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Biomedical subjects

C M Smith

Publications and source records attributed to C M Smith.

At least 253 records · Page 14Linked to original sources
PubMed1983

Identification of receptor mechanism mediating epinephrine-induced arrhythmias during halothane anesthesia in the dog.

The adrenergic receptor mechanism by which halothane sensitizes the myocardium to the ventricular arrhythmogenic properties of catecholamines is unknown. The new generation of selective adrenergic receptor antagonists have been used to determine which receptor blockade causes the greater increase in the dose of epinephrine needed to achieve a threshold for ventricular arrhythmias. Dogs anesthetized with 1.2 MAC halothane had an arrhythmogenic dose of epinephrine (ADE) of 2.2 micrograms X kg X min-1 that significantly increased (P less than 0.01) to 27 micrograms X kg-1 X min-1 after alpha 1 blockade with prazosin. beta 1 blockade with metoprolol also significantly increased the ADE to 12 micrograms X kg-1 X min-1 (P less than 0.05) but was less than the effect noted after prazosin treatment (P less than 0.05). The dramatic increase in the threshold for arrhythmias noted after prazosin could not be ascribed solely to its hemodynamic properties because treatment with sodium nitroprusside did not change the ADE (2.7 micrograms X kg-1 X min-1) significantly; yet nitroprusside treatment resulted in a similar drop in mean arterial pressure (59 mmHg) to that of prazosin treatment (51 mmHg) when compared with the control group. Thus postsynaptic myocardial alpha 1 adrenergic receptors mediate most of the sensitization by halothane to the ventricular arrhythmogenic effects of catecholamines, while a lesser contribution is conferred by the beta 1 adrenoceptors. These results have implications for the treatment and identification of patients particularly at risk from halothane-epinephrine interactions.

Adrenergic alpha-Antagonists↗
PubMed1983

Effects of Salinity on Primary Processes of Photosynthesis in the Red Alga Porphyra perforata.

The effects of salinity on the primary processes of photosynthesis were studied in the red alga Porphyra perforata. The results show that there are at least three sites in the photosynthetic apparatus of this alga that were affected by increased salinity. The first site, photoactivation and dark-inactivation of electron flow on the reducing side of photosystem I, was completely inhibited at high salinity. The second site, electron flow on the oxidizing side (water side) of photosystem II, was inhibited as was the re-oxidation of Q in the presence of 3-(3,4-dichlorophenyl)-1,1-dimethylurea. The third site affected by high salinity was the transfer of light energy probably from pigment system II to I. High salinity reduced the amount of light energy that reached the reaction centers of photosystem II.These effects are discussed in relation to the mechanisms available to this plant to avoid photoinhibition when it is exposed to stresses such as high light and high salinity which are conditions that are commonly found in the intertidal habitat.

Journal Article↗
PubMed1983

An unusual brainstem capillary telangiectasis in a child.

This case report concerns a brainstem telangiectasis that mimicked a tumor causing progressive neurologic symptoms over a period of 6 years prior to death. Intravascular coagulation within the malformation leading to localized ischemia is proposed as the mechanism for the apparent growth of the lesion.

Brain Neoplasms↗
PubMed1983

Hemoglobin North Shore: a variant hemoglobin associated with the phenotype of beta-thalassemia.

Hemoglobin (Hb) North Shore (beta 134 val leads to glu) is a mutant hemoglobin that is associated with the phenotype of mild heterozygous beta-thalassemia. Heterozygotes are characterized low normal hemoglobin levels or mild anemia, microcytosis, increased HbA2, and 34%-38% Hb North Shore. The mechanism of the anemia and microcytosis associated with Hb North Shore was explored by studies of hemolysate thermal instability, peripheral blood globin biosynthesis, and whole blood oxygen affinity. Hb North Shore was mildly heat unstable in comparison to normal adult hemolysate. Pulse labeling of reticulocytes with 3H-leucine showed an alpha/beta ratio of 1.35 (normal 1.0). The beta North Shore/alpha ratio was 0.22-0.27, which was less than expected on the basis of gene dosage and less than that seen for most beta-chain variants. The beta A/alpha ratio was 0.50, as would be expected. The beta North Shore/alpha ratio was 0.26 after a 15-min pulse and did not decrease during 120 min of chase. These findings suggest that suboptimal synthesis rather than posttranslational degradation is responsible for the thalassemic phenotype associated with this variant hemoglobin. These observations parallel the findings in heterozygous HbE. It is not presently known whether the thalassemia phenotype is conferred by the structural mutation itself or by another mutation cis to the beta North Shore gene.

Amino Acids↗
PubMed1982

Deoxyadenosine triphosphate accumulation in erythrocytes of deoxycoformycin-treated mice.

The accumulation of deoxyadenosine triphosphate (dATP) in erythrocytes of mice treated with the adenosine deaminase inhibitor deoxycoformycin was studied in an attempt to establish and evaluate a model system for the study of at least some biochemical aspects of hereditary adenosine deaminase deficiency. Mouse erythrocytes in vitro readily phosphorylated deoxyadenosine to dATP, and this nucleotide was relatively stable once formed. dATP accumulated in vivo in mice treated with deoxycoformycin both as a function of dose from 0.25 to 10 mg/kg, and with time after administration. Major sources of the deoxyadenosine used for dATP formation in vivo appear to be normoblast nuclei produced during erythropoiesis, and dying cells; minor sources would appear to include dietary DNA, overproduction of deoxyribonucleotides, and DNA repair.

