• Journal of Chest Surgery
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• v.29 no.5
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• pp.477-486
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• 1996

Endogenous analgesic systems are known to be activated by peripheral noxious stimulation as well as arterial carbon dioxide elevation. In the present study, neuronal Activities in the rostral ventrolateral med- ulla were identified and classified in according to their rhythmic activities, and their responses to noxious peripheral nerve stimulations before and after elevating the arterial carbon dioxide partial pressure were investigated Using extracellular recording technic, a total of 53 spontaneously active neurons were recorded from the rostral ventrolateral medulla in u-chloralose anesthetized cats. These were classified as cardiovascular (28), respiratory (16), both cardiovascular and respiratory (2) and noncardiovascular - nonrespiratory (7). - Among the 28 cardiovascular neurons eleven showed increased activities during arterial hypercapnia, thirteen showed decreased responses, and four showed no change. Nine respiratory neurons showed increased responses to arterial hypercapnia, six showed decreased responses and one showed no change. neither of the cardiovascular and respiratory neurons showed significant change in its activity during ar- terial hypercapnia, however, four of the noncardiovascular - nonrespiratory neurons exhibited decreased their activities in response to arterial hypercapnia while two exhibited increased activities. Arterial hypercapnia increased the responses of cardiovascular neurons to peripheral nerve stimulation with C-inteniity, while not changing the responses to Ak_stimulation significantly . From the above results it was conclllded that during arterial hypercapnia, some cardiovascular neurons and respiratory neurons have increased activities as well as increased reponses to C-Hber stimulation.

• Tuberculosis and Respiratory Diseases
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• v.46 no.5
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• pp.628-635
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• 1999

Background : Maximal expiratory flow rate is determined by the size of airway, elastic recoil pressure and the collapsibility of airway in the lung. The obstruction of expiratory flow is one of the major functional impairments of emphysema, which represents COPD. Nevertheless, expiratory narrowing of upper airway may be recruited as a mechanism for minimizing airway collapse, and maintaining lung volume and hyperinflation by an endogenous positive end-expiratory pressure in patients with airflow obstruction. We investigated the physiologic role of trachea in respiration in emphysema. Method : We included 20 patients diagnosed as emphysema by radiologic and physiologic criteria from January to August in 1997 at Seoul Municipal Boramae Hospital. Chest roentgenogram, high resolution computed tomography(HRCT), and pulmonary function tests including arterial blood gas analysis and body plethysmography were taken from each patient. Cross-sectional area of trachea was measured according to the respiratory cycle on the level of aortic arch by HRCT and calibrated with body surface area. We compared this corrected area with such parameters of pulmonary function tests as $PaCO_2$, $PaO_2$, airway resistance, lung compliance and so on. Results : Expiratory cross-sectional area of trachea had significant correlation with $PaCO_2$ (r=-0.61, p<0.05), $PaO_2$ (r=0.6, p<0.05), and minute ventilation (r=0.73, p<0.05), but inspiratory cross-sectional area did not (r=-0.22, p>0.05 with $PaCO_2$, r=0.26, p>0.05 with $PaO_2$, and r=0.44, p>0.05 with minute ventilation). Minute ventilation had significant correlation with tidal volume (r=0.45, p<0.05), but it had no significant correlation with respiratory frequency (r=-0.31, p>0.05). Cross-sectional area of trachea had no significant correlation with other parameters of pulmonary function including $FEV_1$, FVC, $FEV_1$/FVC, peak expiratory flow, residual volume, diffusing capacity, airway resistance, and lung compliance, whether the area was expiratory or inspiratory. Conclusion : Cross-sectional area of trachea narrowed during expiration in emphysema, and its expiratory area had significant correlation with $PaCO_2$, $PaO_2$, and minute ventilation.

• The Korean Journal of Physiology
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• v.18 no.1
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.

• Analytical Science and Technology
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• v.34 no.6
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• pp.259-266
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• 2021

Cannabis (Marijuana) is one of the most widely used drugs in the world, and its distribution has been controlled in South Korea since 1976. Identification of 11-nor-Δ⁹-carboxy-tetrahydrocannabinol (THCCOOH) in urine can provide important proof of cannabis use, and it is considered scientific evidence in the forensic field. In this study, we describe a simultaneous quantitative method for identifying THCCOOH and THCCOOH-glucuronide in urine, using simple liquid-liquid extraction (LLE), and liquid chromatography-tandem mass spectrometry (LC-MS/MS). THCCOOH-D₃ and THCCOOH-glucuronide-D₃ were used as internal standards. Validation results of the matrix effect, as well as recovery, linearity, precision, accuracy, process efficiency, and stability were all satisfactory. No carryover, endogenous or exogenous interferences were observed. The limit of detection (LOD) of THCCOOH and THCCOOH-glucuronide were 0.3 and 0.2 ng/mL, respectively. The developed method was applied to 28 authentic human urine samples that tested positive in immunoassay screening and gas chromatography/mass spectrometry (GC/MS) tests. The ranges of concentrations of THCCOOH and THCCOOH-glucuronide in the samples were less than LOQ~266.90 ng/mL and 6.43~2133.03 ng/mL, respectively. The concentrations of THCCOOH-glucuronide were higher than those of THCCOOH in all samples. This method can be effectively and successfully applied for the confirmation of cannabinoid use in human urine samples in the forensic field.