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Biomedical subjects

G D Abrams

Publications and source records attributed to G D Abrams.

At least 37 records · Page 2Linked to original sources
PubMed1991

Penetrating atherosclerotic aortic ulcer with dissecting hematoma: control of bleeding with percutaneous embolization.

A case is presented in which left subpleural hematoma and hemothorax resulted from a penetrating atherosclerotic aortic ulcer with an aortic pseudoaneurysm and intramedial hematoma. Percutaneous transfemoral embolization of the ulcer with use of coils and thrombin resulted in stabilization of the patient's hemodynamic status. The patient died 6 days later of pneumonia. In certain clinical situations, treatment of bleeding from penetrating aortic ulcers with percutaneous embolization may stabilize the patient's condition, allowing elective surgical intervention.

Aged↗
PubMed1991

Evidence for regional catecholamine uptake and storage sites in the transplanted human heart by positron emission tomography.

Positron emission tomography in combination with the newly introduced catecholamine analogue [11C]hydroxyephedrine ([11C]HED) enables the noninvasive delineation of sympathetic nerve terminals of the heart. To address the ongoing controversy over possible reinnervation of the human transplant, 5 healthy control subjects and 11 patients were studied after cardiac transplant by this imaging approach. Regional [11C]HED retention was compared to regional blood flow as assessed by rubidium-82. Transplant patients were divided into two groups. Group I had recent (less than 1 yr, 4.4 +/- 2.3 mo) surgery, while group II patients underwent cardiac transplantation more than 2 yr before imaging (3.5 +/- 1.3 yr). [11C]HED retention paralleled blood flow in normals, but was homogeneously reduced in group I. In contrast, group II patients revealed heterogeneous [11C]HED retention, with increased uptake in the proximal anterior and septal wall. Quantitative evaluation of [11C]HED retention revealed a 70% reduction in group I and 59% reduction in group II patients (P less than 0.001). In group II patients, [11C]HED retention reached 60% of normal in the proximal anterior wall. These data suggest the presence of neuronal tissue in the transplanted human heart, which may reflect regional sympathetic reinnervation.

Blood Pressure↗
PubMed1990

Effect of gastrointestinal flora on body temperature of rats and mice.

The purpose of these experiments was to test the hypothesis that gut flora influences the body temperature of rodents. Rats and mice were implanted with biotelemetry transmitters that enabled us to record both abdominal temperature and activity for long periods of time. Rats given nonabsorbable antibiotics in their drinking water, which reduced their gut flora, had a marked decrease in both their daytime and nighttime temperatures. Similar results were found with germfree mice. The circadian rhythms in body temperature of germfree and conventionalized mice were not different. However, the body temperatures of the germfree mice were lower than those of the conventionalized mice during both the daytime and nighttime. The decrease in body temperature in the germfree mice was not related to changes in activity. These results support the hypothesis that gut flora has a tonic stimulatory effect on both the daytime and nighttime body temperature of rodents.

Abdomen↗
PubMed1989

Treatment of Wilson's disease with zinc. V. Changes in serum levels of lipase, amylase, and alkaline phosphatase in patients with Wilson's disease.

We noted a frequent increase in the serum enzymes amylase, lipase, and alkaline phosphatase in patients with Wilson's disease who are receiving zinc acetate therapy (25 or 50 mg elemental zinc three times daily). Typically, values are normal before the initiation of zinc therapy, increase to slightly above normal after a few weeks of therapy, and stabilize at the high normal range after approximately a year of treatment. Very large dosages of zinc (800 mg/day) produce even further elevation of serum lipase and amylase without the symptoms of pancreatitis. Pancreatic pathologic studies of a zinc-treated rat model receiving dosages equivalent to up to 25 times the effective dosage in a human being, which is based on milligrams of zinc per kilogram of body weight, reveal that no lesions are induced by zinc treatment in the pancreas. We interpret these findings to indicate that extended maintenance therapy with zinc does not pose a risk of pancreatic damage in patients with Wilson's disease.

Adolescent↗
PubMed1988

Protection of reperfused ischemic canine myocardium by CI-922, a new inhibitor of leukocyte activation.

There is increasing evidence that activated neutrophils cause myocardial injury during reperfusion of ischemic myocardium. This study was performed to assess the effect of Ci-922, an inhibitor of neutrophil activation, in a canine preparation of myocardial infarction. Dogs received 15-min infusions of CI-922 1 mg/kg or 5% dextrose beginning 30 min before occlusion of the left circumflex coronary artery. After occlusion for 90 min and reperfusion for 6 h, infarct size was determined by ex vivo perfusion of the left circumflex coronary artery with triphenyltetrazolium chloride. The percentage of the area at risk infarcted was: control, 42 +/- 5; and CI-922, 23 +/- 4 (p less than 0.05 vs. control). There were no significant inter-group differences in heart rate or mean arterial pressure, and CI-922 did not enhance collateral blood flow to the ischemic bed. After incubation with CI-922 (100 microM), production of superoxide anions by canine neutrophils activated by opsonized zymosam decreased from 3.5 +/- 0.2 to 2.0 +/- 0.4 nmol/10 min/10(6) cells (p less than 0.05). Thus, inhibition of neutrophil-mediated damage may explain the cardioprotective effect of CI-922.

