PubMed Health⌕ Search

Biomedical subjects

D D Morris

Publications and source records attributed to D D Morris.

At least 91 records · Page 5Linked to original sources
PubMed1984

Noninvasive prediction of the angiographic extent of coronary artery disease after myocardial infarction: comparison of clinical, bicycle exercise electrocardiographic, and ventriculographic parameters.

To assess alternative criteria for the prediction of multivessel coronary artery disease after myocardial infarction, we compared the clinical, bicycle electrocardiographic, and radionuclide ventriculographic (ejection fraction and wall motion) responses in 110 patients undergoing coronary angiography after myocardial infarction. Ninety-seven of the 110 patients had multivessel coronary artery disease (two or more diseased vessels). Clinical or electrocardiographic abnormalities were observed in 41 of 97 (sensitivity = 43%) patients with multivessel disease, and in only two of 13 (specificity = 85%) patients without multivessel disease. The average information content of these combined clinical and electrocardiographic variables relative to perfect discrimination was 5%. Among the scintigraphic parameters, the conventional criterion for ejection fraction abnormality, a rise of less than 5% had a sensitivity of 72% and a specificity of 62% for multivessel coronary artery disease, while a fall in ejection fraction of 5% or more had a sensitivity of 39% and specificity of 92% for multivessel coronary artery disease. The presence of an exercise wall motion abnormality in the nonadjacent noninfarcted (remote) region had a sensitivity of 82% and specificity of 55% for multivessel coronary artery disease. A more stringent criterion, worsening of remote wall motion with exercise, had a sensitivity of 52% and specificity of 75%. When this latter criterion was combined with a fall in ejection fraction, the sensitivity for multivessel coronary artery disease increased to 62%, specificity remained 75%, and information content increased from 5% to 10%. We conclude that conventional diagnostic criteria for abnormal clinical, bicycle electrocardiographic, or scintigraphic results do not identify patients with additional coronary artery disease after infarction with high accuracy. Two alternative ventriculographic parameters--a fall in ejection fraction and wall motion worsening--are similar to clinical parameters in specificity, but have a higher sensitivity and information content.

Adult↗
PubMed1984

Renal clearance and fractional excretion of electrolytes over a 24-hour period in horses.

Four consecutive 6-hour urine collections were obtained from 10 healthy adult horses given free access to a complete pelleted ration and water. Samples of blood were collected from the jugular vein at the start of the test period and then every 6 hours for 4 consecutive samples. Mean renal clearance of creatinine (CCr) varied significantly during the four, 6-hour collections, ranging from 1.474 in period II to 2.702 ml/min/kg of body weight during period III (P less than 0.05). The CCr in period III was significantly different from the 24-hour mean value of 1.877 ml/min/kg (P less than 0.05). The mean 6-hour clearances of potassium (CK), chloride (CCl), and calcium (CCa) also varied significantly during the 4 collections (P less than 0.05). The 24-hour mean CK and CCl were different from the mean during period III (P less than 0.05). There was significant correlation between mean 24-hour CCr and CK (P less than 0.01); CCr and CCl (P less than 0.05); CNa and CK (P less than 0.01); CNa and CCl (P less than 0.01); and CK and CCl (P less than 0.001). The 95% confidence interval for 6-hour mean values of fractional excretion of Na (FENa) was 0.032% to 0.522%; FEK was 23.345% to 48.074%; FECl was 0.588% to 1.861%; and FECa was -0.158% to 6.723%. Although FENa, FECl, and FECa were highly variable within and between individual horses, mean values for periods I to IV did not differ significantly over time or from 24-hour mean values. The FEK varied less throughout the 24-hour test period. Mean urine volume, urine concentrations of Cr and K, urine osmolality, urine-to-plasma osmolality, urine-to-plasma urea nitrogen, and plasma urea nitrogen varied significantly through time periods I to IV (P less than 0.05); however, means for time periods I to IV were not different from 24-hour means.

