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Biomedical subjects

C G McLeod

Publications and source records attributed to C G McLeod.

At least 19 recordsLinked to original sources
PubMed2006

Intestinal choristoma in the subcutis of a dog.

A 2-year-old, spayed female, Labrador Retriever-cross presented with a subcutaneous mass of several weeks' duration in the right flank region. Surgical excision and histologic examination were performed. The 1.0-cm-diameter mass was circumscribed, unencapsulated, and cystic with a bilayer wall. The inner layer resembled intestinal mucosa, including a tall columnar lining epithelium, crypt-like glands containing scattered neuroendocrine cells that were strongly immunopositive for synaptophysin, and a supporting lamina propria-like fibrovascular tissue that contained lymphocytes and plasma cells. The outer layer was 1- to 2-mm thick and was composed of intersecting and blending bundles of smooth muscle and collagen. Given the presence of organized intestinal tissues in the subcutis, the lesion was consistent with intestinal choristoma.

Animals↗
PubMed2000

Systemic Exophiala jeanselmei infection in a cat.

A 14-year-old spayed domestic shorthair cat was referred for ultrasonographic evaluation of abnormally shaped kidneys. Multifocal lesions were detected ultrasonographically in the liver and kidneys; a fine-needle aspirate of the kidneys was performed, and numerous clumps of fungal hyphae were identified. The following day, the cat was recumbent with advanced neurologic signs. The cat was euthanatized, and a necropsy was performed. Multifocal granuloma-like masses were seen on the liver, kidneys, abdominal wall, mesentery, thoracic wall, pericardium, and epicardium. Similar lesions were found on the cervical portion of the spinal cord, the cerebrum, and cerebellum. Exophiala jeanselmei, an organism of the phaeohyphomycotic group, was identified on fungal culture. To our knowledge, systemic infections caused by this organism have not been reported. However, phaeohyphomycotic infections are believed to be an emerging disease in humans.

Abdomen↗
PubMed1992

Pyloric adenocarcinoma in a ferret.

Pyloric adenocarcinoma was diagnosed in a ferret with clinical signs of gastric distention. The development of this tumor may be related to Helicobacter mustelae infection in the gastric mucosa of ferrets. Pyloric adenocarcinoma has only recently been reported in ferrets and should be considered as a differential diagnosis for gastric distention in this species.

Adenocarcinoma↗
PubMed1987

Direct microinjection of soman or VX into the amygdala produces repetitive limbic convulsions and neuropathology.

Rats were injected in the amygdala and other forebrain sites with nmolar amounts of the highly toxic organophosphate 'nerve agent' compounds soman or VX (O-ethyl-S-(2-diisopropylaminoethyl)-methylphosphonothioate) in an attempt to determine the mechanism(s) responsible for the permanent brain pathology that has been observed following systemic intoxication with these agents. Injections were performed using a stereotaxically guided microsyringe in animals maintained under halothane/oxygen anesthesia or using chronically implanted cannulae in conscious animals. Bilateral microsyringe injections of up to 11.0 nmol soman into the amygdala failed to evoke abnormal behavior or brain pathology. When rats were pretreated with lithium chloride, or when carbachol was coadministered, soman injections evoked repetitive clonic convulsions and neuropathology. Unilateral injections of 3.4 nmol of VX into the amygdala elicited convulsions and brain damage in 67% of the animals tested. Atropine pretreatment (15.0 mg/kg, i.p.) prevented the development of convulsions and brain damage. Neuropathology was observed only in animals that developed repetitive convulsions; the piriform and entorhinal cortex, amygdala, hippocampus and thalamus were the brain structures most consistently damaged. With unilateral injections, the damage was more severe on the side ipsilateral to the injection. The behavioral topography of the convulsions and the neuroanatomical distribution and nature of the subsequent pathology closely resemble that observed with systemic administration of these compounds. The results indicate that the nerve agents are not directly neurotoxic, that peripherally induced hypoxia or anoxia are unlikely mechanisms of the neuropathology, and that the brain damage produced by these compounds is primarily seizure-mediated.

Amygdala↗
PubMed1987

Cardiomyopathy in Soman and Sarin intoxicated rats.

Rats surviving various single dose of the organophosphorus anticholinesterase nerve agents Soman and Sarin were examined by light microscopy at intervals up to 35 days post-exposure. Brain lesions, identical to those that have been reported elsewhere were present, as well as a previously unreported finding associated with Soman or Sarin intoxication: half of all animals that had brain lesions also had areas of myocardial degeneration and necrosis. Depending upon the point in time at which cardiac tissues were examined, findings varied from areas of acute myolysis and necrosis to areas undergoing resolution of damage. The finding of brain lesions in those animals having cardiac lesions suggests a relationship between the convulsion induced neurologic and cardiac lesions. These studies suggest that convulsive doses of chemical warfare agents induce pathological changes in the cardiovascular system of laboratory animals.

