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Biomedical subjects

R M O'Neal

Publications and source records attributed to R M O'Neal.

At least 19 recordsLinked to original sources
PubMed1990

Spinal cord thromboplastin-induced coagulopathy in a rabbit model.

Coagulopathy results from many diverse events, including several neurogenic causes. Using a rabbit model, we produced coagulopathy by injecting autologous spinal cord and extracted thromboplastin intravenously. Serial coagulation panels were performed to evaluate the activation of the thrombotic and fibrinolytic pathways. Group 1 animals (n = 4) received intravenous injections of homogenized spinal cord tissue. Coagulopathy was not produced with 36 mg of homogenized spinal cord tissue, but 50 mg or more resulted in death. Group 2 animals (n = 12) received intravenous injections of extracted rabbit cord thromboplastin, which contained approximately 60% activity of a commercially purified rabbit brain thromboplastin. Five animals receiving 2.5 to 5.5 mg of thromboplastin per kilogram of body weight survived with evidence of coagulopathy. Seven animals receiving 2.5 to 100 mg of thromboplastin per kilogram of body weight died. Group 3 (4 control animals) received normal saline injections without changes in clinical or laboratory status. The thrombotic pathway was activated in all animals as evidenced by decreased platelet counts and fibrinogen levels. Activation of the fibrinolytic system was demonstrated by increased concentrations of protamine sulfate and abnormal euglobulin clot lysis times. The most sensitive parameters were the platelet count, protamine sulfate concentration, and white cell count (margination), which became abnormal within 15 minutes after the injections and returned to normal within 1 hour.

Animals↗
PubMed1985

Functional and histologic changes in vein grafts exposed to crystalloid potassium cardioplegic solution.

A canine external jugular vein to iliac artery interposition model was devised to evaluate the potential deleterious effects of cold potassium cardioplegic solution exposure to saphenous vein grafts during aortocoronary bypass procedures. The right jugular vein was harvested from 11 animals and halved, one segment being perfused with 1 liter of normal saline solution (NS) at 4 degrees C over a period of 31.7 +/- 2.5 min at a perfusion pressure of 50.5 +/- 2.6 mm Hg, and the other segment perfused with 1 liter of crystalloid potassium cardioplegic solution (CP) at 4 degrees C over a period of 24.8 +/- 3.2 min at a perfusion pressure of 53.0 +/- 1.5 mm Hg. The measured differences in the perfusion times and pressures were not significant at P less than 0.05. The grafts were then interposed into the iliac artery systems of their respective animals, and transgraft pressure gradients were measured by direct needle puncture technique and found to be 12.6 +/- 5.9 mm Hg for the CP-treated grafts and 19.9 +/- 9.6 mm Hg for the NS-treated grafts. At the time of graft harvest 7.4 +/- 0.23 months later transgraft pressure gradients were again measured and found to be 2.5 +/- 1.8 mm Hg for the CP-treated and 2.9 +/- 1.7 mm Hg for the NS-treated grafts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Chlordecone-induced potentiation of carbon tetrachloride hepatotoxicity: a light and electron microscopic study.

