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Biomedical subjects

E J Hartley

Publications and source records attributed to E J Hartley.

9 recordsLinked to original sources

Should all children with suspected or confirmed malignant hyperthermia susceptibility be admitted after surgery? A 10-year review.

Children otherwise suitable for same-day discharge may be admitted to the hospital solely because they are known or suspected to be malignant hyperthermia-susceptible (MHS). To determine whether their hospitalization is necessary, the medical charts of 303 children labeled MHS who had undergone surgery with anesthesia free of malignant hyperthermia-triggering agents on 431 occasions between 1981 and 1990 were reviewed. Eighteen of these patients (25 cases) who were subsequently identified as biopsy-negative were excluded from the study. We recorded the reason for the MHS label and the perioperative management and outcome of the cases. Fifty-eight percent of procedures were followed by hospital admission solely because of the patient's MHS label. None of the 25 children (33 cases) with biopsy-proven malignant hyperthermia developed intraoperative or postoperative pyrexia. Ten children suspected to be MHS developed pyrexia greater than 38.5 degrees C. These episodes were not considered to be malignant hyperthermia and were not treated with dantrolene. None of the remaining 275 patients exhibited any features of malignant hyperthermia, although one had an adverse reaction to radiologic contrast medium. On the basis of our retrospective analysis, postoperative admission to the hospital solely on the basis of the MHS label is not warranted.

Adolescent

Determination of bupivacaine in plasma by high-performance liquid chromatography. Levels after scalp infiltration in children.

The local anaesthetic bupivacaine could be very useful for analgesia in pediatric neurosurgery. Since systemic toxic reactions to bupivacaine are correlated with high plasma levels it was important, as an adjunct to clinical evaluation, to measure plasma bupivacaine. This report describes a high-performance liquid chromatography (HPLC) method for the quantitation of plasma bupivacaine. Sample preparation involves extraction into ether followed by back-extraction into HCl. After evaporation, the acid extract is redissolved and separated by reversed-phase chromatography. The assay is linear to 5 mg bupivacaine/L and shows excellent recovery and precision. With samples from children undergoing brain surgery following scalp infiltration with either 0.125% or 0.25% bupivacaine, plasma levels peak within 10 min, then fall rapidly to a plateau by 30 min. This plateau is maintained for at least 120 min. In no case did we find supposed toxic levels of bupivacaine.

Brain

Scalp infiltration with bupivacaine in pediatric brain surgery.

To evaluate whether local anesthetic scalp infiltration blunts hemodynamic responses to craniotomy in anesthetized children (age, 2-18 yr), two concentrations of bupivacaine (0.125% and 0.25%) with vasoconstrictor (epinephrine 1:400,000) were compared with control data when a solution of vasoconstrictor alone was injected. Arterial plasma levels of bupivacaine were measured by high-pressure liquid chromatography. Statistically significant increases in mean arterial pressure and heart rate above baseline measurements occurred in the control group during the period between scalp incision and dural reflection (P less than 0.05). Both concentrations of bupivacaine prevented these increases. Mean arterial pressure and heart rate during scalp incision and scalp reflection were significantly higher in the control group than in both bupivacaine groups (P less than 0.05). Peak bupivacaine plasma levels (mean +/- SD) occurred either 5 or 10 min after infiltration and were significantly higher in the 0.25% group (0.48 +/- 0.31 microgram/mL) than the 0.125% group (0.14 +/- 0.13 microgram/mL) (P less than 0.05). These results suggest that bupivacaine infiltration blocks the hemodynamic response to craniotomy. A concentration of 0.125% bupivacaine with 1:400,000 epinephrine is as effective as 0.25% bupivacaine with 1:400,000 epinephrine at reducing the hemodynamic response to craniotomy. Because the lower concentration of bupivacaine produces lower blood levels, we recommend 0.125% bupivacaine with 1:400,000 epinephrine as a useful, safe adjunct to general anesthesia in children undergoing craniotomy.

Adolescent

Development of receptors for dopamine and noradrenaline in rat brain.

In order to examine the receptor basis for the development of spontaneous locomotion and for the effects of clonidine in the infant rat, we measured the densities of alpha 1-adrenoceptors, alpha 2-adrenoceptors and D2-dopamine receptors in various brain regions of the developing infant Wistar rat. The mesolimbic D2-dopamine receptors paralleled the rise in spontaneous locomotion of the infant rat. No alpha 1-adrenoceptors were detectable at birth in any of the four regions examined (mesolimbic, hippocampus, frontal cortex, and hypothalamus), thus providing no basis for the locomotor-stimulating action of clonidine in the first week of life. Mesolimbic alpha 2-adrenoceptors matured between 21 and 28 days (at which time clonidine yields its usual sedating action).

Animals

The effect of calcium oncardiac phosphorylase activation, contractile force and cyclic AMP in euthyroid and hyperthyroid rat hearts.

Calcium chloride injected into isolated perfused rat hearts produced a positive inotropic effect and increased the levels of phosphorylase a (EC 2.4.1.1). The increase in enzyme activity lagged behind the inotropic effect. Pretreatment of animals with thyroid hormone enhanced the ability of noradrenaline to activate phosphorylase but did not affect the inotropic or phosphorylase activating effect of calcium. Thyroid hormone pretreatment did enhance the chronotropic effect of calcium. Calcium did not affect the cardiac levels of cyclic AMP. It is concluded that calcium can activate phosphorylase by a mechanism other than cyclic AMP and that the enhancement of adrenergic amine-induced phosphorylase activation by thyroid hormone is not a calcium mediated event.

Animals