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Biomedical subjects

G D Abrams

Publications and source records attributed to G D Abrams.

At least 19 recordsLinked to original sources
PubMed1992

Shock-wave thrombus ablation, a new method for noninvasive mechanical thrombolysis.

Successful experimental and clinical experience with thrombus ablation has been attained with high-power acoustic energy delivered in a catheter. The goal of this study was to investigate the feasibility of noninvasive thrombus ablation by focused high-power acoustic energy. The source for high-power acoustic energy was a shock-wave generator in a water tank equipped with an acoustic lens with a fixed focal point at 22.5 cm. Thrombus was prepared in vitro, weighed (0.24 +/- 0.08 g), and inserted in excised human femoral artery segments. The arterial segments wer ligated, positioned at the focal point and then randomized into either test (n = 8) or control (n = 7). An x-ray system verified the 3-dimensional positioning of the arterial segment at the focal point. A 5 MHz ultrasound imaging system continuously visualized the arterial segment at the focal point before, during and after each experiment. The test segments were exposed to shock waves (1,000 shocks/24 kv). The arterial segment content was then flushed and the residual thrombus weighed. The arterial segment and thrombus were fixed and submitted to histologic examination. The test group achieved a significant ablation of thrombus mass (0.25 +/- 0.15 vs 0.07 +/- 0.003 g; p = 0.0001) after application of shock waves. Arterial segments showed no gross or microscopic damage. Ultrasound imaging revealed a localized (1.9 +/- 0.5 cm2), transient (744 +/- 733 ms), cavitation field at the focal point at the time of application of focused shock waves. Thus, focused high-power acoustic energy can effect noninvasive thrombus ablation without apparent damage to the arterial wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Femoral Artery↗
PubMed1992

Hypoxia-induced bacterial translocation in the puppy.

Because hypoxia is one of the most common major stresses to which a neonate is exposed, we postulated that it alone might be the cause of intestinal bacterial translocation, which could be the underlying etiology of neonatal sepsis. An animal model, in which hypoxia is the sole stress, was developed in our laboratory and tested in 18 puppies to determine the effect of hypoxia and reoxygenation on intestinal bacterial translocation. In group I (n = 8), following laparotomy and cannulation of the superior mesenteric vein (SMV), the FIO2 was decreased from 21% to 9% for 90 minutes followed by reoxygenation at 21% for 120 minutes. The abdomen was closed and the animals were allowed to recover. After 24 hours the mesenteric lymph nodes (MLNs), spleen, and liver were harvested for bacterial determination and the ileum and jejunum for histological evaluation. Group II (n = 7) was treated the same as group I with the FIO2 maintained at 21%. Group III (n = 3) animals were killed, without intervention, for bacterial analysis. In group I, the systemic PO2 decreased by 75%, SMV PO2 decreased by 64%, and oxygen delivery to the small bowel decreased by 80% in comparison with group II. The mean arterial pressure and cardiac output were not significantly different between group I and group II; however, the mucosal blood flow was decreased by 60% (P less than .001) in group I. Arterial and SMV blood lactic acid levels were unchanged in group I in comparison with group II, suggesting that anaerobic metabolism was not initiated in the splanchnic circulation during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Intramural methotrexate therapy for the prevention of neointimal thickening after balloon angioplasty.

OBJECTIVES: The study was performed to test the hypothesis that high local, intramural concentrations of antineoplastic agents at the site of balloon injury inhibit vascular smooth muscle cell proliferation without systemic toxicity. BACKGROUND: The predominant mechanism for recurrent stenosis after coronary balloon angioplasty is neointimal thickening due to medial smooth muscle cell proliferation. The clinical use of potent antiproliferative agents to prevent restenosis has been limited by the potential for severe systemic side effects. Local therapy with these agents may be effective and free of systemic complications. METHODS: After bilateral balloon angioplasty of the carotid arteries of 14 juvenile farm pigs, the dilated arterial segments were treated locally with methotrexate (6.25 mg/ml, total dose 25 mg) or 0.9% saline solution through a perforated balloon catheter. The animals were then killed 30 days after balloon injury to determine the effects of this therapy on neointimal thickness. In an additional six animals, tritium-labeled methotrexate was used to determine the concentration and duration of detectability of methotrexate in the wall of the treated arteries and in the systemic circulation. RESULTS: Two hours after drug instillation the concentration of labeled drug was greater than 1,000-fold greater in the wall of the treated artery than in circulating blood, and this ratio remained between 50 and 100 for at least 7 days. Despite this difference, the mean intimal thickness 30 days after the procedure was similar in the 10 methotrexate-treated arteries and the 18 saline-treated arteries (59 +/- 30 vs. 56 +/- 25 microns, p = 0.6). The morphologic appearance of the neointima was similar in each group and suggested an important role for mural thrombus in the genesis of the intimal thickening. CONCLUSIONS: Treatment with intramural methotrexate, delivered through a perforated balloon catheter at the selected concentration and total dose, failed to prevent intimal thickening after balloon injury. Nonetheless, the perforated balloon catheter appears to be a promising means of delivering a high local concentration of drugs with potentially life-threatening systemic side effects. The optimal concentrations and combinations of candidate drug therapies warrant further evaluation.