Animals↗
PubMed1985

Pathology of nerve agents: perspectives on medical management.

Recent investigations at several institutes have demonstrated extensive acute brain pathology in experimental animals exposed to single subcutaneous doses of the chemical warfare nerve agents soman or sarin. Lesions include neuronal and neurophil degeneration, necrosis, and in animals that survive for several weeks, a degenerative encephalopathy characterized by mineralization, encephalomalacia, atrophy, and hydrocephalus. The cerebral cortex, amygdaloid complex, hippocampus, and multiple thalamic nuclei are consistently affected. This pattern of injury resembles that described for epilepsy and ischemic brain injury. Some animals have cardiac lesions characterized by acute necrosis with subsequent mild inflammation and fibrosis. Anticonvulsants protect experimental animals from lesion development. In rats, this encephalopathy causes long-range behavioral changes characterized by hyperactivity during routine handling and variances in traditional behavioral tests. The histopathologic features and distribution of lesions in nerve agent-poisoned animals support the hypothesis that epileptiform seizure activity is a major factor in nerve agent pathology. Other localized insults such as ischemia and hypoxia probably contribute to the pathogenesis.

Animals↗
PubMed1985

Soman-induced brain lesions demonstrated by muscarinic receptor autoradiography.

Repeated exposure of rats to sublethal doses of soman resulted in moderate to severe symptoms of anticholinesterase intoxication and a pronounced weight loss within a small subgroup of these animals. A consistent pattern of cell loss and extensive neuronal necrosis appeared in specific brain areas within this subgroup. This neuropathology was not noted in rats unless they showed marked symptoms of poisoning including a precipitous weight loss. Neuropathology was most notable in the piriform cortex and thalamus. Quantitative receptor autoradiography indicated that these subjects had a significant decrease in muscarinic receptors in the piriform cortex and thalamus. The ratio of the muscarinic receptor densities in soman-treated rats with lesions to soman-treated rats without lesions was 57%, piriform cortex; 64%, ventrolateral thalamus; and 50%, mediodorsal thalamus. These decrements are distinguished from adaptive down-regulation because they are larger, there is no indication of recovery and there is a correspondence between histological lesions and the areas with decreases in muscarinic receptors. Thus, quantitative receptor autoradiography provides, in addition to kinetic information and topographical distribution, radiohistochemical evidence of neuronal damage.

Animals↗
PubMed1984

Acute neuropathology in soman poisoned rats.

Groups of rats received single subcutaneous injections of the highly toxic organophosphate compound, soman, in doses of 106, 133 or 165 micrograms/kg and were observed during the acute phase of intoxication. Survivors were killed at intervals up to fourteen days after exposure, and brain sections were examined by light microscopy. A consistent pattern of neuronal degeneration and necrosis was observed in brains of animals which had experienced convulsions during the intoxication. The lesions had an appearance and distribution similar to that reported for both hypoxic injury and status epilepticus. No lesions were observed in animals which did not experience convulsions. The results indicate that soman, and possibly other similar organophosphate compounds, may produce significant irreversible damage to the central nervous system.

Acute Disease↗
PubMed1982

Experimental Proteus mirabilis burn surface infection.

We established a human burn isolate of Proteus mirabilis as an experimental pathogen. Infliction of a nonfatal scald injury (30%) rendered rats highly susceptible to lethal surface infection with this isolate. Dose-response experiments indicated that the lethal inoculation dose (50%) was less than 10(3) organisms per square centimeter. Histopathologically, surface colonization was followed by progressive growth with subsequent invasion of viable tissue. The invasion was not characterized by the perivascular or perineural lesions observed in experimental Pseudomonas burn sepsis. Bacteriologic examinations showed moribund animals to be bacteremic with the test strain and to have wound biopsy counts exceeding 10(6) organisms per gram of tissue. The role of bacterial motility as a virulence factor in this surface infection was investigated. Substrains selected for loss of subsurface spreading in soft agar lost virulence. This model of burn infection with a member of the Enterobacteriaceae should be used to evaluate topical and parenteral antimicrobial agents needed for the control of wound infections caused by such agents.

Animals↗
PubMed1981

Experimental inhalation injury in the goat.

Inhalation injuries are usually produced by inhalation of gaseous or particulate products of incomplete combustion and are rarely due to heat per se unless steam is inhaled. The clinical and anatomic characteristics of an appropriate animal model should mimic the disease encountered clinically. A model of inhalation injury has been produced in anesthetized goats through the use of a modified bee smoker. The smoke is delivered at a low temperature and contains byproducts of incomplete combustion. This reproducible injury produces necrotic tracheobronchitis and bronchiolitis with pseudomembrane and cast formation in association with mild multifocal atelectasis and bronchopneumonia. These lesions spontaneously resolve within 3 weeks without supportive therapy. The upper trachea, protected from smoke injury by the inflated cuff of the endotracheal tube, showed no evidence of injury. This nonlethal injury is proposed as an appropriate model for evaluation of the pathophysiology and treatment of inhalation injury.

