• The Journal of Korean Medicine
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• v.22 no.3
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• pp.169-178
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• 2001

After initial recovery from acute carbon monoxide (CO) intoxication, some patients occasionally undergo severe neuropsychiatric deterioration, which is called postanoxic delayed encephalopathy (sequelae). This is the clinical report about one patient, a 73-year-old man, diagnosed with delayed encephalopathy after acute CO intoxication. The symptoms of the patient were mental dysfunction including memory impairment and disorientation, abnormal behavior, incontinence and mutism. He had completely recovered after an aonxic episode, but the neurological symptoms that developed were preceded by an interval of apparent normality (the 'lucid interval'). We characterized him as suffering deficiency syndrome of the heart and prescribed for him Bokreongbosim-tang and Guipi-tang, and thereafter his symptoms were remarkably improved. For the evaluation of clinical improvement, we use the Modified Barthel Index (MBI), Canadian Neurologic Scale (CNS), and the Korean version of the Mini-Mental State Examination (K-MMSE)

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.6
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• pp.357-362
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• 2003

Carbon monoxide (CO) is low molecular weight oxide gas that is endogenously produced under physiological conditions and interacts with another gas, nitric oxide (NO), to act as a gastrointestinal messenger. The aim of this study was to determine the effects of exogenous CO on L-type calcium channel currents of human jejunal circular smooth muscle cells. Cells were voltage clamped with 10 mM barium ($Ba^{2+}$) as the charge carrier, and CO was directly applied into the bath to avoid perfusion induced effects on the recorded currents. 0.2% CO was increased barium current ($I_{Ba}$) by $15{\pm}2$% ($mean{\pm}S.E.$, p<0.01, n=11) in the cells. To determine if the effects of CO on barium current were mediated through the cGMP pathway, cells were pretreated with 1-H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, $10{mu}M$), a soluble guanylyl cyclase inhibitor, and exogenous CO (0.2%) had no effect on barium currents in the presence of ODQ ($2{\pm}1$% increase, n=6, p>0.05). CO mediates inhibitory neurotransmission through the nitric oxide pathway. Therefore, to determine if the effects of CO on L-calcium channels were also mediated through NO, cells were incubated with $N^G-nitro-L-arginine$ (L-NNA, 1 mM), a nitric oxide synthase inhibitor. After L-NNA pretreatment, 0.2 % CO did not increase barium current ($4{\pm}2$% increase, n=6, p>0.05). NO donor, SNAP ($20{\mu}M$) increased barium current by $13{\pm}2$% (n=6, p<0.05) in human jejunal smooth muscle cells. These data suggest that CO activates L-type calcium channels through NO/cGMP dependant mechanism.

• Journal of Ginseng Research
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• v.19 no.3
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• pp.225-230
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• 1995

The effect of long-term ginseng (Panax ginseng C.A. Meyer) administration on the clearance of carboxyhemoglobin (CO-Hb) and the property of blood gases was investigated in rats. Rats were received ginseng water extract (0.025% in drinking water) for 42 weeks starting at the age of 6 weeks. They were exposed to the diluted mainstream smoke generated from 15 filter cigarettes for 20 min in a round polycarbonate chamber (D37 cmXH13 cm). Under this condition, the mean CO-Hb content of control and the ginseng-treated rats immediately after the exposure was nearly the same as 13.8$\pm$2.9 f) and 13.9$\pm$1.6%, respectively. However, CO-Hb was more rapidly removed from blood in the ginseng treated rats than in untreatEd control with the laps of time, namely, its biological half life In the former was 36.9$\pm$1.5 min and in the latter was 56.9$\pm$13.2 min. Although long-term ginseng treatment did not affect the content of hemoglobin and blood pH of rats, it slightly increased blood oxygen content and its partial pressure value, and decreased levels of carbon dioxide and bicarbonate. These results suggest that long-term administration of rats with ginseng extract accelerate the elimination of CO from the blood. This effect seems to be related to the enhancement of oxygen consumption of the rat by a certain action of ginseng components as previously reported.