Head and Neck Infections in Pediatric Cardiac Transplant Patients

A retrospective chart review was undertaken at Columbia Presbyterian Medical Center to assess the incidence, etiology and management of head and neck infections in pediatric cardiac transplant patients on immunosuppression. From June 1984 to February 1992, 59 cardiac-transplants were performed on 57 pediatric patients. Standard immunosuppressive therapy was used. Thirteen of these patients died within three months of transplant and were not included. Of the 44 patient charts reviewed, 82 head and neck infections were documented in 27 patients (61%). There were 26 episodes of sinusitis, 27 episodes of otitis media and 20 episodes of tonsillitis/pharyngitis. Unusual middle-ear pathogens seen included Morganella morgagni and Pseudomonas aeruginosa. These preliminary data suggest that children on immunosuppression for cardiac transplant may be at risk for head and neck infections from unusual or unsuspected organisms, and tympanocentesis plays an important role in diagnosis and treatment. A prospective study is planned to gain further data. </jats:p

Interaction of verapamil with human platelet alpha-adrenergic receptors

Platelet aggregation induced by epinephrine is an alpha-adrenergic event and is inhibited in vitro by the calcium-channel blocker, verapamil. We wondered whether this inhibition might be mediated by an interaction of verapamil with platelet alpha-adrenergic receptors. Verapamil inhibited the specific binding of [3H]dihydroergocryptine ([3H]DHE), a nonselective alpha-adrenergic antagonist, to intact platelets in a concentration-dependent and competitive manner. At 10 microM verapamil caused a fivefold decrease in the affinity of binding of [3H]DHE to platelet alpha-adrenergic receptors (P less than 0.001) with no change in the number of receptors per platelet. The inhibition of binding was not reversed by excess calcium. Verapamil also inhibited the binding of a selective alpha 2-adrenergic antagonist, [3H]yohimbine, to intact platelets, and inhibited the binding of an alpha 2-partial agonist, [3H]clonidine, to platelet membranes. Moreover there was a strong correlation between verapamil's effect on [3H]DHE binding and its effect on epinephrine-induced aggregation (r = 0.98). Although verapamil is commonly used as an inhibitor of calcium flux across cell membranes, the present studies demonstrate that verapamil also inhibits epinephrine-induced aggregation at the level of the platelet alpha-adrenergic receptor. </jats:p