Animals↗
PubMed1983

Disseminated intravascular coagulation in six horses.

Disseminated intravascular coagulation (DIC) was diagnosed as a secondary disease in 6 horses. Four horses had localized and/or systemic sepsis, one horse had disseminated neoplasia, and one had idiopathic ulcerative enteropathy. The diagnosis of DIC was based on the finding of at least 3 of 4 abnormalities: thrombocytopenia, prolonged prothrombin time, prolonged activated partial thromboplastin time, and a high concentration of fibrinolytic degradation products. The most common clinical signs other than those attributable to the primary disease process were abnormal hemorrhage (4 hours) and venous thrombosis (4 horses). All horses eventually died or were euthanatized because of the severity of the primary disease.

Animals↗
PubMed1983

Thyroid-stimulating hormone: response test in healthy horses, and effect of phenylbutazone on equine thyroid hormones.

Adult horses showed a mild diurnal variation in equine plasma thyroxine (T4) concentrations, but not triiodothyronine (T3). Plasma T4 concentrations tended to be higher between 5 PM and 8 PM than at 8 AM. Increases in plasma T4 and T3 were similar in adult healthy horses given 5, 10, or 20 IU of thyroid-stimulating hormone (TSH). The T4 peaked at approximately twice (2.0 +/- 0.4 times) as high as the base line at 6 to 12 hours after the TSH was given. The greatest change from base line T3 occurred at 1 to 3 hours after the TSH was given, but the magnitude of increase was widely variable (4.36 +/- 2.49 times as high as base line). The following method for doing the equine TSH-response test was suggested: (i) prepare plasma or serum sample for determining base line T4 and T3, (ii) inject 5 IU of TSH IM, (iii) prepare plasma or serum samples at 3 and 6 hours after the TSH was injected, and (iv) freeze samples at -20 C until T4 and T3 determination by radioimmunoassay. Treatment of horses with phenylbutazone for 5 days caused a significant decrease in base line T4 and T3 in horses (P less than 0.05). However, phenylbutazone-treated horses responded to the injection of TSH, and the increase in T4 at 6 hours was greater than in the controls (not given phenylbutazone) (P less than 0.02).

Animals↗
PubMed1983

Fecal leukocytes and epithelial cells in horses with diarrhea.

Fecal samples from 74 horses with diarrhea were examined microscopically for leukocytes and epithelial cells. The diarrhea was categorized as either acute (less than two weeks) or chronic, Salmonella positive or negative, and mild or severe (based on the fecal consistency). A large number of fecal leukocytes was strongly suggestive of salmonellosis; however, approximately 1/3 of the horses with Salmonella-negative diarrhea also shed fecal leukocytes. Fecal leukocytes were more common in horses with acute and/or severe diarrhea regardless of cause. Numbers of fecal colonic mucosal epithelial cells were increased in severe diarrhea, and their presence in horses with chronic diarrhea was correlated with salmonellosis. The study supports the concept that fecal leukocytes and epithelial cells occur in increased numbers in equine salmonellosis but also occur in other types of diarrhea.

Animals↗
PubMed1982

Atrial fibrillation in horses: factors associated with response to quinidine sulfate in 77 clinical cases.

Seventy-seven horses with atrial fibrillation (AF) were treated orally with quinidine sulfate (QS) at the University of Pennsylvania, School of Veterinary Medicine, Thirty-seven horses (48%) had adverse reactions to QS, the most common of which were nasal mucosal edema, anorexia, colic, and diarrhea. The mean highest daily QS dose was slightly greater in horses showing toxicity (P less than 0.1) and their conversion rate was less (P less than 0.05). A schedule of gradually increasing QS dose was time consuming, costly and not associated with fewer adverse reactions. Horses were compared by their response to QS: conversion for at least 12 months (Group I; 25 horses); reversion with 12 months (Group II; 8); nonconversion (Group III; 14). All horses with congestive heart failure (CHF) failed to convert. The mean age (P less than 0.05), total QS dose and highest daily QS dose (P less than 0.05) were significantly greater in Group III horses. The mean duration of signs before treatment and occurrence of adverse reactions to QS were greater in horses in Group II and III than Group I. (P less than 0.05). All horses in Groups I and II returned to performance, and many (81%) were successful. Most Group III horses (13/14) are known to have died. It was concluded that most horses with AF uncomplicated by CHF have a good prognosis when treated early with QS. Delayed QS therapy may reduce chances for conversion of AF or increase the probability of reversion.