Animals↗
PubMed1980

Control of blood flow in a large surface wound.

To study the factors which control the increased blood flow to a large granulating wound, Doppler flow probes were implanted around the external iliac arteries bilaterally in 20-40 kg goats. Following operative recovery and basal measurements, skin was excised from one hind limb. Blood flow in the injured leg of five awake, resting goats rose above that of the uninjured leg by the fourth postoperative day and plateaued at 70-90% above uninjured leg flows for the next two weeks. The increase in injured leg blood flow was associated in time with the formation of a highly vascularized wound. This increased blood flow to the injured leg persisted in 11 anesthetized goats studied 9-12 days postinjury (186 +/- 27 ml/minute versus 107 +/- 19, p < 0.01, mean +/- SEM). Substrate turnover revealed that elevated blood flow to the injured leg was not the result of increased oxygen consumption, but was associated with increased glucose uptake (7.8 +/- 1.1 mg/minute versus 2.7 +/- 0.6, p < 0.001) and lactate release (3.6 +/- 1.3 mg/minute versus 1.1 +/- 0.7, p < 0.05). Limitations in oxygen delivery failed to explain the increased blood flow to the injured leg, since raising arterial PO(2) or exposing the leg to a high oxygen environment had no effect on limb perfusion. Although lactate and potassium, both potential vasodilators, were elevated in the femoral vein blood from the injured leg, a series of cross perfusion studies failed to reduce vascular resistance in another leg on the same or a second uninjured animal. Additional studies revealed that changes in leg vascular resistance were markedly diminished in the injured leg following hemorrhage, spinal anesthesia, or intravenous infusion of epinephrine or norepinephrine. These studies of large granulating wounds reveal: 1) elevated injured leg flow is not the result of local hypoxia; 2) any wound vasodilators have no impact on systemic circulation; 3) the wound vasculature appears relatively insensitive to circulating and neurogenic vasomotor drives.

Animals↗
PubMed1979

The use of lyophilized vein grafts in vascular access for chronic hemodialysis.

The feasibility of utilizing lyophilized veins for creation of A-V fistulas was examined in two studies. In Study I, the longevity of lyophilized vein fistulas was found to be comparable to that of fresh veins in the experimental animal. Study II showed that lyophilized cadaveric veins performed at least as well as bovine grafts when used for vascular access in chronic hemodialysis patients. The advantages of lyophilized veins for creation of A-V fistulas in dialysis patients are described.

Animals↗
PubMed1979

Evaluation of Pseudomonas aeruginosa toxin A in experimental rat burn wound sepsis.

The search for methods to achieve control of Pseudomonas aeruginosa infection continues with the introduction of aluminum-absorbed toxoid developed from P. aeruginosa exotoxin. This toxoid induces significant titers of neutralizing and precipitating antibodies for toxin A when given with appropriate adjuvants. These experiments show that immunization with aluminum phosphate-absorbed toxoid failed to protect burned rats infected with P. aeruginosa. These and previous experiments show that active immunization with live P. aeruginosa provides good strain-specific protection in the same model. No cross-protection was demonstrated between strains of P. aeruginosa in these experiments.

Animals↗
PubMed1979

The role of cimetidine in the prevention of stress induced gastric mucosal injury.

The results of these studies assessed the value of pretreatment with cimetidine in the prevention of gastric mucosal erosions secondary to stress. Ninety-four female C-D rats were divided into two trials using cold restraint stress. In trial 1, intraperitoneal cimetidine, administered prior to stress, significantly reduced the number of glandular mucosal lesions per animal, X +/- S.E.M., compared with saline solution controls, 1.2 +/- 0.5 versus 8.4 +/- 1.7. In trial 2, addition of hydrochloric acid given intragastrically to rats pretreated with cimetidine resulted in the same lesion rate per stomach as in the saline solution control group, 5.9 +/- 0.7 versus 6.1 +/- 0.6. Rats receiving cimetidine alone exhibited a reduced lesion rate, 1.2 +/- 0.4. The results demonstrate the ability of cimetidine to reduce gastric injury produced by cold induced stress. Furthermore, this action appears to be related to the pharmacologic effects which decrease gastric acid production.

Animals↗
PubMed1978

"Fruiting bodies" of aspergillus on the skin of a burned patient.

A case of a young man with an extensive total-body-surface burn complicated by wound infection is presented. One of the fungal organisms in the cutaneous burn wound had morphologically characteristic and diagnostic features by development of conidiophores ("fruiting bodies") pathognomonic of Aspergillus spp.

Adult↗