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Biomedical subjects

P F Lord

Publications and source records attributed to P F Lord.

At least 19 recordsLinked to original sources
PubMed2003

Pulmonary oedema in Swedish hunting dogs.

A syndrome of acute dyspnoea after hunting in 16 Swedish hunting dogs is characterised. Radiographic pulmonary infiltrates interpreted as pulmonary oedema were found in the acute stage. In 12 dogs, the infiltrates regressed after five to 14 days. Subendocardial necrosis and pulmonary oedema were found at postmortem examination in four other dogs with acute and recurrent dyspnoea after hunting, and myocardial fibrosis in a further three dogs with a history of recurrent dyspnoea after hunting; none of these pathological changes was seen in dogs which had no previous history of dyspnoea after hunting. A pathogenetic mechanism is proposed whereby high catecholamine levels, present during hunting due to the stress of excitement and exercise, cause acute cardiac and pulmonary lesions in some susceptible dogs, similar to neurogenic or postictal pulmonary oedema.

Acute Disease↗
PubMed1998

Quantitative estimation of intestinal dilation as a predictor of obstruction in the dog.

Mechanical obstruction is a major differential diagnosis for dogs presented with gastrointestinal problems. Small intestinal dilation is a cardinal sign of obstruction but its recognition depends upon the observer's experience and anecdotally derived parameters for normal small intestinal diameter. The objective of this study was to formulate a quantitative index for normal intestinal diameter and evaluate its usefulness in predicting small intestinal obstruction. The material consisted of survey abdominal radiographs of 50 normal dogs, 44 cases of intestinal obstruction and 86 patients which subsequently had an upper gastrointestinal examination. A ratio of the maximum small intestinal diameter (SI) and the height of the body of the fifth lumbar vertebra at its narrowest point (L5) was used, and a logistic regression model employed to determine the probability of an obstruction existing with varying degrees of intestinal dilation. A value of 1.6 for SI/L5 is recommended as the upper limit of normal intestinal diameter for clinical use. The model showed that obstruction is very unlikely if the SI/L5 value is less than this. Higher values were significantly associated with obstruction.

Animals↗
PubMed1990

Accuracy of formulae for calculating left ventricular volumes of the equine heart.

Echocardiography may be an accurate method of measuring left ventricular (LV) volumes and mass of the horse's heart. If so, studies of the heart size and hypertrophy would be possible. This study evaluated geometric models of the external and internal LV shapes, to determine which could be applied to echocardiographic measurements. We preserved 30 horses' hearts and measured their dimensions and cross sectional areas. These measurements were entered into seven formulae representing different geometric models of the ventricle and its chamber. We derived a correction factor to estimate the long axis as a fixed proportion of the external diameter, so that volumes could be determined from an M-mode or a cross sectional echocardiogram. Statistical analysis of the regressions of known volumes against calculated volumes measured by water displacement, demonstrated that the ellipsoid formula using cross sectional areas was very accurate in representing the external shape of the left ventricle (slope = 1.01 r2 = 96.3) and its chamber (slope = 0.83, r2 = 94.3). Myocardial volume, measured by subtracting internal (chamber) volume from external volume, was also calculated accurately (slope = 1.01, r2 = 96.5). The ellipsoid formula using directly measured diameter was only slightly less accurate. LV mass could be calculated by applying the specific gravity of equine myocardium, 1.05, to the myocardial volume. Formulae recommended for evaluating are, with M-mode echocardiography: [equation: see text] and with 2D echocardiography [equation: see text] where De is the external diameter, Di is the internal diameter, Ae the external area and Ai the internal area.

Animals↗
PubMed1989

Development and decay of systemic thermotolerance in rats.

