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Biomedical subjects

Y J Kao

Publications and source records attributed to Y J Kao.

At least 19 recordsLinked to original sources
PubMed2001

Induction and regulation of nitric oxide synthase in airway epithelial cells by respiratory syncytial virus.

In this study, we evaluated the effects of respiratory syncytial virus (RSV) infection on nitric oxide (NO) production in human airway epithelial cells. In addition, we evaluated whether T-helper type 1 (Th1)- and Th2-type cytokines modulate the release of NO in response to RSV infection. To do this, we infected monolayers of A549 cells with RSV and determined nitrite levels in the supernatant fluids. We also measured nitrite levels in human small-airway epithelial cells (SAEC) in primary culture and in the bronchoalveolar lavage fluid (BALF) obtained from Balb/c mice after RSV infection. To further support our observations in these analyses, we performed immunocytochemistry and Western blot analysis for inducible nitric oxide synthase (iNOS) in A549 cells. To evaluate the regulation of NO production in response to RSV, we performed experiments in the absence and presence of the Th1 and Th2 type cytokines: interferon (IFN)-gamma, interleukin (IL)-4, and IL-13. In addition, we assessed the inhibitory effect of dexamethasone on iNOS in RSV infected A549 cells. Results were expressed in terms of nmol/mg protein and shown as percents of control values (mean +/- SE). RSV increased the release of nitrites in A549 cells, SAEC, and BALF. The increase in nitrite levels was supported by immunocytochemistry and Western blot analysis for iNOS protein in A549 cells, indicating activation of iNOS in response to RSV infection. IFN-gamma and IL-13 did not affect the RSV-induced increase in NO production. By contrast, IL-4 and dexamethasone suppressed the release of NO in response to RSV infection. These observations show that RSV infection leads to activation of iNOS within the airway epithelium and that IL-4 and dexamethasone inhibit the production of NO in response to RSV infection.

Carcinoma, Small Cell↗
PubMed2000

Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats.

The purpose of the present investigation was to determine whether the sensitivity to systemic toxic effects of cocaine is altered in genetically epilepsy-prone rats (GEPRs). Moderate seizure (GEPR-3) and severe seizure (GEPR-9) rats, and the control strain, Sprague-Dawley rats, 10 weeks of age, were lightly anesthetized with halothane and nitrous oxide. Following surgical preparation and stabilization, the animals were given a constant intravenous infusion of cocaine (4 mg/kg per min) until death. Blood pressure, ECG, and EEG were monitored continuously throughout the experiment. Cocaine doses required to produce seizures (i.e., epileptiform activity on the EEG) were not significantly different between GEPRs and control rats (16.8+/-0.6 mg/kg in GEPR-3, 18.7+/-0.7 mg/kg in GEPR-9, and 14.7+/-1.3 mg/kg in Sprague-Dawley). Seizure duration, amplitude and the number of epileptiform bursts were also similar among the three strains. Additionally, there was no significant difference in cocaine doses that produced arrhythmias and cardiac asystole between GEPRs and control. The results indicate that genetically epilepsy-prone rats do not exhibit altered sensitivity to cocaine-induced seizures despite the marked susceptibility to sound-evoked seizures. Local anesthetic-induced seizures and acoustically-evoked seizures apparently have different underlying mechanisms.

Animals↗
PubMed1996

The reversal of profound mivacurium-induced neuromuscular blockade.

PURPOSE: Mivacurium is metabolized by plasma cholinesterase catalyzed ester hydrolysis. Acetylcholinesterase antagonists used in the reversal of muscle relaxation may also inhibit plasma cholinesterase and, therefore, delay the hydrolysis of mivacurium. The clinical interaction between acetylcholinesterase antagonists and mivacurium induced neuromuscular blockade was studied. METHOD: Intraoperative muscle relaxation was maintained with a mivacurium infusion to achieve a constant intense block (first twitch, T1, 2-3% of control). Patients were randomly divided into three groups. Patients in Group 1 received no anticholinesterase, in Group 2 neostigmine 0.07 mg.kg-1, and in Group 3 edrophonium 1 mg.kg-1. The times between termination of the mivacurium infusion (Group 1) or the administration of the anticholinesterase (Groups 2 and 3) to 25%, 50%, 75% and 95% T1 recovery, and to 50%, 70% and 90% recovery in the ratio, T4/T1 (TR) were recorded. RESULT: In the neostigmine Group, T1 recovery to 25%, 50% and 75% (2.32 +/- 1.41, 3.90 +/- 1.85 and 6.88 +/- 2.66 min) was accelerated compared with control (3.36 +/- 1.34, 5.78 +/- 2.22, and 8.58 +/- 3.60, and), but recovery to 95% (18.53 +/- 9.09 vs 13.29 +/- 5.24 min) was delayed. Also, TR recovery to 50%, 70%, and 90% was slower (14.47 +/- 8.73, 21.25 +/- 11.06 and 31.37 +/- 12.11 min vs 11.75 +/- 3.74, 13.78 +/- 4.39 and 17.86 +/- 6.44 min). However, all T1 and TR recovery times were decreased in the edrophonium group (0.88 +/- 0.51, 2.00 +/- 1.50, 4.97 +/- 2.96, and 9.35 +/- 5.24 min for T1 and 6.86 +/- 3.93, 9.05 +/- 4.51 and 12.24 +/- 6.66 min for TR). CONCLUSION: Neostigmine reversal of intense mivacurium neuromuscular block should be avoided, as this may result in prolongation of the block.