Angioplasty, Balloon↗
PubMed1992

Design and testing of a high-flow autoperfusion catheter: an experimental study.

An autoperfusion catheter is similar to an angioplasty balloon catheter with side holes in the guide-wire lumen proximal to the balloon. When the balloon of the autoperfusion catheter is deployed and inflated in an artery, the guide wire is removed, and the hub of the guide-wire lumen is capped. The catheter then allows passive distal perfusion by using ambient pressure to drive blood into the guide-wire lumen, through the balloon, and out the end hole. This article discusses the requirements and constraints of a high-flow autoperfusion catheter, summarizes attempts to modify standard angioplasty catheters for use as an autoperfusion catheter, and describes the design and testing of a custom autoperfusion catheter capable of delivering approximately 3 mL/sec at physiologic pressures. In a model of canine acute renal artery occlusion lasting 90 minutes, the custom autoperfusion catheter provided marked protection from acute tubular necrosis compared with conventional percutaneous transluminal angioplasty catheters. The authors conclude that the high-flow autoperfusion catheter may be useful as a temporary stent in cases of rupture, dissection, or penetrating wounds involving large arteries.

Angioplasty, Balloon↗
PubMed1991

Hemodynamics versus biopsy findings during cardiac transplant rejection.

Before the use of cyclosporine as the major component for immunosuppression after cardiac transplantation, rejection was accompanied by catastrophic hemodynamic decompensation. However, the hemodynamic changes that occur during rejection after cardiac transplantation in patients treated with cyclosporine have not been clearly described. Between July 1986 and October 1989, 89 adults underwent orthotopic heart transplantation at the University of Michigan Medical Center. All patients received triple-drug therapy immunosuppression consisting of steroids, cyclosporine, and azathioprine. Cardiac hemodynamics were measured and correlated with the histologic assessment of rejection. There have been ten deaths among these 89 patients for an overall survival of 89%. There were no deaths from rejection. One hundred fifty-three of the biopsy specimens were read as grade 0, 31 were grade 1, 75 were grade 2, 103 were grade 3, and 9 patients had grade 4 biopsy specimens. No hemodynamic differences were noted in patients with increasing grade of rejection. Five patients (5/9, 55%) with severe rejection (grade 4) had symptoms of congestive heart failure at the time of biopsy. These symptomatic grade 4 patients differed from asymptomatic grade 4 patients only in cardiac output (2.9 versus 5.2 L/min). Overall hemodynamic decompensation was not evident as rejection grade increased. Routine serial endomyocardial biopsies remain the procedure of choice in the diagnosis of rejection in the asymptomatic patient after cardiac transplantation as hemodynamics do not predict degree of rejection.

Adult↗
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↗
PubMed1978

Clindamycin-induced enterocolitis in hamsters.

A lethal enterocolitis was induced in hamsters by oral or parenteral administration of clindamycin in amounts comparable to those used in treatment of humans. The intestinal lesions were characterized histologically as an acute inflammatory reaction with pseudomembrane formation and resembled the lesions seen in humans with antibiotic-induced colitis. Results of quantitative stool cultures showed the numbers of Peptostreptococcus and Corynebacterium decreased in animals with colitis after challenge with 100 mg of clindamycin/kg, while numbers of Escherichia coli, Streptococcus faecalis, and clindamycin-resistant Clostridium sordellii and Clostridium difficile increased. Bacteria were not seen within the intestinal lesions. Viruses were not isolated from hamsters with colitis. Although the pathogenesis of this syndrome is not completely established, the evidence is consistent with the hypothesis that the disease is caused by clostridial toxins and that the production of these toxins by organisms within the intestines is enhanced by the effects of clindamycin upon the bowel flora.

Administration, Oral↗
PubMed1978

Production of an antibiotic substance by Bacillus licheniformis within the digestive tract of gnotobiotic mice.