The development and decay of thermotolerance to the lethal effect of systemic hyperthermia was investigated in Sprague-Dawley rats. Systemic hyperthermia was induced by partial submersion of gas-anesthetized rats into a temperature-controlled water bath. Survival was determined in rats challenged for periods of 10 to 90 min at 42.5 C, 24 to 144 h after a sublethal conditioning exposure of 41.8 C for 1 h. Survival curves of various exposure times at 42.5 C lethal to 50% of the animals (LD50) were determined for the conditioned animals and compared with those obtained for simultaneously treated control (unconditioned) rats. The thermotolerance ratios (TTR-LD50 for conditioned animals at various times after sublethal conditioning exposure divided by the LD50 for the control animals) were calculated and compared with the ratios reported in the literature for cells heated in vitro and for tissues heated locally in vivo. Pretreatment of rats at 41.8 C for 1 h resulted in an increase in the LD50 when rats were challenged 24 to 96 h later, with a maximum increased noted at 48 h (56.5 vs. 25.0 min for control; TTR = 2.3). The animals remained relatively resistant to the second heat treatment at 96 h and returned to control levels of heat sensitivity by 120 h. The development and kinetics of thermotolerance to lethality induced by whole-body hyperthermia need to be considered when multiple-fraction hyperthermia treatment plans are designed.

Adaptation, Physiological↗
PubMed1987

Coumadin and 111In-labeled platelet uptake on experimental thrombi in dogs. Preliminary observations.

The effect of coumadin treatment upon the uptake of 111In platelets (111In-P) in dogs by experimental jugular thrombi and intravascular catheters was studied. Coumadin, in doses sufficient to raise the PT to the "therapeutic" range, did not impair scintigraphic visualization of thrombi on images obtained 4 hours after 111In-P injection. In addition, there was no obvious effect upon postmortem measurements of thrombus:blood or catheter:blood 111In activity ratios, consistent with the imaging data. However, slight delay in 111In-P accumulation on thrombi and catheters appeared to be present in dogs treated with coumadin, based on images obtained at 1, 2, and 3 hours after 111In-P injection. It is unlikely that coumadin's effect upon 111In-P uptake by thrombi would be significant in a clinical setting, although further studies would be required to confirm this.

Animals↗
PubMed1984

Production of systemic hyperthermia in the rat.

The design of clinical trials employing whole-body hyperthermia in cancer therapy has been hampered due to lack of a suitable animal model. We describe a technique for reproducibly and efficiently inducing whole-body hyperthermia in Sprague-Dawley rats, using halothane and oxygen anesthesia and immersion in a hot water bath. Core body temperatures of between 41.5 and 43 degrees C were induced and maintained for periods of up to 200 min and survival curves were determined. The time of exposure at a given temperature that resulted in death in 50% of the animals within 24 hr after heating (LD50/24 hr) was calculated by linear logistic regression analysis. LD50 24 hr values of 115, 61, 57, 25 and 16 min were obtained for temperatures of 41.75, 42.0, 42.25, 42.5 and 42.75 degrees C respectively. This heating technique is compared to several more toxic methods for inducing whole-body hyperthermia with respect to possible pharmacological and physiological differences.

Anesthesia, Inhalation↗
PubMed1984

Villus atrophy and malabsorption in a rhesus monkey.

Villus atrophy involving the proximal small intestine was diagnosed in a rhesus monkey (Macaca mulatta) at necropsy. A juvenile, male, captive-born monkey exhibited weight loss, hypoalbuminemia, patchy alopecia, eosinophilia, and vomiting. D-xylose absorption was impaired. Contrast radiography revealed thickening of the gastric and intestinal walls, gaseous distension of intestines and a rapid transit rate. There was no clinicopathologic evidence of involvement of organs other than the gastrointestinal tract. The intestinal villus atrophy was similar in distribution and morphology to that of human celiac disease.

Animals↗
PubMed1984

Development and decay of systemic thermotolerance in rats.

The development and decay of thermotolerance to the lethal effect of systemic hyperthermia were investigated in Sprague-Dawley rats. Systemic hyperthermia was induced by partial submersion of gas-anesthetized rats in a controlled-temperature water bath. Survival was determined for rats challenged for periods of 10 to 90 min at 42.5 degrees at intervals of 24 to 144 hr after a sublethal conditioning exposure of 41.8 degrees for 1 hr. Survival curves and times of exposure at 42.5 degrees lethal to 50% of the animals (LD50) were determined for the conditioned animals and compared with those obtained for simultaneously treated control (unconditioned) rats. The thermotolerance ratios (LD50 for conditioned animals at various times after sublethal conditioning exposure divided by the LD50 for the control animals) were calculated and compared with the ratios reported in the literature for cells heated in vitro or for tissues heated locally in vivo. Pretreatment of rats at 41.8 degrees for 1 hr resulted in an increase in the LD50 for rats challenged 24 to 96 hr later, with a maximum increase noted at 48 hr (56.5 min compared with 25 min for control; thermotolerance ratio, 2.3). The animals remained relatively resistant to the second heat treatment at 96 hr and returned to control levels of heat sensitivity by 120 hr. The development and kinetics of thermotolerance to lethality induced by wholebody hyperthermia need to be considered in the design of multiple-fraction treatment plans.

