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Biomedical subjects

R Ramsey

Publications and source records attributed to R Ramsey.

At least 19 recordsLinked to original sources
PubMed1992

Antiradical effects in L-propionyl carnitine protection of the heart against ischemia-reperfusion injury: the possible role of iron chelation.

L-Propionyl carnitine has been shown to improve the heart's mechanical recovery and other metabolic parameters after ischemia-reperfusion. However, the mechanism of protection is unknown. The two dominating hypotheses are: (i) L-propionyl carnitine can serve as an energy source for heart muscle cells by being enzymatically converted to propionyl-CoA and subsequently utilized in the Krebs cycle (a metabolic hypothesis), and (ii) it can act as an antiradical agent, protecting myocardial cells from oxidative damage (a free radical hypothesis). To test the two possible pathways, we compared the protection afforded to the ischemia-reperfused hearts by L-propionyl carnitine and its optical isomer, D-propionyl carnitine. The latter cannot be enzymatically utilized as an energy source. The Langendorff perfusion technique was used and the hearts were subjected to 40 min of ischemia and 20 min of reperfusion. In analysis of ischemia-reperfused hearts, a strong correlation was found between the recovery of mechanical function and the presence of protein oxidation products (protein carbonyls). Both propionyl carnitines efficiently prevented protein oxidation but L-propionyl carnitine-perfused hearts had two times greater left ventricular developed pressure. The results indicate that both metabolic and antiradical pathway are involved in the protective mechanism of L-propionyl carnitine. To obtain a better insight of the antiradical mechanism of L-propionyl carnitine, we compared the ability of L- and D-propionyl carnitines, L-carnitine, and deferoxamine to interact with: (i) peroxyl radicals, (ii) oxygen radicals, and (iii) iron. We found that none of the carnitine derivatives were able to scavenge peroxyl radicals or superoxide radicals. L- and D-propionyl carnitine and deferoxamine (not L-carnitine) suppressed hydroxyl radical production in the Fenton system, probably by chelating the iron required for the generation of hydroxyl radicals. We suggest that L-propionyl carnitine protects the heart by a dual mechanism: it is an efficient fuel source and an antiradical agent.

Animals↗
PubMed1990

Drug-related problems: their structure and function.

In order to better focus the role of the pharmacist on patient need and patient outcome, a means of categorizing drug-related problems (DRPs) is presented. A DRP exists when a patient experiences or is likely to experience either a disease or symptom having an actual or suspected relationship with drug therapy. Eight different categories of DRPs are described and examples of each category are offered. This categorization serves a number of functions, such as: (1) to illustrate how adverse drug reactions form but one category of extant DRPs, (2) to make tangible the pharmacist's role for the future, (3) to serve as a focus for developing a systematic process whereby the pharmacist contributes significantly to the overall positive outcome of patients, (4) to bring to pharmacy practice a vocabulary consistent with that of other healthcare professionals, and (5) to aid in the development of standards of practice for pharmacists.

Diagnostic Errors↗
PubMed1988

Influence of age on the pharmacokinetics of butorphanol.

Butorphanol kinetics were studied in 8 young (23-34 years of age) and 9 elderly (65-79 years of age) healthy male subjects following a single, intravenous 2-mg dose of butorphanol tartrate. Plasma and blood concentrations collected over 24 h were analyzed by a second antibody radioimmunoassay for unchanged drug. Systemic blood clearance (21.29 +/- 7.18 ml/min/kg), apparent steady-state volume of distribution (9.02 +/- 2.40 liters/kg), distribution half-life (7.67 +/- 4.66 min), and the blood/plasma concentration ratio (1.21 +/- 0.36) in the elderly did not differ from those in the younger subjects. However, the terminal elimination half-life was significantly prolonged in the elderly (5.51 +/- 2.49 versus 3.67 +/- 0.52 h, p less than 0.05). Positive correlations between age and terminal elimination half-life and volume of distribution were noted. Our data suggest that young and old subjects attain similar plasma concentrations after single doses; however, longer dosing intervals may be necessary for multiple dosing in the elderly. The appropriate dosing interval for butorphanol needs to be assessed in elderly patients.

Adult↗
PubMed1987

Physiological and immunologic disturbances associated with shock in a primate model of Lassa fever.

The degree of cell and organ damage in clinical and histological studies of patients dying of Lassa fever has been insufficient to explain the catastrophic shock characteristic of the fatal illness. To explore this issue further, we conducted a study of the evolution of shock in three Lassa virus-infected rhesus monkeys. By the sixth day after infection, a marked, progressive reduction of in vitro platelet aggregation occurred despite normal numbers of circulating platelets and a normal platelet survival time and was accompanied by loss of prostacyclin production by postmortem endothelium. Both of these functions recovered rapidly in a surviving animal. There was no evidence of disseminated intravascular coagulation, nor were clotting factors significantly abnormal. We observed association of viral antigen with neutrophils and progressive neutrophilia. Viremia was not reduced by a brisk antibody response in our animals, and there was a general depression of response to mitogens in mixed lymphocyte stimulation assays. Our findings suggest that shock in Lassa fever is due to biochemical dysfunctions of platelets and endothelial cells and results from loss of intravascular plasma volume, effusions, and hemorrhage.