Animals↗
PubMed1988

Pathogenesis of gastrointestinal infections.

The normal gastrointestinal tract is constantly "infected" by a large and varied microbial population. This normal flora plays a significant role in establishing and maintaining the normal state of the digestive tract. Although the digestive ecosystem thus constituted has a high degree of stability, some microbes have evolved virulence factors or characteristics that allow them to gain a foot-hold in the tract. Given the variety of virulence factors found in different organisms, gastrointestinal infectious diseases are characterized by a broad spectrum of patterns which differ with respect to the relationship between microbe and host, i.e., the degree of tissue penetration by the organism. Genetic analysis of virulence factors promises to deepen our understanding of the pathogenesis of these diseases and to lead ultimately to effective means of prevention.

Bacteria↗
PubMed1987

Prostacyclin protects ischemic reperfused myocardium in the dog by inhibition of neutrophil activation.

Prostacyclin (PGI2) and the stable PGI2 analogue SC39902 (6,9 alpha-epoxy,5S-fluoro-11 alpha, 15S-dehydroxyprosta-6,13E-dien-1-oic acid, sodium salt) were studied in anesthetized open-chest dogs subjected to 90 minutes of left circumflex coronary artery (LCCA) occlusion and 6 hours of reperfusion. PGI2 (50 ng/kg/min, infused into the left atrium) reduced infarct mass by 59% compared to control, but SC39902 (1.5 micrograms/kg/min) failed to produce a significant reduction in infarct size. Both PGI2 and SC39902 reduced mean arterial blood pressure, heart rate, and rate-pressure product to the same extent. Regional myocardial blood flow measured with radiolabelled tracer microspheres did not demonstrate an increase in regional blood flow to the ischemic myocardium during the 90 minutes of LCCA occlusion in the PGI2 and control treatment groups. Canine neutrophils were isolated from whole blood and activated with opsonized zymosan. PGI2 produced a concentration-dependent inhibition of neutrophil activation as measured by superoxide production in vitro, whereas SC39902 failed to effectively inhibit neutrophil activation. Neutrophil migration into inflammatory skin lesions was effectively attenuated when dogs were pretreated with PGI2 (50 ng/kg/min, intravenously). Therefore, it is suggested that the cytoprotective effect of PGI2 during myocardial ischemia and reperfusion is related to an inhibition of neutrophil migration and the production of cytotoxic activated oxygen species.

Animals↗
PubMed1987

Superoxide dismutase does not cause scar thinning after myocardial infarction.

Previous studies demonstrated that treatment with superoxide dismutase, a scavenger of superoxide anions, limits the extent of myocardial injury in a canine preparation of regional myocardial ischemia and reperfusion. Little is known, however, about the effects of superoxide dismutase on the healing of a myocardial infarct. Therefore, this study was performed to determine whether treatment with superoxide dismutase during myocardial ischemia impairs formation of scar tissue after infarction. Dogs received 2 hour infusions of superoxide dismutase or albumin (controls) by way of the left atrium beginning 15 minutes before and ending 15 minutes after a 90 minute occlusion of the left circumflex coronary artery. Six weeks later the animals were killed. Two-dimensional echocardiography was performed before surgery and before induced death. Wall thickening in the central ischemic zone was decreased at 6 weeks compared with baseline studies (p less than 0.05), but the decrease was similar for both groups. The hydroxyproline concentrations (microgram/mg dry weight) of the scar tissue in the superoxide dismutase and control groups, respectively, were 35.3 +/- 3.8 and 28.7 +/- 5.0 (p less than 0.05). The ratios of the scar thickness to normal wall thickness were superoxide dismutase 0.91 +/- 0.03 and control 0.89 +/- 0.03 (p greater than 0.05). Thus, superoxide dismutase had no adverse effect on wall thickening or scar formation assessed 6 weeks after myocardial infarction, and may be useful to limit oxygen radical-mediated damage during reperfusion of the ischemic myocardium.

Animals↗
PubMed1987

Surgical pathology of the infected gut.

