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Biomedical subjects

G D Abrams

Publications and source records attributed to G D Abrams.

97 records · Page 6Linked to original sources
PubMedDate not supplied

Effects of lodoxamide on ischemic reperfused myocardium.

The beneficial effects of lodoxamide tromethamine (U42585E) have been examined in a canine model of myocardial ischemic injury. Lodoxamide was infused 20 mg/kg/h i.v. starting 30 min before occlusion of the proximal left circumflex coronary artery (LCX) and continuing through 90 min of ischemia. Lodoxamide produced a significant reduction in ultimate infarct size measured at 24 h by postmortem tetrazolium perfusion staining. Infarct size expressed as a percent of the anatomical area at risk was 21.7 +/- 2.7 in the treated group vs. 47.0 +/- 3.1 in the control group (mean +/- SEM). No significant difference in area at risk was observed between treated and control groups. Salvage occurred primarily in subepicardial and midmyocardial tissue without apparent lateral protection. Histological examination confirmed gross results of postmortem staining. The protection appeared to be unrelated to myocardial oxygen demand since no hemodynamic differences between groups were observed at the time of occlusion of throughout the 24-h experimental course. Concurrent studies of ex vivo platelet aggregation showed no effect of lodoxamide on adenosine diphosphate (ADP), collagen, and arachidonic acid-induced aggregation. In vivo antithrombotic effects were evaluated in four conscious dogs by inducing LCX thrombosis with low-amperage stimulation (50 microA for 24 h) of the intimal surface. Occlusive thrombi occurred in all four dogs and were similar to controls. These results suggest that lodoxamide reduces myocardial ischemic injury by a mechanism unrelated to oxygen demand or antiplatelet effects.

Amino Acids↗
PubMedDate not supplied

Delayed pentobarbital therapy of acute focal cerebral ischemia.

The efficacy of pentobarbital in the delayed treatment of acute cerebral ischemia was investigated in cats. Cerebral ischemia was produced by left middle cerebral artery (LMCA) ligation. Ten cats received 50 mg/kg of pentobarbital prior to ligation; a second group of 10 cats received the same dose of pentobarbital 2 hrs after ligation, and the control group of 7 cats received no pentobarbital. Brains were removed after spontaneous or induced death and the volume infarction was determined histologically. It was found that the volume of brain infarction in the group receiving pentobarbital 2 hrs after ligation was significantly less than that of the control group, which received no pentobarbital; but the volume of infarction in the former group was significantly greater than that found in the experimental group, which received pentobarbital prior to ligation. However, the mortality after LMCA ligation was higher in the 2 experimental groups, which received pentobarbital therapy, than in the control group, which did not receive pentobarbital. An hypothesis was advanced, which speculated that secondary adrenal insufficiency and altered cardiovascular function accounted for the increased mortality after pentobarbital treatment of patients with ischemic stroke.

Animals↗
PubMedDate not supplied

Canine myocardial reperfusion injury: protection by a free radical scavenger, N-2-mercaptopropionyl glycine.

Oxygen-derived free radicals and their metabolites may contribute to the extension of irreversible cellular injury, which occurs on reperfusion of the previously ischemic myocardium. Therefore, therapy directed against the toxic effects of reactive oxygen species may provide protection to the ischemic myocardium, which undergoes subsequent reperfusion. We evaluated the effectiveness of N-2-mercaptopropionyl glycine (MPG), a free radical scavenger, to limit the extent of irreversible injury resulting from 90 min of ischemia followed by 6 h of reperfusion in a canine model of myocardial infarction. In three groups of dogs, MPG (20 mg/kg) was administered as a constant infusion into the left atrium. Group I received MPG for 2 h, starting 15 min before occlusion of the left circumflex coronary artery and ending 15 min after reperfusion. Group II received MPG for 1 h, starting 15 min before reperfusion. Group III received MPG for 1 h beginning 45 min after reperfusion. Each group was compared with its respective saline control group. Infarct size was reduced by 35% in Group I (32.2 +/- 5.1% vs. 47.7 +/- 3.4% of the area at risk, p less than 0.05) and Group II (31.4 +/- 3.6% vs. 47.5 +/- 5.1% of the area at risk, p less than 0.025) in comparison with the saline treated control animals. In contrast, in Group III infarct size did not differ significantly from the saline-treated control group (45.9 +/- 3.3% vs. 47.7 +/- 3.5% of the area at risk). The percent of left ventricle at risk did not differ among the groups. The beneficial effects of MPG could not be explained on the basis of hemodynamic differences. In addition, MPG did not influence regional myocardial blood flow. In vitro studies indicated that MPG effectively scavanges O2- generated by the hypoxanthine-xanthine oxidase reaction, as well as by PMA-activated polymorphonuclear leukocytes. Based on these observations, we propose that MPG exerts its beneficial effects by protecting against free radical-mediated damage during the early phase of reperfusion.

Amino Acids, Sulfur↗
PubMedDate not supplied

Cytoimmunologic monitoring and heart transplantation.

Cytoimmunologic monitoring (CIM) combines morphological quantitation of activated lymphocytes and immunoblasts with immunophenotyping of peripheral blood in an effort to identify patients at risk for heart transplant rejection. In this study, CIM and endomyocardial biopsy (EMB) results were correlated in 55 paired blood and tissue specimens obtained from 18 heart transplant patients after operation. We found that 83% of patients with rejection and 81% of patients without rejection had increased levels of morphological activated lymphocytes. Multiple other criteria for determining levels of activation were used without improving the sensitivity or specificity. The use of CD4:CD8 ratios to discriminate between activation caused by rejection and those from viral infections and other inflammatory conditions yielded a sensitivity of 43% and specificity of 56%. The presence of activation markers such as I2, TAC, and T9 did not correlate with either CIM or EMB findings. CD4:CD8 alone was not predictive of cardiac rejection as increased, normal, and decreased CD4:CD8 ratios were seen in patients with and without rejection. Other measurements such as percentage of activated lymphocytes, total lymphocyte count, and whole blood cell count did not correlate with EMB or immunophenotypic findings. These results indicate that neither CIM, as currently conducted, nor immunophenotyping alone is sensitive or specific enough to substitute for EMB in screening for tissue rejection.

Antibodies, Monoclonal↗