Animals↗
PubMed1985

Transformed T lymphocytes infected by a novel isolate of human T cell leukemia virus type II.

Human T cell leukemia virus type II (HTLV-II) has been isolated from a patient (Mo) with features of leukemic reticuloendotheliosis (LRE) and from a patient with acquired immunodeficiency syndrome (AIDS). We have obtained another isolate of HTLV-II from a patient (CM) with severe hemophilia A, pancytopenia, and a 14-year history of staphylococcal and candidal infections but no evidence of T cell leukemia/lymphoma, AIDS, or LRE. Fresh mononuclear cells and cultured lymphocytes from CM express retroviral antigens indistinguishable by molecular criteria from HTLV-IIMo. Leukocyte cultures from CM yield hyperdiploid (48,XY, +2, +19) continuous lymphoid lines; human fetal cord blood lymphocytes (CBL) are transformed by cocultivation with these CM cell cultures but retain normal cytogenetic constitution. Electron microscopic examination of the CM cultures and transformed CBL reveals budding of extracellular viral particles, intracellular tubuloreticular structures, and viral particles contained within intracellular vesicles. CM cell cultures and the transformed CBL do not require exogenous interleukin 2, have T cell cytochemical features and mature T helper phenotypes, and exhibit minimal T helper and profound T suppressor activity on pokeweed mitogen-stimulated differentiation of normal B cells. These characteristics, which are similar to those observed with the first HTLV-II isolate, may represent properties of all HTLV-II-infected T cells.

Adult↗
PubMed1982

Block of locust muscle glutamate receptors by delta-philanthotoxin occurs after receptor activations.

One component (delta-philanthotoxin (delta-PTX) of the venom from the wasp Philanthus triangulum blocks transmission postsynaptically at excitatory synapses on locust muscle. delta-PTX depresses both the iontophoretic glutamate potential and the excitatory junctional current (e.j.c.) in a glutamate receptor activation-dependent manner. The rate of recovery from the effects of the toxin is reduced following either prolonged application of L-glutamate or repetitive iontophoretic application of this amino acid or high frequency neural stimulation of the muscle in the presence of delta-PTX. The decay phase of the e.j.c. is shortened by delta-PTX. The effects of delta-PTX on the e.j.c. are not voltage dependent. The open-close kinetics of glutamate channels in extrajunctional muscle membrane are modified by delta-PTX as shown by patch clamp analysis. The mean life time of the glutamate channel is reduced, whilst the mean interval between single opening events is increased with the events often occurring in bursts. These data are consistent with glutamate channel blocking by this toxin. It is proposed that the toxin blocks open channels gated by both junctional and extrajunctional glutamate receptors on locust muscle. It is further proposed that delta-PTX enters a compartment of the muscle through the glutamate open channels and that it can also block the open channels from this site.

Animals↗
PubMed1979

Factors promoting colony stimulating activity (CSA) production in macrophages and epithelial cells.

The regulation of colony stimulating activity (CSA) release from CSA producing cells is a poorly understood process. Using freshly isolated mouse peritoneal cells and a continuous line of mouse thymic epithelial cells a precise and reproducible method of short term culture was developed to study this phenomenon. Serum, endotoxin, lithium, and cyclic GMP stimulated CSA release from both cell types. Particles such as zymosan, inulin, latex, and iron filings stimulated CSA release from mouse peritoneal cells but not from thymic epthelial cells. Theophylline and cyclic AMP inhibited CSA release from both cell types. Trypsin activated guinea pig C3 and C5 did not stimulate CSA release. Cycloheximide, an inhibitor of protein synthesis, completely inhibited CSA release. We believe these findings may reflect mechanisms of in vivo regulation of CSA release.

Animals↗
PubMed1976

Correlation between diffuse EEG abnormalities and cerebral atrophy in senile dementia.

Thirty-five elderly patients were investigated because of clinical signs of dementia. The presence or diffuse cerebral atrophy, and its severity, were determined by the use of computed tomography (CT scan). All of the patients were also examined by electroencephalography (EEG), and the presence of diffuse abnormalities, especially diffuse slowing, was noted. Specifically, patients with normal or near-normal EEGs were compared with those with severe diffuse slowing. No correlation between the presence or severity of diffuse EEG abnormalities and the degree of cerebral atrophy as measured by CT scan was found. Though the EEG is clearly identifying physiological dysfunction of nerve cells in demented patients it does not appear to be reliable tool for the prediction of diffuse cerebral atrophy in this population.

Age Factors↗