In the normal digestive tract, interaction of the mucosa with a large and varied microbial flora is inevitable. In fact, the "normal" state of the digestive tract reflects the impact of the resident flora to a significant degree. The pathogenesis of various infectious conditions encountered by the surgical pathologist in the gut is understood more readily when the gastrointestinal tract is viewed as a complex ecosystem. Significant disease may result from perturbation of the normal flora, as well as from exogenous infection, and susceptibility of the host may vary with disturbances of the digestive ecosystem. An ecologic perspective is essential in the consideration not only of the "infected" gut, but of conditions as diverse as ischemia or even carcinogenesis in the gastrointestinal mucosa.

Animals↗
PubMed1987

Physiologic assessment of the four commonly performed endorectal pullthroughs.

The popularity of the endorectal pullthrough for the treatment of benign mucosal diseases of the rectum has created a controversy regarding the need for a reservoir. The four currently advocated procedures, the straight endorectal anastomosis, the J pouch, the S pouch, and the lateral isoperistaltic ileal reservoir were evaluated in a puppy model with four animals in each experimental group. Measurement of rectal capacitance showed that all groups achieved 80-85% of control values at 6 months after surgery. Intestinal transit time decreased by one-half in all groups. Stool consistency, stool culture, water, and electrolyte absorption did not show any statistical superiority of one group over another. Stool frequency varied widely at 6 months; 10 stools per 8-hour period were counted in the lateral reservoir group versus 25 with the J pouches, and 16 with the straight and S groups. Stool frequency did not correlate with transit time, stool consistency, or rectal capacitance. Barium enemas showed that straight pullthroughs more closely resembled the measurements of the normal animal's endorectal canal. Based on these studies, there appears to be no advantage to adding a reservoir to the endorectal pullthrough.

Anal Canal↗
PubMed1986

Ascorbic acid chronic alcohol consumption in the guinea pig.

Protection against the toxic effects of chronic alcohol consumption was observed in male guinea pigs maintained on a high-ascorbic-acid diet (vitamin C-deficient chow plus 2.0 mg ascorbic acid/ml drinking water) as compared to animals on a low-ascorbic-acid diet (vitamin C-deficient chow and from 0.025 to 0.050 mg ascorbic acid/ml drinking water). Alcohol was orally administered to the guinea pigs at a dose of 2.5 g/kg for up to 14 weeks. Levels of serum aspartate aminotransferase and serum alanine aminotransferase were significantly elevated in animals on the low-ascorbic-acid diet that received alcohol, 120 and 250%, respectively. In contrast, in animals on the high-ascorbic-acid diet that received alcohol, levels of alanine aminotransferase were not significantly elevated and levels of aspartate aminotransferase were elevated 50%. In addition, some of the animals on the low-ascorbic-acid diet that received alcohol for 12 to 14 weeks developed hepatic steatosis and necrosis, whereas none of the animals on the high-ascorbic-acid diet that received alcohol for the same length of time manifested these changes.

Administration, Oral↗
PubMed1986

Reduction of myocardial infarct size by neutrophil depletion: effect of duration of occlusion.

Experiments were performed in the dog to examine the effects of neutropenia on ultimate infarct size resulting from short (90 minutes) or prolonged (4 hours) circumflex coronary artery occlusion. Sheep antiserum to canine neutrophils was used to produce neutropenia. Control animals received nonimmune serum. Neutrophil infiltration into myocardial infarcts was examined using histopathologic techniques and a semiquantitative scoring system. In 90-minute occlusions with 24-hour reperfusion, neutropenia was associated with the development of significantly smaller infarcts: normopenic group, 43.2% +/- 3.3% (n = 7) vs. neutropenic group, 26.6% +/- 3.7% (n = 10) of the area at risk, means +/- SEM. However, in 4-hour occlusion with 6-hour reperfusion experiments, the tendency of neutrophil depletion to reduce infarct size did not reach statistical significance (46.4% +/- 7.2% vs. 31.5% +/- 6.0% of the area at risk, normopenic vs. neutropenic) despite differences in neutrophil infiltration into the reperfused region. The observed differences in ultimate infarct size could not be attributed to differences in myocardial oxygen consumption. The results suggest that a significant amount of myocardial infarction induced by a limited duration of coronary artery occlusion followed by reperfusion is neutrophil dependent and appears to be less important in determining the fate of myocardium subjected to more prolonged periods of ischemia followed by reperfusion.

Agranulocytosis↗
PubMed1986

Reduction of the size of infarction by allopurinol in the ischemic-reperfused canine heart.