Animals↗
PubMed1966

Threshold for conditioned suppression using x-rays as the pre-aversive stimulus.

Four male, 12-week-old Sprague-Dawley rats were used to determine the threshold for behavioral response to X-irradiation using the conditioned suppression technique. They were maintained at 80 per cent body weight and initially trained to stable performance on a VI 1 min schedule with 16 per cent sucrose solution as reinforcement. After a stable baseline was obtained, animals were placed in the instrumental conditioning box beneath the X-ray machine for a half-hour session each day. While subjects were actively pressing the lever for reinforcement, 15-sec X-ray exposures of 0.5 R/sec were administered, followed immediately by electric shock. After all animals had exhibited conditioned suppression, the dose-rate was decreased in subsequent sessions in an effort to establish threshold. The results indicate that X-rays at a dose-rate as low as 0.004 R/sec can be an effective pre-aversive stimulus for the rat.

Animals↗
PubMedDate not supplied

Therapy of suspected septicemia in neonatal foals using plasma-containing antibodies to core lipopolysaccharide (LPS).

Equine antiserum to core lipopolysaccharide (LPS) was evaluated in a double-blind prospective study for therapeutic benefit in suspected septicemia in neonatal foals. Forty foals younger than 7 days of age were included in the study by satisfaction of clinical and laboratory criteria, suggestive of gram-negative septicemia. Twenty-two foals were treated with core LPS antiserum (plasma produced from horses which were hyperimmunized with rough gram-negative mutant bacterin) and 18 foals received "nonimmune" plasma (from horses prior to immunization against core LPS). All foals received antimicrobials, fluids, and other supportive care measures, depending on clinical signs and according to accepted current practice. The clinical and laboratory data of each foal were monitored and recorded daily for 14 days after plasma treatment or until death. The overall survival rate of these 40 foals with septicemia was 52.5%. The most prevalent diagnoses in addition to septicemia were enteritis and pneumonia. Of 30 positive bacterial cultures, 93% were due to gram-negative organisms. There was no statistically significant increase in survival rate in the 22 foals given core LPS antiserum (P greater than 0.05).

Animals↗
PubMedDate not supplied

Endotoxemia in horses. A review of cellular and humoral mediators involved in its pathogenesis.

Endotoxemia remains the leading cause of death in horses, being intimately involved in the pathogenesis of gastrointestinal disorders that cause colic and neonatal foal septicemia. Endotoxins, normally present within the bowel, gain access to the blood across damaged intestinal mucosa, or endotoxemia occurs when gram negative organisms proliferate in tissues. Endotoxins are removed from the circulation by the mononuclear phagocyte system, and the response of mononuclear phagocytes to these lipopolysaccharides (LPS) play an important role in determining the severity of clinical disease. Macrophages become highly activated for enhanced secretory, phagocytic and cidal functions by LPS. Macrophage-derived cytokines are responsible for many of the pathophysiologic consequences of endotoxemia. The arachidonic acid metabolites, prostacyclin and thromboxane A2 likely mediate early hemodynamic dysfunction and the leukotrienes may potentiate tissue ischemia during endotoxemia. Interleukin 1 (IL-1) induces fever and is responsible for the inflammatory cascade, which constitutes the acute phase response. Tumor necrosis factor (TNF), an important proximal mediator of the effects of LPS, acts to initiate events and formation of other molecules that affect shock and tissue injury. Systemic administration of TNF produces most of the physiologic derangements that are associated with endotoxemia and antibodies that are directed against TNF significantly reduce LPS-induced mortality in experimental animals. In response to endotoxins, mononuclear phagocytes express thromboplastin-like procoagulant activity (PCA), which initiates microvascular thrombosis. Both IL-1 and TNF induce PCA expression, creating a positive feedback loop for LPS-induced coagulopathy. A macrophage-derived platelet activating factor contributes to coagulation dysfunction and further stimulates arachidonic acid metabolism. The ultimate consequences of endotoxemia are multiple system organ failure and death. The numerous feedback loops and intertwining cascades of mediators during endotoxemia defy simplistic methods of treatment. The optimal therapy likely involves methods to alter the generation of inflammatory mediators by mononuclear phagocytes.

