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Biomedical subjects

L B Thomas

Publications and source records attributed to L B Thomas.

17 recordsLinked to original sources
PubMed1991

Immunohistochemical detection of a monoclonal antibody directed against the NGF receptor in basal forebrain neurons following intraventricular injection.

It has been shown by autoradiography that, following intraventricular administration, a monoclonal antibody directed against the rat nerve growth factor (NGF) receptor is specifically accumulated bilaterally by numerous cholinergic neurons of the basal forebrain. This is consistent with the evidence that cholinergic basal forebrain neurons have NGF receptors and respond to NGF under a variety of experimental conditions. The present study demonstrates that the immunohistochemical detection of unmodified monoclonal antibody in cholinergic forebrain neurons following transport from CSF is feasible, although injection of larger amounts of the antibody is required to obtain an image equivalent to the one obtained with the autoradiographic method. The location of the immunohistochemical product clearly indicates that the antibody has been internalized, probably in an endosomal compartment.

Animals↗
PubMed1989

Effect of lidocaine after experimental cerebral ischemia induced by air embolism.

To investigate possible approaches to the treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, somatosensory evoked potentials (SEP's) were measured after cerebral air embolism in the anesthetized cat. Air was introduced into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to approximately 10% or less of baseline values. Either a saline or lidocaine infusion was begun 5 minutes after inducing cerebral ischemia. In the saline-treated group, SEP amplitude was reduced to 6.7% +/- 1.6% (mean +/- standard error of the mean) of baseline, with a return to 32.6% +/- 4.7% of baseline over a 2-hour period. In the lidocaine-treated group, SEP amplitude was reduced to 5.9% +/- 1.5%, with a return to 77.3% +/- 6.2% over a 2-hour period. The results suggest that lidocaine administration facilitates the return of neural function after acute cerebral ischemia induced by air embolism.

Animals↗
PubMed1987

Hormonal changes during decompression sickness.

Changes in plasma hormone levels were studied in anesthetized dogs during decompression sickness. Hormone levels were measured in 4 groups: control (no dive, n = 9); air group (air dive, ventilated with air postdive, n = 6); helium-oxygen (He-O2) group (air dive, ventilation changed to He-O2 at 30 min postdive, n = 9); nonsurvivor group (air dive, died within 30 min postdive, n = 9). Dived animals were subjected to repetitive dives until pulmonary artery pressure doubled. Plasma epinephrine (Epi) and norepinephrine (NE) concentrations rapidly increased postdive in all animals. Serum angiotensin-converting enzyme (ACE) activity increased postdive in the He-O2 group only, and these increases were small. Diving did not alter serum concentrations of cortisol, thyroxine (T4), or triiodothyronine (T3); however, T4 and T3 fell in all animals, probably as a consequence of anesthesia. He-O2 breathing did not affect concentrations of Epi, NE, cortisol, T4, T3, or serum ACE activity.

Animals↗
PubMed1987

Effects of He-O2 breathing during experimental decompression sickness following air dives.

The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.

Animals↗
PubMed1987

Failure of heparin, superoxide dismutase, and catalase to protect against decompression sickness.

The effects of heparin (HEP), superoxide dismutase (SOD), and catalase (CAT) on the course of decompression sickness (DCS) were studied in anesthetized dogs (Canis familiaris). Animals were divided into 4 groups: a drug assay group (n = 4) received HEP + SOD or HEP + SOD + CAT but were not dived; a control group (n = 14) was dived without drug treatment; a HEPSOD group (n = 11) received HEP + SOD predive and postdive; and a HEPSODCAT group (n = 15) received HEP + SOD + CAT before diving. All dived animals were subjected to repetitive air dives to 10 ATA until pulmonary artery pressure at least doubled within 10 min postdive. Physiologic variables were measured for 3 h postdive or until death. Animals were not recompressed. More early deaths occurred in the HEPSOD (7/11) and HEPSODCAT (8/15) groups than in the control group (5/14). All dived animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, acidosis, hypoxemia, and interstitial pulmonary edema postdive. Drug therapy did not alter these responses to decompression. We conclude that without recompression, treatment with either HEP + SOD OR HEP + SOD + CAT does not improve the outcome of severe DCS in this animal model.

Animals↗
PubMed1979

Hepatic angiosarcoma associated with androgenic-anabolic steroids.

A retrospective epidemiological study of deaths from hepatic angiosarcoma (HAS) in the U.S. showed that during 1964--74 there were 168 such cases, of which 37 (22%) were associated with previously known causes (vinyl chloride, 'Thorotrast', and inorganic arsenic) and 4 (3.1%) of the remaining 131 cases with the use of androgenic-anabolic steroids. It is suggested that the long-term use of androgenic-anabolic steroids is the fourth cause of HAS, the majority of cases still being of unknown aetiology. Moreover, the presented cases serve as a link in a spectrum of hepatic disorders recently recognised to be caused by environmental agents such as vinyl chloride, arsenic, and thorotrast, and by contraceptive and anabolic steroids. Similar precursor stages, usually not recognised by clinical laboratory tests and consisting of areas of hyperplasia of hepatocytes and sinusoidal cells and sinusoidal dilatation, lead potentially to hepatic adenoma, carcinoma, peliosis, and angiosarcoma.