This study was performed to assess the effect of allopurinol in a canine preparation of myocardial infarction. Dogs underwent occlusion of the left circumflex coronary artery for 90 min, followed by reperfusion for 6 hr. Three groups were studied: (1) control, (2) dogs receiving 25 mg/kg allopurinol 18 hr before occlusion and 50 mg/kg 5 min before occlusion, and (3) dogs receiving allopurinol as above plus 5 mg/kg superoxide dismutase over 1 hr beginning 15 min before reperfusion. Infarct size expressed as a percentage of the area at risk was 40 +/- 4 in the control group, 22 +/- 5 in the allopurinol group (p less than .05 vs control), and 17 +/- 4 in the allopurinol plus superoxide dismutase group (p less than .05 vs control). The differences in infarct size were not due to differences in myocardial oxygen supply or demand. Neutrophil superoxide anion production was not altered by allopurinol treatment. The results suggest that myocardial xanthine oxidase may generate oxygen radicals that play a role in myocardial injury due to ischemia and reperfusion.

Allopurinol↗
PubMed1986

Protective effects of N-2-mercaptopropionyl glycine against myocardial reperfusion injury after neutrophil depletion in the dog: evidence for the role of intracellular-derived free radicals.

Reperfusion of the previously ischemic myocardium is associated with the production of oxygen free radicals and their metabolites, which contribute to the ultimate extent of irreversible myocardial injury. The relative importance of polymorphonuclear leukocytes vs intracellular-derived oxygen metabolites has remained uncertain. We evaluated the effectiveness of a free-radical scavenger, N-2-mercaptopropionyl glycine (MPG), in limiting infarct size after ischemia/reperfusion in dogs that were depleted of neutrophils with specific antisera. Twenty-four urethane-anesthetized open-chest dogs were subjected to 90 min of ischemia by occlusion of the left circumflex coronary artery followed by 6 hr of reperfusion. Dogs were randomly assigned to receive nonimmune serum, neutrophil antiserum, or neutrophil antiserum plus MPG (20 mg/kg intra-atrially 15 min before reperfusion was initiated and for 45 min after reperfusion). Infarct size, as a percent of the area at risk, was reduced by 33% in the neutrophil antiserum group as compared with the nonimmune group (30.7 +/- 2.7% vs 45.6 +/- 3.7%, p less than .01). The combined administration of neutrophil antiserum plus MPG reduced the size of infarction by 63% of the area at risk compared with that in the nonimmune group (17.0 +/- 2.7% vs 45.6 +/- 3.7%, p less than .01). The reduction in infarct size with neutrophil antiserum plus MPG was significantly greater than that with the neutrophil antiserum alone (p less than .01). The areas at risk did not differ among the groups. Myocardial protection could not be explained on the basis of hemodynamic differences. The observation that MPG enhances the protective effects of neutrophil depletion suggests that both extramyocardial- and intramyocardial-derived oxygen free radicals contribute significantly to reperfusion-induced myocardial injury.

Amino Acids, Sulfur↗
PubMed1986

Cytomegalovirus cholangitis in a homosexual man with acquired immune deficiency syndrome.

A 29-year old white homosexual man with acquired immune deficiency syndrome presented initially with right upper quadrant pain and progressive cholestasis. Diffuse mucosal irregularities were seen at endoscopic retrograde cholangiography. Histopathological examination of the gallbladder and wedge liver biopsy showed evidence of cytomegalovirus infection. A repeat endoscopic retrograde cholangiography for persistent symptoms of right upper quadrant pain and cholestasis showed progressive mucosal irregularities of the intra- and extrahepatic bile ducts consistent with progressive cholangitis. Subsequently the patient developed evidence of disseminated infection and died. Postmortem examination revealed histologic features of cytomegalovirus infection in lungs, pancreas, small bowel, adrenal glands, and liver. Immunohistochemical staining of liver confirmed the presence of cytomegalovirus infection of the biliary duct system.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Malignant fibrous histiocytoma of the heart presenting as unilateral pulmonary thromboembolism and infarct.

A malignant fibrous histiocytoma of the heart located at the pulmonic valve and thrombotic occlusion of branches of the left pulmonary artery with pulmonary infarct were found at autopsy in a 77-year-old man. The thrombi contained malignant cells. The patient had undergone left upper lobectomy four years earlier for thromboembolism with infarct, and review of the slides from that procedure revealed similar malignant cells within thrombi. This case is remarkable for the slow growth of the neoplasm and the prolonged survival of the patient, without specific therapy.

Aged↗
PubMed1985

Scintigraphic characterization of amyloid cardiomyopathy.

Amyloidosis is an important entity in the differential diagnosis of cardiac failure of undetermined etiology. In this case report, the typical pattern of combined systolic and diastolic impairment in amyloid cardiomyopathy was demonstrated by analysis of the cardiac blood pool study. In addition, the patient described had mild uptake of Ga-67 citrate, as well as the characteristically intense myocardial uptake of Tc-99m pyrophosphate. Scintigraphic assessment may be particularly helpful when the diagnosis of amyloidosis is being considered in a patient with unexplained cardiac failure.

Aged↗