Animals↗
PubMed1983

Thermal tolerance to whole body hyperthermia.

Thermal tolerance, that is, a reduced sensitivity to a succeeding heat treatment, has been noted in vitro and following local hyperthermia in normal tissues and malignant tumors. However, information is sparse concerning thermal tolerance following systemic hyperthermia, thereby limiting our ability to design optimally fractionated systemic hyperthermia treatment protocols. A technique for reproducibly inducing systemic hyperthermia in the rat is described, and the survival curve for rats exposed at 42.5 degrees C for periods of up to 75 minutes is presented. Using this system, increased survival of rats to systemic hyperthermia at 42.5 degrees C was demonstrated 30 hours after an initial sublethal conditioning exposure (41.8 degrees C for 1 hour). The LD50 (the time of exposure lethal to 50% of the rats) at 42.5 degrees C was increased by a factor of approximately 2 in the animals exposed to the sublethal conditioning. This increase in LD50 demonstrates the development of thermal tolerance to killing by whole body hyperthermia.

Acclimatization↗
PubMed1982

Epizootic coronaviral typhlocolitis in suckling mice.

Multiple epizootics of typhlocolitis associated with high morbidity and mortality occurred among suckling mice in an arbovirology research laboratory. Affected mice had necrosis and hyperplasia of cecal, colonic, and less often, small intestinal mucosa. Epithelial syncytia were present throughout the affected areas. Other organs generally were not involved. The etiologic agent was a coronavirus antigenically related to mouse hepatitis virus strains 1 and S. Sera from dams of affected litters and recovered animals did not contain detectable complement fixing antibody to coronavirus antigen. The lesions and the causative agent differed from previously reported coronaviral syndromes in mice. The source of the infection was not definitely found.

Animals↗
PubMed1980

Iatrogenic arteriovenous fistula in a cynomolgus macaque (Macaca fascicularis): a case report.

A juvenile male cynomolgus macaque was slightly depressed and had a rough haircoat. Cardiomegaly and pulmonary interstitial edema were found. A distinct fremitus was palpable over the right femoral canal. The only abnormal laboratory finding was an elevated total leukocyte count. A femoral arteriogram confirmed the diagnosis of femoral arteriovenous fistula. Surgical correction of the fistula was successful in reversing the heart failure. The history and anatomic location of the lesion suggested an iatrogenic cause.

Animals↗
PubMed1978

Patent ductus arteriosus with pulmonary hypertension in a cat.

Patent ductus arteriosus with pulmonary hypertension and right to left shunting of blood flow was diagnosed in a 9-month-old female cat. Because of the pulmonary hypertension, the cat did not have typical signs of patent ductus arteriosus; thus, cardiac angiography and catheterization were utilized to confirm the diagnosis. The patent duct was successfully occluded with a vascular clip.

Animals↗
PubMed1977

Primary myocardial disease in the cat. A model for human cardiomyopathy.

Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).

Age Factors↗
PubMed1976

Left ventricular diastolic stiffness in dogs with congestive cardiomyopathy and volume overload.

Mean functional diastolic stiffness, an estimate of the left ventricular resistance to filling during diastole, was measured in 10 normal dogs, 7 dogs with diseases causing volume overload (patent ductus arteriosus and primary mitral valve insufficiency), and 4 dogs with idiopathic congestive cardiomyopathy. It was measured as the increase in pressure during diastole (deltaP), divided by the corresponding increase in volume (deltaV). The pressure was measured at cardiac catheterization, and the volume was derived by a cineangiocardiographic method. There was no increase in diastolic stiffness of the hearts with volume overload compared with the normal hearts, but those with cardiomyopathy had a large increase, although the end-diastolic volumes in cardiomyopathy were generally less than in volume overload.

Animals↗