, and bile canaliculi and the occasional appearance of whorls of smooth endoplasmic reticulum. Hepatocytes from liver neoplasms, all identified as well-differentiated hepatic cell neoplasms, contained voluminous whorls and large phagosomes filled with whorls, myelin figures, and cellular debris. The phagosomes were present both intracytoplasmic and intrasinusoidal, either partially or completely surrounded by Kupffer cell extensions. These cellular alterations are interpreted as evidence of adaptive cellular responses.

Age Factors↗
PubMed1980

Elimination of excess smooth endoplasmic reticulum after phenobarbital administration.

Livers from Charles River rats during and after treatment with phenobarbital were studied in order to investigate possible mechanisms involved in the elimination of excess smooth endoplasmic reticulum. The most pronounced structural change during compound administration was proliferation of smooth endoplasmic reticulum; depletion of glycogen and an increase in lipid deposits were also observed. After termination of treatment, these changes were reversed. The appearance of an increased number of autophage vacuoles and lysosomes plus the localization of acid phosphatase reaction product in these bodies suggests autophagy as one possible mechanism for the elimination of excess smooth endoplasmic reticulum. Cytoplasmic blebs and fragments replete with smooth endoplasmic reticulum were observed within the sinusoids. The presence of Kupffer cell cytoplasmic extensions surrounding these fragments and acid phosphatase reaction product within Kupffer cell inclusions suggests heterophagy as another process participating in the removal of excess smooth endoplasmic reticulum.

Animals↗
PubMed1976

Chenodeoxycholic acid induced liver injury in pregnant and neonatal baboons.

The prolonged feeding of chenodeoxycholic acid produces hepatic injury in both pregnant and non-pregnant baboons. CDC feeding does not adversely affect ovarina function and no teratogenic effects of this bile acid were noted in 16 live birth and two stillborn progeny of CDC fed animals. However, 10 of the 16 live birth neonates and one stillborn had focal hepatic lesions histologically similar to those observed in the adult animals. In addition one neonate had gross hepatic necrosis. The severity of the liver damage was related to the content of lithocholic acid in the bile of both the neonates and their mothers. Experiments with 14C-chenodeoxycholic and 14C-lithocholic acid demonstrate that the lithocholate in the enterohepatic circulation of the neonate is derived from the CDC fed to the pregnant adult. In the gallbladder bile of the neonate most, but not all, of the lithocholate is conjugated but unsulfated. Both newborn and adult baboons sulfate lithocholic acid but to an extent less than that reported for man. Less efficient sulfation of lithocholic acid in the baboon may exaggerate the toxicity of CDC feeding in this species compared to man. Nevertheless, the potential for adverse effects on the fetal liver must be recognized as a risk associated with the use of chenodeoxycholic acid in women of child-bearing age.

Animals↗
PubMed1976

Electron microscopic study of virus particles in yolk sac and placenta and in hematopoietic organs of newborn C3Hf mice.

Examination of yolk sac from a C3Hf and a C3H mouse with the electron microscope revealed the presence of C-type virus particles in the blood islands. Particles were observed budding from the plasma membrane of hemocytoblasts, from erythroblasts, and occasionally from reticulocytes. C-type particles were also found in similar cells in hematopoietic foci in the liver, spleen, and bone marrow of embryos, and they continued to be present in newborn C3Hf mice up to 11 days of age. Particles consistently appeared in the thymus, even in older suckling mice. A comparison is made between the presence of C-type particles in organs of embryonic, newborn, and adult C3Hf mice. C-type particles were not observed in the chorioallantoic placentas from mice that were given injections of mouse leukemia virus (Gross) or from normal noninjected mice; however, intracisternal A-type particles were present in cytotrophoblast cells from these placentas.

Age Factors↗
PubMed1975

Toxicity of chenodeoxycholic acid in the nonhuman primate.

Toxicologic aspects of long-term therapy with the gallstone-dissolving agent, chenodeoxycholic acid (CDC) are under study in the baboon. Eighteen animals, subdivided into low (20 mg. per kilogram per day), incremental (18 to 38 mg. per kilogram per day), and high (38 mg. per kilogram per day) dose groups were fed CDC daily for 8 to 15 months. During that period they maintained on appearance of excellent, unchanged health and behavior indistinguishable from that of eight control animals. However, 15 of the 18 CDC-fed animals showed significant elevations of monthly serum glutamic pyruvic transaminase-serum glutamic oxalacetic transaminase determinations, and 14 of the 18, from all dose groups, developed significant focal histologic changes in serial liver biopsies. Histologic changes are similar to those described for lithocholic acid toxicity and correlate with an elevated percentage of chenodeoxycholic acid and, particularly, with lithocholic acid (8 to 14 percent) in gallbladder bile of the CDC-fed animals. A few CDC-fed animals showed histologic changes without enzymatic changes and vice versa. To date none of the focal hepatic lesions appears irreversible; it is too early to determine whether continued CDC feeding results in progression, stabilization, or regression of changes. More intensive surveillance of human subjects receiving chenodeoxycholic acid is indicated.

Alanine Transaminase↗