Adolescent↗
PubMed1995

Cerebral metabolism during propofol anesthesia in humans studied with positron emission tomography.

BACKGROUND: Although the effects of propofol on cerebral metabolism have been studied in animals, these effects have yet to be directly examined in humans. Consequently, we used positron emission tomography (PET) to demonstrate in vivo the regional cerebral metabolic changes that occur in humans during propofol anesthesia. METHODS: Six volunteers each underwent two PET scans; one scan assessed awake-baseline metabolism, and the other assessed metabolism during anesthesia with a propofol infusion titrated to the point of unresponsiveness (mean rate +/- SD = 7.8 +/- 1.5 mg.kg-1.h-1). Scans were obtained using the 18fluorodeoxyglucose technique. RESULTS: Awake whole-brain glucose metabolic rates (GMR) averaged 29 +/- 8 mumoles.100 g-1.min-1 (mean +/- SD). Anesthetized whole-brain GMR averaged 13 +/- 4 mumoles.100 g-1.min-1 (paired t test, P < or = 0.007). GMR decreased in all measured areas during anesthesia. However, the decrease in GMR was not uniform. Cortical metabolism was depressed 58%, whereas subcortical metabolism was depressed 48% (P < or = 0.001). Marked differences within cortical regions also occurred. In the medial and subcortical regions, the largest percent decreases occurred in the left anterior cingulate and the inferior colliculus. CONCLUSION: Propofol produced a global metabolic depression on the human central nervous system. The metabolic pattern evident during anesthesia was reproducible and differed from that seen in the awake condition. These findings are consistent with those from previous animal studies and suggest PET may be useful for investigating the mechanisms of anesthesia in humans.

Adult↗
PubMed1994

A new method to evaluate cardiovascular response in anesthetized rats. Hypertension after variable intensity, brief electrical stimuli.

To establish and standardize a nociceptive response in anesthetized rats, the hypertensive responses to defined electrical and mechanical stimuli were studied. Rats (n = 7) were given etomidate, 3.8 mg/kg/hr intravenously (i.v.) 2 hr following carotid artery and jugular vein cannulation. At 15 min after beginning the infusion, four types of noxious stimuli were administered sequentially at 1-min intervals (14 stimuli total): Type 1: Square electrical waves, 125 cps, 1.6 msec, 2-sec train duration, varying current from 0.4 to 12 mA (11 stimuli); Type 2: A single 10-mA electrical stimulus, 5-sec train duration; Type 3: Tail clamping; and, Type 4: Skin incision. After each stimulus, maximum change in systolic blood pressure (delta SBP) was measured. delta SBP after the most intense stimuli was as follows: Type 1 (12 mA, 2 sec), 32.1 +/- 2.14 mmHg; Type 2 (10 mA 5 sec), 42.9 +/- 2.4 mmHg; Type 3 (tail-clamping), 34.3 +/- 3.3 mmHg; Type 4 (skin incision), 14.2 +/- 2.8 mmHg. For the multiple Type-2 stimuli, a relationship between current and delta SBP was present. The authors believe that characterized graded electrical stimulation will allow a more quantitative evaluation of the hypertensive response to noxious stimuli in etomidate anesthetized rats, as compared to observing a single response to a single stimulus. The characterization of the electrical stimulation by amplitude, frequency, and wave form makes research work on nociception under anesthesia easily reproducible.

