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Biomedical subjects

W W Hurd

Publications and source records attributed to W W Hurd.

58 records · Page 4Linked to original sources
PubMed1980

Acquired functional asplenia. Association with spontaneous rupture of the spleen and fatal spontaneous rupture of the liver in amyloidosis.

A 45-year-old woman who had lower extremity ecchymoses and vague abdominal and back complaints was found to have acquired functional asplenia manifested by Howell-Jolly bodies and poikilocytosis on peripheral blood smear. On spleen scan there was inability to take up radioactive colloid. Shortly thereafter, she was found to have a spontaneous rupture of the spleen. At operation, the spleen, liver, and periaortic lymph nodes were found to be diffusely involved with amyloidosis. Five months later, an acute, serious, intra-abdominal condition developed secondary to spontaneous rupture of the liver, and the patient died. To our knowledge, neither acquired functional asplenia nor spontaneous rupture of the liver has been reported previously in association with amyloidosis.

Amyloidosis↗
PubMedDate not supplied

Cocaine downregulates beta-adrenergic receptors in pregnant sheep myometrium.

Cocaine abuse is associated with premature labor. Although cocaine is known to competitively inhibit beta-adrenergic receptor binding, cocaine's effect on receptor downregulation is uncertain. This study was designed to determine the in vitro effect of cocaine on downregulation of beta-adrenergic receptors in pregnant myometrium. Pregnant sheep myometrium was incubated with either cocaine, isoproterenol, or a cocaine metabolite, benzoylecgonine. Membrane fractions were assayed for beta-adrenergic receptors using (125I)-cyanopindolol and the beta 2-adrenergic antagonist ICI 118,551. We found that cocaine (10(-6) to 10(-4) mol/L), but not benzoylecgonine, downregulated both beta 1- and beta 2-adrenergic receptors, but did not further augment receptor downregulation by isoproterenol. The 46% decrease in beta-adrenergic receptors seen after exposure to cocaine was similar to the 53% decrease seen after isoproterenol. We hypothesize downregulation of beta-adrenergic receptors by cocaine may play a role in the association of cocaine abuse with premature labor.

Animals↗
PubMedDate not supplied

Effect of cocaine on intracellular calcium regulation in myometrium from pregnant women.

OBJECTIVE: To evaluate the effect of cocaine on intracellular free calcium ([Ca2+]i) regulation in human myometrial cells by determining the sources of Ca2+ it might mobilize, as well as assess the role cocaine might play in the catecholamine's effect on the cell's [Ca2+]i. METHODS: Primary culture of myometrial cells from pregnant women was used as an experimental model. [Ca2+]i relative changes in response to cocaine and norepinephrine were measured with fura-2 fluorometry and analyzed by means of one-way analysis of variance. RESULTS: Cocaine alone (10(-8) to 10(-3) mol/L) increased [Ca2+]i by up to 43 +/- 18% over basal level in a dose-dependent manner. Norepinephrine also elevated [Ca2+]i in a concentration-dependent manner (202 +/- 24% over basal level at 10(-4) mol/L). The norepinephrine-evoked increase was inhibited in Ca(2+)-free media by 48%, whereas the cocaine response was not affected. The Ca(2+)-channel antagonist nifedipine caused decrease in the [Ca2+]i response to 10(-5) mol/L of norepinephrine by 84%, whereas the [Ca2+]i rise to 10(-5) mol/L cocaine was not significantly changed. Inhibitor of the sarcoplasmic reticulum Ca2+ pump, thapsigargin, completely blocked cocaine-evoked increases in [Ca2+]i, whereas norepinephrine responses were greatly reduced. At the same time, cocaine (10(-8) to 10(-3) mol/L) did not potentiate norepinephrine-evoked Ca2+]i increases in the cells. CONCLUSION: These results indicate that cocaine increases [Ca2+]i in pregnant human myometrial cells, primarily by stimulating release of Ca2+ from intracellular stores rather than by direct stimulation of Ca2+ influx.

Adrenergic alpha-Agonists↗