Previous studies have shown that a chlorinated pesticide, chlordecone (Kepone), greatly potentiates carbon tetrachloride (CCl4) hepatotoxicity and lethality (Curtis, L.R., Williams, W.L., and Mehendale, H.M. (1979). Toxicol. Appl. Pharmacol. 51, 283-293; Curtis, L.R., and Mehendale, H.M. (1980). Drug Metab. Dispos. 8, 23-27). The present study describes sequential morphologic changes which occurred in livers of rats given a "nontoxic" level of chlordecone (10 ppm for 15 days) followed by a single injection of CCl4 (0.1 ml/kg). The hepatic alterations were examined 1 to 36 hr after exposure of the rats to CCl4. Those changes were compared to hepatic alterations which occurred in rats that received the same dose of chlordecone (10 ppm for 15 days) or a single injection of CClr (0.1 ml/kg) alone. The only change noted in livers from rats that received chlordecone alone was focal increase in smooth endoplasmic reticulum (SER) of hepatocytes at 24 hr and continuing throughout the time course of the experiment. Livers from animals that received CCl4 alone showed morphologic changes at 6 hr consisting of glycogen loss, increase in SER, and dilatation of rough endoplasmic reticulum (RER) in pericentral hepatocytes. Accumulation of small lipid droplets was also noted in midzonal hepatocytes. After 6 hr, there was no further increase in severity of injury. At 12 hr recovery was noticeable and, by 36 hr, livers from the CCl4 group appeared normal. Prior administration of chlordecone greatly potentiated pathologic changes in livers of animals that received CCl4. By 4 hr, there was total loss of glycogen in hepatocytes throughout the entire lobule. Small lipid droplets were present in pericentral, midzonal and periportal hepatocytes. Hepatocytes with extremely dilated RER were randomly scattered throughout the entire lobule. At 6 hr, there was further accumulation of lipid in the form of large droplets in hepatocytes. Focal, necrotic cells surrounded by polymorphonuclear leukocytes were randomly distributed throughout the lobule. The number of necrotic foci had progressively increased at the 12- and 24-hr intervals. By 36 hr, confluent areas of necrosis in pericentral and midzonal areas were observed in livers of some animals. This study indicates that although the combination of chlordecone and CCl4 produces much greater hepatic injury resembling damage due to a massive dose of CCl4, histologically, some differences in the progression and distribution of hepatocellular damage within the lobular architecture of the liver are evident.

Animals↗
PubMed1983

Chlordecone-induced potentiation of carbon tetrachloride hepatotoxicity: a morphometric and biochemical study.

The present study, conducted over a time course of 36 hr after CCl4 administration, describes sequential morphometric and biochemical changes which occur in livers of rats exposed to a combination of low levels of chlordecone (10 ppm for 15 days) and a single ip injection of CCl4 (0.1 ml/kg). Those changes were compared to hepatic alterations which occur in rats that received the same dose of chlordecone or CCl4 alone. Biochemical studies showed only trivial increases in levels of glutamic-pyruvic transaminase (GPT), glutamic-oxalacetic transaminase (GOT), and moderate but temporary increases in isocitrate dehydrogenase (ICD) after CCl4 alone. The combination of chlordecone and CCl4 resulted in significantly greater elevations of all three serum enzymes at all time intervals examined. Morphometric data showed no difference between normal diet controls and animals exposed to chlordecone alone as far as numerical density of hepatocytes or volume densities of hepatocytes with glycogen, lipid, dilated rough endoplasmic reticulum (RER), pyknosis, or mitoses. Morphometric analysis of livers from animals that received CCl4 alone showed decreases in numerical density, temporary decrease in percentage of hepatocytes containing glycogen, an increase in hepatocytes containing lipid, temporary increase in hepatocytes with dilated RER, and temporary increases in pyknotic nuclei. Soon after the initial hepatic injury was histologically evident between 4 and 6 hr, the number of mitoses increased dramatically and this progressed until complete recovery from CCl4 damage. From all indices of damage, complete recovery was evident by 36 hr after CCl4 administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1980

Multiple pulmonary scar carcinomas in a patient with Hodgkin's disease: report of a case and review of the literature.

A case of multiple pulmonary scar carcinomas arising in a 53-year-old woman with Hodgkin's disease is reported. Review of the literature reveals that scar carcinoma is generally thought to arise in areas of bronchiolar epithelial proliferation occurring in association with pre-existing lung scars. However, we and others have emphasized that, given the usual gross and histologic picture of scar carcinoma, it is impossible to state with certainty whether the carcinoma arose in response to the scar tissue, or the scar tissue formed consequent to the occurrence of repeated small foci of tumor necrosis. The association of Hodgkin's disease and multiple malignancies is also discussed.

Carcinoma↗
PubMed1980

Fatal hemorrhage from a ruptured aneurysm of a submucosal gastric artery.