Animals↗
PubMedDate not supplied

Hypercoagulable state associated with a deficiency of protein C in a thoroughbred colt.

Protein C is a vitamin K-dependent serine protease with anticoagulant and profibrinolytic activity which is synthesized in the liver. Decreased protein C activity was detected in a Thoroughbred colt with clinical and histopathologic evidence of recurrent venous thrombosis. Although protein C activity was reduced, protein C antigen concentration was normal. Consumptive coagulopathies produce a decrease in both the functional and antigenic concentrations of protein C, thus a defect in protein C synthesis was suspected. Inhibition of gamma-carboxylation secondary to vitamin K antagonism results in the synthesis of a protein C molecule with antigenicity, but without biological activity. However, there was no evidence of vitamin K antagonism. The hypercoaguable state resulting from the reduced activity of protein C in this colt was associated with uncomplicated renal disease, rather than a protein C consumptive process such as endotoxemia. A primary hypercoagulable state due to a deficiency of protein C activity was diagnosed. Primary deficiencies of protein C activity have not been previously documented in horses.

Animals↗
PubMedDate not supplied

Hemostatic and fibrinolytic indices in neonatal foals with presumed septicemia.

Thirteen coagulation tests evaluating hemostatic and fibrinolytic indices and serum cytokine and plasma endotoxin concentrations were obtained in 34 foals with a positive sepsis score (septic group) and 46 age-matched healthy foals. Compared to healthy foals, the prothrombin, activated partial thromboplastin, and whole blood recalcification times were significantly longer in septic foals. The fibrinogen and fibrin degradation products concentrations, percent plasminogen, alpha-2 antiplasmin, and plasminogen activator inhibitor activities, and tumor necrosis factor and interleukin-6 activities were greater in septic foals. Protein C antigen and antithrombin III activity were significantly lower in septic foals. Blood cultures were positive for growth and endotoxin was detected in 19 of 29 and 15 of 30 septic foals, respectively. In septicemic foals with detectable endotoxin in the plasma, the prothrombin and activated partial thromboplastin times were significantly longer and the plasminogen and antithrombin III activities were significantly less than in septic foals in which endotoxin was not detected. Twenty-three of the 34 septic foals did not survive. Septic foals that did not survive were most likely to have a positive blood culture in which a gram-negative organism was isolated. Histopathologic evidence of hemorrhage was evident in 11 foals at postmortem examination and thrombosis was identified in 2 foals. The prothrombin time was significantly longer in foals that had multisite hemorrhage at postmortem examination. The results of this study indicate that clinically relevant alternations in hemostatic and fibrinolytic indices occur in neonatal foals with septicemia and that derangements can be correlated with the presence of endotoxin in plasma. Derangements in hemostatic or fibrinolytic indices were helpful in identification of septic foals with increased risk of coagulopathy, but were not helpful in predicting hemorrhage as compared to thrombus formation. Survival of septicemic foals was correlated with gram-negative bacteremia, but not with the presence of endotoxin or coagulopathy.

Aging↗