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Biomedical subjects

V C Lee

Publications and source records attributed to V C Lee.

11 recordsLinked to original sources
PubMed2000

UVA-induced oxidative damage in retinal pigment epithelial cells after H2O2 or sparfloxacin exposure.

Retinal impairment is one of the leading causes of visual loss in an aging human population. To explore a possible cause for retinal damage in the human population, we have monitored DNA oxidation in human retinal pigment epithelial (RPE) cells after exposure to hydrogen peroxide (H2O2) or the quinolone antibacterial sparfloxacin. When H2O2- or sparfloxacin-exposed cells were further exposed to ultraviolet A (UVA) irradiation, oxidative damage to the DNA of these cells was greatly increased over baseline values. This RPE+pharmaceutical-UVA cell system was developed to mimic in vivo retinal degeneration, seen in mouse studies using quinolone and UVA exposure. DNA damage produced by sparfloxacin and UVA in RPE cells could be remedied by the use of antioxidants, indicating a possible in vivo method for prevention or minimization of retinal damage in humans

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2000

Restructuring patient financial services for maximum effectiveness.

Following its formation as a regional IDS, John Muir/Mt. Diablo Health System in Walnut Creek, California, adopted an innovative approach to reorganizing its patient financial services (PFS) functions. Instead of consolidating all PFS functions into a single centralized business office, the IDS divided PFS leadership responsibilities into two areas: daily operations and technical functions. The director of daily operations oversees PFS clerical staff who are responsible for admitting functions, billing, follow-up, and related activities. The director of technical functions is responsible for implementing, uploading, and maintaining the various information systems; contract tracking and compliance; and regulatory compliance.

California↗
PubMed1998

Propofol sedation produces dose-dependent suppression of lidocaine-induced seizures in rats.

UNLABELLED: The association of propofol with excitatory motor activity, such as myoclonic jerking and opisthotonus, in humans and in animals suggests that it may aggravate clinical seizure activity in some circumstances, although evidence suggests that under other circumstances, propofol inhibits seizure activity. In the current study, we assessed the effect of sedating doses of propofol on lidocaine-induced seizure activity in spontaneously breathing rats receiving no other anesthetics. Adult Sprague-Dawley male rats, 300-400 g, were divided into a control group and three experimental groups representing three graded levels of propofol sedation. The control rats then received a lidocaine infusion at the rate of 150 mg x kg(-1) x h(-1), resulting in a slow, progressive increase in systemic lidocaine concentrations. At the onset of electroencephalographic (EEG) seizure activity, arterial lidocaine concentrations were obtained. The treated rats received propofol according to three different dose schedules: Dose 1 = 10 mg x kg(-1) x h(-1) after a 2.5-mg/kg bolus; Dose 2 = 20 mg x kg(-1) x h(-1) after a 5-mg/kg bolus; Dose 3 = 40 mg x kg(-1) x h(-1) after a 10-mg/kg bolus. After 30 min, a steady level of sedation, dependent on the dose of propofol, was achieved. The lidocaine infusion was then started, and systemic lidocaine levels were obtained at the onset of EEG seizure activity. The lidocaine was continued until the onset of death by cardiac arrest. Plasma lidocaine was measured by gas chromatography. Analysis of variance and Dunnett's t-test were used for comparisons with the control values. Continuous propofol sedation increased the seizure dose of lidocaine from 37.7 +/- 3.5 mg/kg (mean +/- SEM) to 52.5 +/- 2.6 mg/kg (Dose 1, P < 0.05) and 67.9 +/- 8.6 mg/kg (Dose 2, P < 0.05), and completely abolished lidocaine seizures at Dose 3. The lethal dose of lidocaine, 89.4 +/- 10.5 mg/kg control versus 108.7 +/- 10.3 mg/kg (Dose 1), 98.3 +/- 10.1 mg/kg (Dose 2), and 93.5 +/- 10.4 mg/kg (Dose 3) did not differ among groups. The lidocaine levels at seizure threshold were increased in the propofol-treated rats: 16.9 +/- 0.5 microg/mL control versus 19.2 +/- 0.7 microg/mL (Dose 1, P = not significant) and 23.7 +/- 1.8 microg/mL (Dose 2, P < 0.05). Continuous propofol sedation in spontaneously breathing rats receiving no other anesthetics exerts a protective effect against lidocaine-induced seizures in a monotonic, dose-dependent fashion. The cardiac arrest dose of lidocaine is unaffected by propofol under these conditions. IMPLICATIONS: The i.v. anesthetic drug propofol, given to rats to produce sedation, was found to suppress seizure activity caused by overdosage of the local anesthetic lidocaine.