We have described a case of rupture of a microaneurysm of a submucosal gastric artery, discovered at autopsy. Most patients with this condition present with upper gastrointestinal hemorrhage for which no obvious cause can be found clinically, and even laparotomy may fail to disclose the cause. Because the predence of this lesion may easily elude even experienced pathologists, increased awareness of this entity is needed for correct diagnosis and prompt surgical treatment, whithout which the condition has proved to be almost invariably fatal.

Aneurysm↗
PubMed1977

Effect of thiamine deficiency, pyrithiamine and oxythiamine on pyruvate metabolism in rat liver and brain in vivo.

Rats were fed either a thiamine-deficient diet of diets containing pyrithiamine or oxythiamine. When symptoms of thiamine deficiency appeared, the animals were injected intraperitoneally with [2-14C] pyruvate six to twelve minutes prior to sacrifice. Free glutamic and aspartic acids were isolated from liver and brain and degraded. The results indicate that, in thiamine-deficient or oxythiamine-treated rats, pyruvate metabolism in liver and brain is similar to that in normal animals. In contrast, pyrithiamine drastically decreases the oxidative decarboxylation of pyruvate by rat liver.

Animals↗
PubMed1977

Experimentally induced bleomycin sulfate pulmonary toxicity: histopathologic and ultrastructural study in the pheasant.

Morphological alterations in the lungs of pheasants after prolonged high-dosage administration of bleomycin sulfate were studied by light and electron microscopy. Nontreated birds acted as controls, and their lungs showed no abnormalities. Lungs of bleomycin-treated pheasants revealed collapse alternating with overexpansion, marked cuboidalization of atrial epithelium, and incipient interstitial fibrosis. There were neither lymphoplasmacytic or eosinophilic infiltrates, nor evidence of vasculitis. Ultrastructurally, type 1 alveolar epithelial cells were either reactive or conspicuously absent in the air capillaries. Type 2 alveolar epithelial cells appeared hyperplastic with numerous lamellar bodies, many of which extruded into air spaces. Immature fibroblasts were noted in the vicinity of collagen fibrils or amorphous material resembling elastin. No immune deposits were present in basement membranes. These findings are consistent with a direct toxic effect of bleomycin to the pheasant lung rather than a drug hypersensitivity reaction. Reproduction of the bleomycin lesion in a nonmammalian species corroborates even further the high propensity of the drug to affect the lung.

Animals↗
PubMed1977

Derivation of intimal smooth muscle cells in normal arteries and atherosclerotic plaques. An overview.

We have no evidence of the precise derivation of myointimal cells, either in 'normal' intima or in atherosclerotic lesions. Neither has any derivation been eliminated. Efforts to establish the origin of the cells might be as helpful to our understanding of the lesions as have been the studies of proliferation of SMC, regardless of which one of the various theories of the pathogenesis of atherosclerosis we happen to support.

Arteries↗
PubMed1976

The incidence of anemia in residents of Missouri.

A state-wide nutritional health survey of Missouri residents conducted in 1973 included hemoglobin, hematocrit, and serum iron determinations on approximately 1,164 persons and dietary iron intake estimates, based on a diet history, for 530 persons. Based on the criteria used for interpretation of the Ten-State Nutrition Survey data, over 19% of all preschool age white children and over 10% of the white children six to 10 years old had low or deficient hemoglobin levels. Between 8 and 17% of the white males between 10 and 60 years old and over 30% of the white males over 59 years old were anemic. Between 3 and 9% of all white females over 9 years of age had low or deficient hemoglobin levels. The levels of anemia for most age and sex groups of Negroes were at least twice as great as for corresponding groups of white persons. Low or deficient hemoglobin levels within the age and sex groups were associated with low hematocrit and serum iron levels; suggesting that some of the anemia was a reflection of iron deficiency. Estimates of the dietary intake of iron indicated that less that 20% of the females 10 to 35 years old and less than 60% of older females and boys under 17 years of age were consuming the Recommended Dietary Allowances. Over 35% of the preschool children and females between 10 and 60 years old were consuming less than two-thirds of their Recommended Dietary Allowances for iron. At least part of the iron deficiency was, therefore, indicated to be related to insufficient dietary intake.

Adolescent↗