Adenosine Deaminase↗
PubMed1982

Phenotype of human T helper and suppressor cells in an in vitro specific antibody response.

Monoclonal anti-human T cell antibodies have been used to identify cells which provide help for an in vitro specific antibody response to influenza virus and also those which suppress the response of allogeneic peripheral blood mononuclear cells. The helper cells carry antigens defined by the Leu 3a and OKT4-antisera, whereas the suppressor cells are predominantly Leu 2a- and OKT8-positive. Help and suppression in this secondary in vitro antibody response are therefore provided by antigenically distinct T cell subsets.

Antibodies, Monoclonal↗
PubMed1982

A human-hybridoma system based on a fast-growing mutant of the ARH-77 plasma cell leukemia-derived line.

A rapidly-growing, HAT-sensitive cell line LICR-LON-HMy2 has been derived from the ARH-77 human plasma cell leukemia-derived line. It lacks the enzyme hypoxanthine phosphoribosyltransferase (EC 2.4.2.8). Hybrids have been reproducibly made for more than a year and in independent laboratories with lymphocytes from tonsils, lymph nodes and peripheral blood and tonsil lymphocytes cultured with antigens. The parent line and hybrids are very robust in culture and double in 20-30 h. Hybrids clone easily and have stable karyotypes, most with modal numbers in the sixties. Stable Ig secretion patterns have been observed over 20-30 passages, and after cloning. It was estimated that about half the hybrids produce new immunoglobulin chains in addition to the parent cell line's IgG1 (kappa light chain). High, but not limiting, density hybridoma cultures (approximately 5 x 10(5) cells/ml) typically produce 0.25-2 micrograms/ml immunoglobulin per day, but some hybrids produce more. A high-secreting variant of LICR-LON-HMy2 has been derived. The LICR-LON-HMy2 line is human and is distinct from the HAT-sensitive human B cell-lines SKO-007 and GM 1500-6TG Al 2. It is available for distribution.

Antibodies, Monoclonal↗
PubMed1982

High frequency discharges in sensory nerves following ischemia.

The effects of ischemia and recovery from ischemia on afferent discharges recorded from dorsal root filaments were assessed in anesthesized cats. During ischemia produced by cross-clamping the lumbar aorta, some of the hindlimb afferents originating in muscle spindles exhibited a sustained high frequency discharge of 120--160 Hz, the so-called "explosion." During recovery from ischemia, nerve discharges appeared in previously inactive dorsal root afferent nerve fibers not of muscle spindle origin. The post-ischemic high frequency discharges appeared in bursts of action potentials at frequencies of 200--500 per second, with 6--32 spikes per burst; the bursts recurred at intervals of 120--600 msec. The nerve fibers exhibiting post-ischemic bursts could not be activated by muscle stretch, muscle tension, palpation, or tactile skin stimulation prior to or during the ischemia. No post-ischemic burst discharges could be detected in analogous experiments with the sural nerve. Intermediate size fibers from normal cutaneous and muscle mechanoreceptors were eliminated as possible origins of the post-ischemia activity. Possible sources include dorsal root ganglion cells or fibers whose sensory endings lie in deep structures such as the walls of the larger blood vessels.

Animals↗
PubMed1982

Association between age, blood lead concentration, and serum 1,25-dihydroxycholecalciferol levels in children.

Serum levels of 1,25-dihydroxycholecalciferol (1,25-CC), the form of vitamin D active in stimulating intestinal absorption of calcium, phosphorus, and lead, were determined in 177 human subjects ages 1 to 16 yr. Significant negative association (r = -0.88) was observed between serum 1.25-CC levels and blood lead concentrations over the entire range of blood lead levels, 12 to 120 micrograms/dl. Adolescents ages 11 to 16 yr had serum 1,25-CC levels higher than those observed among children 10 yr old or younger. No effect of sex or season on serum 1,25-CC level was observed. When the 1,25-CC values for children with blood lead concentrations greater than 30 micrograms/dl were excluded from the analysis, no significant effect of geographic location on 1,25-CC levels was observed.

Adolescent↗
PubMed1982

Filtration deformability of rabbit pulmonary macrophage.

Rabbit PAM deformability was evaluated by positive-pressure filtration through Nucleopore membranes of well-specified pore diameter. The PAM filtration method was standardized and was influenced by apparatus variations (pore size, flow rate, cell concentration), environment (temperature, pH, divalent cations, protein concentration), and differences in PAM cell volume. The influence of phagocyte function on filtration deformability was evaluated by exposing PAMs to pharmacologic and physiologic agents with somewhat exclusive influences on phagocyte physiology. Agents that interact with microfilament contractile protein (N-ethylmaleimide, cytochalasin B) altered deformability profoundly, but no effect was observed with agents interacting with microtubules (vinblastine, colchicine). Agents that cause general PAM activation (phorbol myristate acetate) or stimulate chemotaxis (F-Met-Leu-Phe) increased deformability. On the contrary, PAM deformability was not changed by phagocytosis of Staphylococcus aureus or latex beads. Pharmacologic agents that alter PAM adhesion (aspirin, indomethacin, physiologic dose hydrocortisone) or inhibit glycolysis (2-deoxyglucose) had no influence on filtration deformability. Filtration PAM deformability reflects passive whole cell rigidity, which appears to be determined by the state of polymerization of the actin-myosin microfilament complex.

Animals↗