Anesthetics, Local↗
PubMed1994

Spinal and cortical evoked potential studies in the ketamine-anesthetized rabbit: fentanyl exerts component-specific, naloxone-reversible changes dependent on stimulus intensity.

This study examined the changes in spinal and cortical evoked potentials (EPs) produced by fentanyl in the rabbit. The reversibility of these effects by naloxone and the effects of varying stimulus intensity also were examined. Eleven ketamine-anesthetized rabbits underwent analysis of spinal and cortical EPs produced by posterior tibial nerve electrical stimulation. Progressive fentanyl doses up to 100 micrograms/kg total were given intravenously. Stimulus intensities of two to eight times the motor threshold (MT) were used. The lowest stimulus (2 x MT) was insufficient to activate A delta fibers whereas the highest (8 x MT) produced consistent A delta activation. Two spinal potential waveform components (N1, P2), at 4 and 10 ms, and four cortical components (P1, N2, P3, N4), at 15, 30, 60, and 95 ms, were analyzed. Significant amplitude reductions in spinal P2 (46%), cortical N2 (54%), cortical P3 (47%), and cortical N4 (45%), P < 0.01, as well as latency prolongation in cortical P1 (11%), P < 0.01, resulted from administration of a total dose of 100 micrograms/kg of fentanyl. The effect of fentanyl was critically dependent on stimulus intensity for the cortical P3 component (P < 0.01). All changes were reversed by naloxone. Fentanyl produced dose-related changes in specific spinal and cortical EP waveform components in the ketamine-anesthetized rabbit. This effect was significantly dependent on stimulus intensity in at least one cortical component (P3). Such an interaction between drug dose and stimulus intensity may be relevant to interpreting other human and animal evoked potential studies.

Anesthesia↗
PubMed1990

Non-narcotic modalities for the management of acute pain.

The possible options for the management of acute pain are quite numerous and continue to expand as our understanding of the mechanisms of pain becomes increasing sophisticated. Many of the options discussed have been available for years, and their present underutilization may be a reflection of the lack of emphasis on the importance of management of acute pain. An illustration of this would be our present ritual of prescribing narcotics postoperatively, a longstanding, but unfortunately inadequate practice. Because of poor selection and scheduling of doses, postoperative analgesia is typically a less than satisfactory experience for many patients convalescing in a hospital following surgery. The clinician should of course be guided by the clinical situation itself in order to determine what modality or combination of modalities may be appropriate for pain management. Certain techniques, such as continuous local anesthetic infusions, may warrant an escalated level of monitoring and ancillary care. Other techniques, such as the infiltration of a wound with local anesthetic or the addition of a nonsteroidal anti-inflammatory agent to a regimen of mild oral narcotics are so simple that excluding them from patient care is almost callous and inconsiderate. Attention to the mechanisms of pain that may be present in a given situation, whether it be muscle spasm, ischemia, inflammation, edema, or nerve injury, may guide the clinician toward a more rational approach in managing that pain.

Acute Disease↗
PubMed1984

Clearance from cerebrospinal fluid of intrathecally administered beta-endorphin in monkeys.

Five adult male monkeys (Macaca mulatta) weighing 7.1-9.9 kg were given synthetic human beta-endorphin (800 micrograms) and [14C]methoxy-inulin (50 microCi) in 400 microliters of normal saline intrathecally. Serial samples of cerebrospinal fluid were drawn through a previously positioned indwelling spinal catheter and were assayed for concentrations of beta-endorphin (determined by radioimmunoassay) and inulin (determined by liquid scintillation counter). Spinal fluid concentrations of beta-endorphin and inulin peaked and declined in a parallel manner. The clearance ratio (calculated from the reciprocal of the ratio of the areas under the respective curves of elimination of the two species) remained remarkably similar from animal to animal, giving a mean value of 1.060 +/- 0.090 (SEM). This ratio, being near unity, suggests that beta-endorphin is eliminated from spinal fluid in a fashion similar to that of inulin, which is removed exclusively by bulk absorption.

Absorption↗