In monoxenic mice, vegetative cells and spores of Bacillus licheniformis were enumerated and in vivo antibiotic production was measured at various levels of the digestive tract and in the feces. The apparent independence of vegetative cell and spore populations in the cecum and feces, as well as the marked fluctuations of these two populations in the stomach and small intestine, suggested that sporulation of B. licheniformis and production of antibiotic occur only in the upper levels of the digestive tract. Study of dixenic models wherein B. licheniformis was inoculated after Clostridium perfringens or Lactobacillus sp. or before Lactobacillus sp. revealed the simultaneous disappearance of B. licheniformis from the stomach and antibiotic from the feces. This strain persisted in the cecum, but only in the form of vegetative cells. These models demonstrate that the activity of the microflora in the upper segments can affect the equilibrium of the microflora throughout the digestive tract.

Animals↗
PubMed1977

Pilot studies on recombinant cold-adapted live type A and B influenza virus vaccines.

Recombinant live attenuated type A and B influenza virus vaccines derived from standardized cold-adapted parent strains were given singly and in combination to volunteers. The vaccine viruses were well tolerated, functioned as good antigens, and failed to spread to intimate household contacts. Thirty-nine isolates that were recovered after a single passage in humans appeared genetically stable. The results of histopathologic studies in ferrets encourage development of an animal model for attenuation of the virus.

Animals↗
PubMed1977

Antagonistic effect of extremely oxygen-sensitive clostridia from the microflora of conventional mice and of Escherichia coli against Shigella flexneri in the digestive tract of gnotobiotic mice.

Two extremely oxygen-sensitive strains of Clostridium sp., designated Clostridium E and P, were obtained from digestive microflora of conventional mice and found to constitute a barrier against Shigella flexneri SF-2 when associated in vivo with Escherichia coli K-12. These and other simplified fractions of the conventional microflora were demonstrated to have an effect comparable to that of the total flora. When K-12 and Clostridium E were established in gnotobiotic mice before the introduction of SF-2, the latter was reduced to a level below detection in the digestive tract. Whe SF-2 was established first, the antagonistic effect exerted by Clostridium E and K-12 was variable and, apparently, related to the rate of establishment of Clostridium E. Mutants of SF-2 resistant to the barrier effect of Clostridium E and K-12 appeared at the end of 3 months when SF-2 was established in gnotobiotic mice alone or with K-12, and after only a week when SF-2 was associated only with Clostridium E. These results suggest that the bacterial antagonsim in this model is related to the production in vivo of an antibiotic substance active against SF-2. It appears that the substance may be produced by Clostridium E, stimulated by K-12.

Anaerobiosis↗
PubMed1977

Inability of methylprednisolone sodium succinate to decrease infarct size or preserve enzyme activity measured 24 hours after coronary occlusion in the dog.

Methylprednisolone sodium succinate (50 mg/kg) was given 30 minutes before or after the start of a 90 minute occlusion of the left circumflex coronary artery (LCX) in one group of dogs. In a second group, methylprednisolone sodium succinate was given 15 minutes after permanent occlusion of the left anterior descending artery (LAD). Infarct size was determined by dehydrogenase staining after 24 or 96 hours. Heart slices were incubated with nitro-blue tetrazolium and nonstaining infarcted tissue was dissected and weighed. Myocardial depletion of creatine phosphokinase activity (CPK) and lactate dehydrogenase activity (LDH) were determined 24 hours after temporary LCX occlusion. When measured after 24 hours, methylprednisolone sodium succinate treatment did not reduce infarct size or decrease enzyme loss. After temporary LCX occlusion infarct size was 30.4 +/- 3.6% of left ventricular weight in control dogs and 30.0 +/- 2.3% in treated dogs. No significant difference in infarct size was observed in hearts examined 24 or 96 hours after myocardial infarction. After permanent LAD occlusion, infarct size in control dogs was 39.2 +/- 1.6% of left ventricular weight and 33.7 +/- 3.5% in treated dogs. CPK activity in the LCX area decreased by 26.5 +/- 7% in controls and by 28.1% +/- 7% in treated dogs. Treated dogs sustained a significantly greater fall in arterial blood pressure after LCX occlusion than did controls. During LCX occlusion and upon reperfusion, methylprednisolone sodium succinate treated dogs exhibited a significantly greater number of premature ventricular beats. Since infarct size and enzyme depletion were not reduced when measured after 24 hours, methylprednisolone sodium succinate treatment does not appear to have enhanced myocardial cell viability.

Animals↗