Androstanes↗
PubMed1978

Development of hepatic angiosarcoma in man induced by vinyl chloride, thorotrast, and arsenic. Comparison with cases of unknown etiology.

Examples of human angiosarcoma following exposure to vinyl chloride, Thorotrast, or arsenic (medicinal and industrial) and cases, including children, of unknown etiology were studied to establish diagnostic criteria and to study their evolution. The uniform evolution suggests an environmental factor also in the cases of unknown etiology, which may be established by epidemiologic studies. A precursor stage is charaterized by areas of combined hyperlasia of hepatocytes and a variety of sinusoidal and perisinusoidal cells associated with excess of reticulin and with sinusoidal dialation. The diagnostically useful picture in silver impregnations indicated reticulum formation by the perisinusoidal cells, presumably the libocytes. The hepatocytic proliferation suggests a hepatocarcinogenic but usually not fully expressed potential. The mixed hyperplasia of the various sinusoidal cells proceeds to an overgrowth of angiosarcoma cells, presumably derived from endothelial cells. In early stages they are usually in contact with hepatocytes (intralobular growth). A trabecular arrangement results from loosening of the lobular plate arrangement by dilatation of sinusoids, leading to primary peliosis. With disappearance of the hepatocytes, various growth patterns develop, terminating in nodular, solid angiosarcoma composed of either spindle-shaped or polyhedral cells which undergo necrosis or hemorrhage (secondary peliosis). The interaction between hepatocytes and sinusoidal cells requires elucidation.

Adolescent↗
PubMed1975

Alterations of liver and spleen among workers exposed to vinyl chloride.

Preliminary review of hepatic biopsy and autopsy specimens obtained from workers engaged for prolonged periods in the polymerization of vinyl chloride indicates a fibrotic precursor lesion in the liver. It is the only lesion in some instances but also was found in the uninvolved liver of patients with angiosarcoma and in two instances in liver biopsy specimens obtained before angiosarcoma developed. This precursor stage is characterized by a conspicuous subcapsular fibrosis, a nonpathognomonic progressive portal fibrosis, and a borderline increase of intralobular connective tissue, all associated with focal stimulation of sinusoidal lining cells and hepatocytes. This precursor stage is often accompanied by splenomegaly with enlarged Malpighian follicles and in some instances by portal hypertension requiring portacaval shunt because of variceal hemorrhage. The portal hypertension is explained by increased splenic blood flow in the face of nondistensible fibrotic portal tracts as well as Glisson's capsule. Transition to angiosarcoma is preceded by focal dilatation of sinusoids with even greater activation but dedifferentiation of their lining cells. This lesion is presumably the result of stimulation of various hepatic as well as splenic cells by vinyl chloride or its metabolites. The demonstrated evolution is identical with that following prolonged exposure to inorganic arsenicals. It is postulated also that other instances of inconspicuous hepatic fibrosis associated with splenomegaly and often with portal hypertension, a combination designated as Banti's syndrome or "idiopathic portal hypertension," are the result of a toxic, possibly environmental agent, particularly since the disease is found with greater frequency in some parts of the world. The delineation of the fibrotic precursor stage in the liver may assist in the epidemiologic studies of the vinyl chloride-induced injury.

Arsenic Poisoning↗
PubMed1975

Pathology of angiosarcoma of the liver among vinyl chloride-polyvinyl chloride workers.

We described the histologic features of 13 hepatic angiosarcomas which developed in workers engaged in the polymerization of vinyl chloride to polyvinyl chloride. Although the histologic features varied considerably in different portions of the angiosarcoma in the same liver and in the angiosarcomas of the liver from different patients, many features were similar such as sinusoidal, papillary, and cavernous growth patterns coincident with the precursor lesions of proliferation and atypia of sinusoidal lining cells.

Hemangiosarcoma↗
PubMed1975

Vinyl-chloride-induced liver disease. From idiopathic portal hypertension (Banti's syndrome) to Angiosarcomas.

Histologic examination of liver tissue (eight autopsy and 18 biopsy specimens) and five spleens from 20 workers with vinyl chloride polymerization showed hepatic angiosarcomas in 15. In addition, a peculiar pattern of progressive portal-tract, inconspicuous intralobular and conspicuous capsular fibrosis was observed in the five workers without angiosarconma, in all the seven patients with angiosarcoma from whom tumor-free portions of the liver were available, and in two tumor-free biopsies from patients subsequently found to have angiosarcoma. The fibrosis was accompanied by splenomegaly. Hypertrophy and hyperplasia of both hepatocytes and hepatic and splenic mesenchymal cells were also seen. The histologic similarity to chronic inorganic arsenical poisoning, in which angiosarcomas also occur, and to idiopathic portal hypertension (Banti's syndrome) suggests that the latter syndrome at times results from unknown toxic, possible environmental, chemicals.

Autopsy↗