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Biomedical subjects

T Croxton

Publications and source records attributed to T Croxton.

4 recordsLinked to original sources

Severe haemolysis after an ABO unmatched kidney transplant - a nonsecretor transplanted from a donor with high anti-A titre.

A case of severe haemolysis following an ABO unmatched renal transplant is reported in a group A nonsecretor who received a kidney from a group O living related donor. Following the haemolytic episode, group A donor units were incompatible and the patient was transfused with group O blood. Serological investigation of the recipient revealed anti-A present in the serum and on the red cells. Investigation of the donor revealed the presence of high-titre anti-A. The association of such high-titre donor antibody with haemolysis in ABO unmatched grafts has not been reported before. We discuss the risk factors for developing haemolysis in an ABO unmatched organ transplant and explore the possible relevance of such high donor antibody titre to recipients who are nonsecretors.

ABO Blood-Group System↗

Is it necessary to administer anti-D to prevent RhD immunization after the transfusion of RhD-positive platelet concentrates?

Serology for the presence of anti-D after RhD-incompatible platelet transfusions was performed in 24 RhD-negative patients with haematological disease and 59 RhD-negative patients with non-haematological disease. None of the patients were given prophylaxis with anti-D to prevent RhD immunization. Eight out of 59 (13.5%) non-haematology patients developed detectable anti-D, whereas 0 out of 24 (0%) of the haematology patients formed anti-D (P = 0.06). The risk of alloimmunization after RhD-incompatible platelet transfusions using platelet concentrates prepared by modern technical methods appears to be small in patients with haematological disease, but is significant in non-immunocompromised patients.

Adolescent↗

Physiologic modulation of bronchial epithelial cell barrier function by polycationic exposure.

Bronchial epithelial cells provide a functional barrier to the movement of water and solutes between the luminal and interstitial compartments of the lung. Barrier integrity can be compromised by a variety of factors, including polycationic proteins released by inflammatory cells. We investigated the characteristics of epithelial barrier function and its modulation by cationic stimuli in canine bronchial epithelial (CBE) cells grown in culture. Morphologic characteristics were examined, and barrier function was assessed by measurements of transepithelial mannitol flux (flux) and electrical resistance (RT) during a stable, 3- to 14-day culture period. CBE cultures exhibited progressive mucociliary differentiation and contained nonciliated, ciliated, and neutral and acidic mucin-secretory cells. The synthetic polycation, poly-L-lysine (PLL), from 2.5 to 10 micrograms/ml, caused dose-related increases in flux and decreases in RT that were not accompanied by detectable release of lactate dehydrogenase (LDH) or changes in histochemical appearance. The effect on RT spontaneously reversed over a 15-h recovery period. The action of PLL on flux was not attenuated by treatment of the cells to stabilize cytoskeletal contractile elements but was immediately attenuated by the addition of heparin to the challenged cells. These results indicate that modulation of the barrier integrity of bronchial epithelial cells by cationic proteins, such as those released by inflammatory cells, represents a physiologic process that may be regulated by endogenous anionic factors.

Animals↗

Halothane inhibition of ion transport of the tracheal epithelium. A possible mechanism for anesthetic-induced impairment of mucociliary clearance.

Significant depression of mucociliary function occurs during general anesthesia. One possible mechanism to account for this effect is a change in ion and water transport across airway epithelium. To determine if anesthetics alter epithelial cell function, we used electrophysiologic techniques to measure the effects of halothane on ion transport of in vitro canine tracheal epithelial. Epithelial tissues were mounted in an Ussing chamber and the short-circuit current (Isc) (a measure of active ion transport) and transepithelial resistance were determined in the absence and presence of halothane. Halothane induced a rapid and reversible decrease in Isc that was dose-dependent. Four percent halothane reversibly decreased Isc from 90 +/- 11 to 39 +/- 6 microA/cm2 (n = 12; P = 0.001) and increased transepithelial resistance. Isoproterenol is a well-known activator of chloride secretion that acts via beta-adrenergic receptors and cyclic adenosine monophosphate (cAMP). Pretreatment with isoproterenol or dibutyryl cAMP (a cell permeable analogue of cAMP) increased the percent inhibition of Isc by 4% halothane. These effects are consistent with preferential inhibition of chloride secretion by halothane but rule out a primary action of halothane on the beta-adrenergic system. In the presence of indomethacin, which eliminates the contribution of chloride secretion to Isc, 4% halothane induced a much smaller but still significant inhibition. This suggests that sodium absorption is also affected. We conclude that halothane significantly decreases ion and water transport in canine epithelia and that impaired fluid secretion may contribute to decreased mucous clearance in the perioperative period.

Animals↗