Biomedical subjects
S M Glover
Publications and source records attributed to S M Glover.
Making the most of computer-assisted instruction.
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Getting published. Guidelines for prospective authors.
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Retention. The economics of using an agency.
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Introduction: how bad is the shortage?
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Halothane stimulates the aggregation of platelets of both normal individuals and those susceptible to malignant hyperthermia.
Platelet responses to halothane in normal individuals and in patients susceptible to malignant hyperthermia were evaluated. Platelets in platelet-rich plasma from both normal controls and patients underwent aggregation in response to halothane. There was no significant difference in the degree of aggregation between normal subjects and patients. Aggregation by halothane was associated with a change in platelet shape, centralization of platelet granules, and phosphorylation of platelet actin binding protein, myosin light chain, and a 40 000-dalton protein. Aggregation induced by halothane could be inhibited by EGTA, PGE1, adenosine and verapamil, but not by aspirin. Aggregation induced by halothane could be potentiated by small doses of adrenaline or ADP and in some individuals by caffeine. However, previous exposure of platelets to halothane made them subsequently less aggregable to ADP. The results of these studies do not support a use of halothane-induced aggregation of platelets to detect an abnormality in individuals susceptible to malignant hyperthermia, but do provide new evidence of the effects of halothane on cellular function.
Epinephrine reduction of heme: implication for understanding the transmission of an agonist stimulus.
Alpha-adrenergic agonists that promote platelet aggregation were found to reduce ferric heme to ferrous heme. Agents that bind iron in heme inhibited epinephrine-induced platelet aggregation. It is proposed that epinephrine first binds to its receptor and then reduces an adjacent heme group to transmit its agonist stimulus.