Anesthesia↗
PubMed1993

Hyperkalaemia: a complication of warm heart surgery.

A case is presented of hyperkalaemia (13.6 mEq.L-1) occurring during cardiopulmonary bypass using warm blood cardioplegia (K+ 40-60 mEq.L-1). Treatment with epinephrine, calcium chloride, sodium bicarbonate, and furosemide reduced K+ to 6.5 mEq.L-1 within 30 min and myocardial performance was enhanced with amrinone and cardiac rhythm was controlled with A-V segmental pacing. It is believed that the hyperkalaemia resulted from a combination of the surgical procedure (mitral valve replacement) and the use of warm cardioplegia. The purpose of this report is to increase the awareness of the possibility of hyperkalaemia with warm cardioplegia and to describe a successful therapeutic regimen.

Anesthesia, Intravenous↗
PubMed1993

The effect of sensor malpositioning on pulse oximeter accuracy during hypoxemia.

BACKGROUND: Previous studies have shown that pulse oximeters whose sensors are positioned improperly may yield erroneously low saturation (SpO2) values on normoxemic subjects. The behavior of oximeters with malpositioned sensors during hypoxemia has not been studied. The current study is aimed at determining the behavior of several different pulse oximeters over a wide range of arterial oxygen saturation (SaO2). METHODS: In each of 12 healthy volunteers, a radial artery cannula was inserted, and eight different pulse oximeters, five of which had malpositioned sensors, were applied. Subjects breathed controlled mixtures of nitrogen and oxygen to slowly vary their SaO2 from 100% to 70%. Arterial blood samples were analyzed and pulse oximeter data were recorded at five stable SaO2 values for each subject. RESULTS: The oximeters with malpositioned sensors vary greatly in their behavior, depending on both the actual SaO2 and the manufacturer and model. One oximeter underestimated saturation at all SaO2 values, while three others underestimated at high SaO2 and overestimated at low SaO2. Linear regression analysis shows a decrease in the slope of SpO2 versus SaO2 in most cases, indicating a loss of sensitivity to SaO2 changes. Between-subject variation in response curves was significant. CONCLUSIONS: The calibration curves of the pulse oximeters studied were changed greatly by sensor malpositioning. At low SaO2 values, these changes could cause the oximeter to indicate that a patient was only mildly hypoxemic when, in fact, hypoxemia was profound. It is recommended that sensor position be checked frequently and that inaccessible sensor locations be avoided whenever possible.

Adult↗
PubMed1990

Dose-dependent effect of metoclopramide on cholinesterases and suxamethonium metabolism.

In obstetric patients undergoing postpartum tubal ligation, we found that metoclopramide produced dose-dependent prolongation of suxamethonium-induced neuromuscular block. Mean block times after suxamethonium 1 mg kg-1 were 8.0 min, 9.83 min and 12.45 min for control and metoclopramide 10 mg and metoclopramide 20 mg groups, respectively. A laboratory study was therefore conducted on the inhibition of human plasma cholinesterase (PCHE) and erythrocyte acetylcholinesterase (ACHE) activity by varying concentrations of metoclopramide using acetylthiocholine as substrate. PCHE showed a greater sensitivity to inhibition by metoclopramide; the concentration of metoclopramide producing 50% inhibition of activity (I50) was 3.16 x 10(-7) mol litre-1, which is within the therapeutic range. ACHE was less sensitive to inhibition by metoclopramide (I50 2.24 x 10(-5) mol litre-1). Analysis of enzyme kinetics at varying substrate concentrations revealed that metoclopramide produced a potent non-competitive, dose-dependent inhibition of both ACHE and PCHE. The inhibition constant, Ki, was 1.88 x 10(-7) mol litre-1 for PCHE and 9.5 x 10(-8) mol litre-1 for ACHE. As metoclopramide is a potent inhibitor of PCHE, interactions might be expected to occur between metoclopramide and drugs that require PCHE for biotransformation, such as suxamethonium and ester local anaesthetics.

Cholinesterase Inhibitors↗
PubMed1990

Loss of consciousness after emergence from anaesthesia. A case of suspected micturition syncope.

A case of postanaesthesia micturition syncope with respiratory arrest is described. If syncope occurs, the temporary myocardial ischaemia and cerebral hypoperfusion may increase anaesthetic risk in the marginally compensated patient. The loss of airway protection during the syncopal period is also a cause of concern. We recommend the use of an indwelling bladder catheter during any prolonged surgical procedure.

Anesthesia Recovery Period↗