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B J Chen

Publications and source records attributed to B J Chen.

40 records · Page 3Linked to original sources

Desflurane potentiates atracurium in humans: a comparative study with isoflurane.

STUDY OBJECTIVE: (1) To evaluate the neuromuscular effects of desflurane and its interactions with atracurium and (2) to compare desflurane and isoflurane in these effects. DESIGN: Sequential entry of informed and consenting patients randomly assigned to receive desflurane (n = 25) or isoflurane (n = 25). SETTING: Operating suite of a county-university medical center. PATIENTS: Fifty adults, ASA physical status I, undergoing elective orthopedic surgery. INTERVENTIONS: Following establishment of steady desflurane or isoflurane anesthesia, at 1.25 minimum alveolar concentration (MAC) exhaled for 15 minutes, a randomly predetermined dose of atracurium (0.05, 0.1, or 0.15 mg/kg) was injected intravenously (IV). At the end of surgery, neostigmine 0.04 mg/kg IV was given to reverse the residual block. The neuromuscular effects of desflurane or isoflurane alone, and the dose-response relationship, time course, and reversibility of the neuromuscular effects of atracurium with either anesthetic, were examined in detail and compared using electromyographic quantification of the response of the first dorsal interosseous muscle to train-of-four (TOF) stimulation of the ulnar nerve. MEASUREMENTS AND MAIN RESULTS: TOF fade and depression of the first response (T1) of the TOF were measured in response to desflurane or isoflurane, atracurium, and neostigmine. Desflurane caused more TOF fade than isoflurane prior to atracurium administration. The TOF ratios were 0.91 +/- 0.02 and 0.98 +/- 0.01, respectively (p < 0.05). For other measured neuromuscular parameters, atracurium-induced depression tended to be greater in the presence of desflurane than in the presence of isoflurane, but none of the measured differences reached the statistical significance level of p < 0.05. The ED50, ED95, and 25-75% recovery index of atracurium were 0.038 mg/kg (95% confidence level; range 0.030 to 0.047 mg/kg), 0.11 mg/kg (0.095 to 0.14 mg/kg), and 31 +/- 4 minutes (means +/- SEM) with desflurane anesthesia, versus 0.043 mg/kg (0.035 to 0.052 mg/kg), 0.13 mg/kg (0.11 to 0.16 mg/kg), and 23 +/- 4 minutes with isoflurane anesthesia (p = 0.1-0.2). Continuation of either anesthetic at 1.25 MAC prevented complete recovery of neuromuscular functions spontaneously or following neostigmine 0.04 mg/kg. CONCLUSION: In ASA physical status I adults, 9% desflurane has neuromuscular effects equal to or slightly in excess of those of 1.6% isoflurane.

Adolescent↗

Hydromediastinum following insertion of a central venous pressure line via the right external jugular vein.

The insertion of a central venous pressure (CVP) catheter has been known to be associated with a variety of complications. Among these, isolated hydromediastinum is relatively rare. We recently encountered a patient who developed hydromediastinum due to extravascular penetration of a CVP line inserted via the right external jugular vein. The clinical manifestations and significance of this complication are discussed.

Catheterization, Central Venous↗

Acute and subacute toxicity study of water-soluble polyalkylsulfonated C60 in rats.

Polyalkylsulfonated C60, or FC4S, a highly water-soluble caged fullerene derivative, is believed to be a free radical remover or an antioxidant in biological systems. A 50 mg/ml aqueous solution was prepared as a master solution and administered to female Sprague-Dawley CD(Crl:CD(SD)BR) rats in a single-dose acute toxicity study or a 12-day subacute toxicity study where rats were given the solution daily. In a study of the median lethal dose (LD50), no rats died after oral administration, and thus FC4S was considered to be nontoxic if administered orally. In an LD50 intraperitoneal injection study, rats died within 30 hr after injection; the LD50 was determined to be approximately 600 mg per kilogram of body weight. Rats injected with the compound intraperitoneally or intravenously immediately eliminated the compound through the kidney; the kidney appeared to be the primary target organ. The compound induced a distinct lysosome-overload nephrosis, a phagolysosomal nephropathy characterized by a tinctorial difference between the outer cortex and the inner cortex and the medulla. The affected outer cortex showed a diffuse degeneration, with the presence of numerous large vacuoles and cytoplasmic aggregates in the tubular epithelium. The phagolysosomal nephropathy was detected in rats after acute exposure as well as in the surviving rats following 1 intraperitoneal injection of 500 mg/kg or intravenous injection of 100 mg/kg. Ultrastructural investigation revealed numerous membranous conglomerates characteristic of phagolysosomal and/or lysosomal inclusions in the cytoplasm of the renal tubular epithelium. These conglomerates were confined to the vacuole, electron-dense, and unevenly stained. They varied in size and shape and were fused or aggregated. Occasional phagolysosomes were also observed in the endothelial cells of the peritubular plexus. A preliminary study of microsomal enzyme activity analysis revealed a suppression effect of liver cytochrome P-450-dependent monooxygenase activities, including cytochrome P-450, cytochrome b5, and benzo(a)pyrene hydroxylase, but an increased level of kidney cytochrome P-450-dependent monooxygenase activities, including NADPH-cytochrome P-450 reductase. The significance of these enzyme alterations was not well determined. Further study is needed to clarify the correlation between the alterations of microsomal enzyme activity and the nephropathy of lysosomal overload-induced changes. These changes may serve as a biological marker in toxicity screening tests for this class of compound.

Administration, Oral↗