Biomedical subjects

C B Berde

Publications and source records attributed to C B Berde.

76 records · Page 5Linked to original sources

PubMedDate not supplied

Effects of adrenergic agonists and antagonists on tetrodotoxin-induced nerve block.

BACKGROUND AND OBJECTIVES: The relative contributions of alpha(1)-, alpha(2)-, and beta-adrenergic receptors to adrenergic agonists' prolongation of nerve block by tetrodotoxin (TTX) are unknown. We investigated which receptor agonists prolong TTX block, and whether delayed injection of antagonists can interrupt prolonged blocks after coinjection of TTX and agonists. METHODS: Rats received percutaneous sciatic nerve block with 120 micromol/L TTX with and without adrenergic agonists and antagonists. Block duration was assessed by a modified hot-plate test. Functional deficits in the uninjected leg were used to assess systemic distribution of TTX. Data were expressed as medians with 25th and 75th percentiles. RESULTS: Coinjection of 5.5 micromol/L phenylephrine (alpha(1)-specific), 10 micromol/L clonidine (alpha(2)-specific), and 1.1 micromol/L epinephrine (mixed alpha- and beta-agonist) prolonged TTX nerve block, but 5.5 micromol/L isoproterenol (mixed beta-agonist) did not. Yohimbine inhibited TTX block prolongation by clonidine (median inhibitory concentrations, IC(50) = 130 nmol/L); phentolamine similarly inhibited epinephrine (IC(50) = 45 nmol/L). Adrenergic antagonists did not inhibit the prolongation of TTX block by agonists when injected 3 or 6 hours after the initial block. Subcutaneous injection of adrenergic agonists at a remote site did not prolong TTX block, except for a modest prolongation by clonidine. CONCLUSION: TTX block can be prolonged by alpha(1)- and alpha(2)-, but not beta-adrenergic agonists via locally mediated events of relatively brief duration. Delayed injection of adrenergic antagonists does not interrupt the prolonged blocks produced by coinjection of TTX and adrenergic agonists unless administered soon after block is established. Reg Anesth Pain Med 2001;26:239-245.

Adrenergic Agonists↗

PubMedDate not supplied

Monitoring intravenous fat emulsions in neonates with the fatty acid/serum albumin molar ratio.

Weekly determinations of the fatty acid/albumin molar ratio (FA/SA) were obtained 136 times on 50 neonates (birthweight range, 675-4300 grams; median, 1360 grams) to determine if our use of intravenous fat (IVF) was putting these newborns at risk for kernicterus. The FA/SA was measured using a convenient spectrophotometric technique which we have previously described (Berde CB, Kerner JA, Johnson JD: Clin Chem 26:1173-1177, 1980). Twenty-nine infants received IVF with doses from 0.5 to 3.3 gram/kilogram/day (mean 1.5 gram/kilogram/day), given over 24 hours whenever possible, most commonly begun in the second week of life when the bilirubin level was less than one half of the potential exchange level. Twenty-one infants received no IVF. Previous studies show that fatty acids do not begin to displace bilirubin from albumin until the FA/SA is greater than 6 in vivo, and greater than 4 in vitro. All our infants had safe values with mean FA/SA values of approximately 1.0. Continuous IVF as we administer it does not place neonates at risk for kernicterus. Centers administering IVF in the first week of life or by bolus should consider close monitoring of their infants with the FA/SA.

Fat Emulsions, Intravenous↗

PubMedDate not supplied

Continuous subarachnoid analgesia in two adolescents with severe scoliosis and impaired pulmonary function.

We report postoperative pain management of two adolescents after upper abdominal procedures, one with Hurler-Scheie syndrome and a second with Duchenne muscular dystrophy, and both had progressive spinal scoliosis with poor pulmonary function. A combined technique of subarachnoid and general anesthesia was used during surgery. Postoperative administration of small intermittent doses of subarachnoid morphine produced profound analgesia, which eliminated the need for systemic opioids, restored preoperative arterial oxygenation within 48 hours after the operation, and expedited postoperative recovery.

Abdomen↗

PubMedDate not supplied

Chronic exposure to lidocaine does not alter flux through sodium channels in cultured neuronal cells.

BACKGROUND AND OBJECTIVES: Although tachyphylaxis to local anesthetics has been reported in the clinical literature for more than two decades, the molecular mechanism(s) remain unknown. The authors described an attempt to create an in vitro model for tachyphylaxis to local anesthetics using cultured neuronal cells. METHODS: Murine neuroblastoma cells (N1E115) and rat pheochromocytoma cells (PC-12) were grown in the presence or absence of lidocaine or tetrodotoxin for between 1 and 14 days. Thereafter, the authors tested flux through sodium channels by measuring total and tetrodotoxin-sensitive flux of 14C-labeled guanidinium (a ligand for the sodium channel) into the cells using the technique of Jacques et al. RESULTS: Chronic lidocaine or tetrodotoxin treatment caused no change relative to control cells in total or tetrodotoxin-sensitive guanidinium flux, or in the subsequent ability of lidocaine in the flux assay mixture to inhibit guanidinium flux. CONCLUSIONS: The authors concluded that chronic lidocaine or tetrodotoxin application did not produce changes in stimulated sodium channel activity or subsequent lidocaine susceptibility in this model. To the extent that this model simulated the clinical situation, mechanisms other than up-regulation of sodium channel number or maximal stimulated flux per channel may have been responsible for producing tachyphylaxis.

Animals↗