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실험견의 급성 저산소성 폐고혈압증에서 K+ Channel 의 역할
조재연(Jae Youn Cho),박상면(Sang Myun Park),박희남(Hee Nam Park),이진구(Jin Goo Lee),심재정(Jae Jeong Shim),인광호(Kwang Ho In),강경호(Kyung Ho Kang),유세화(Se Hwa Yoo) 대한내과학회 1996 대한내과학회지 Vol.50 No.3
N/A Objectives: Numerous studies about mediators in acute hypoxic process have been done. These studies revealed that endothelium derived relaxing factor(EDRF, known as nitric oxide) contributed greatly to the pathogenesis of hypoxic pulmonary hypertension and endothelium derived hyperpolarizing factor(EDHF) regulated the tone of vascular smooth muscle. EDHE is known to open K+ channel, hyperpolarizes vascular smooth muscle cells, closes voltage-dependent Ca++ channel and finally relaxes vascular smooth muscle. Some studies revealed that acute hypoxic pulmonary hypertension was developed by inhibition of EDRF &EDHF. To investigate the role of K+ channel in pulmonary hypertension during acute hypoxia, we measured changes of hemodynamic parameters in experimental dogs after adding glibenclamide(K+ channel blocker), methylene blue(S-guanylate cyclase inhibitor), L-NNA(NO synthase inhibitor) and nicorandil(K+ channel opener and S-guanylate cyclase activator). Methods: Six dogs were anesthetized with thiopental sodium and mechanically ventilated with Harvard volume-cycled animal ventilator. Venous and arterial catheters were placed in the limb vein for infusion and femora} artery to measure systemic arterial pressure. Swan-Ganz catheter was inserted via right internal jugular vein for measuring pulmonary arterial pressure, pulmonary capillary wedge pressure asnd cardiac output. We measured the influence of glibenclamide (3mg/kg). methylene blue(lmg/kg), L-NNA (30mg/kg) and nicorandil(300μg/kg) on the changes of hemodynamic parameters during normoxia and hypoxia. Results: The infusion of nicorandil did not affect mean pulmonary arterial pressure during normoxia and significantly inhibited the increase of mean pulmonary arterial pressure during hypoxia. Glibenclamide did not change mean pulmonary arterial pressure during normoxia, but significantly augmented the increase of mean pulmonary arterial pressure during hypoxia. Methylene blue infusion did not affect mean pulmonary arterial pressure during normoxia, but moderately augmented the increase of mean pulmonary arterial pressure during hypoxia. The infusion of L-NNA did not affect mean pulmonary arterial pressure during normoxia and augmented the increase of mean pulmonary arterial pressure singnificantly during hypoxia, The increase of pulmonary arterial pressure induced by glibenclamide, methylene blue, and L-NNA, under hypoxic state was inhibited by nicorandil. Conclusion: Glibenclamide (K channel blocker) did not affect the mean pulmonary arterial pressure in normoxic state, but augmented the pulmonary hypertension during hypoxia and this effect was inhibited by nicorandil. It is suggested that K+ channel contributes to pulmonary hypertension developed during hypoxia, and the depressive effect of nicorandil seems to be attributable to its dual actions as a K' channel opener and an activator of S-guanylate cyclase.
산화질소 ( Nitric Oxide ) 의 기도내 신경성 염증 조절에 관한 연구
심재정(Jae Jeong Shim),박상면(Sang Myun Park),이진구(Jin Goo Lee),조재연(Jae Yeun Cho),인광호(Kwang Ho In),유세화(Se Hwa Yoo),강경호(Kyung Ho Kang),김철환(Chul Hwan Kim) 대한내과학회 1994 대한내과학회지 Vol.47 No.4
N/A Baekground: Asthma is classified as an inflammatory disease because there are inflammatory changes in the asthmatic airways. There are many evidences that sensory neuropeptides are involved in these inflammatory responses. Neurogenic inflammation is caused by the antidromic nonadrenergic noncholinergic (NANC) release of neuropeptides from vagal nerves. Recently nitric oxide (NO) has received considerable attention as a messenger molecule in the peripheral nervous system and relaxes airway smooth muscle. Also NO is a potent vasodilator and involved in plasma exudation from airway vessels, To investigate the role of nitric oxide in neurogenic inflammation, neurogenic inflammatory responses in rat airways according to duration of NANC stimuation and effects of NO were evaluated, Method: Neurogenic inflammation was produced in rat airways of 2 experimental groups of 1 min and 2 min stimulation with 5V, 1mSec, 5Hz after cholinergic and adrenergic blockade and compared with sham NANC, The magnitude of airway microvascular leakages was checked in the trachea, main bronchus, peripheral bronchus, and lung parenchyme and the leakeage was measured by Evans blue dye extravasation. NW-nitro-L-arginine (L-NNA, 5 mg/kg iv), L-NNA and L-arginine (50 mg/kg iv) were given 15 min before 2 min stimulation on 3 separate groups for evaluation of NO effects, and microvascular leakage was compared with 2 min NANC stimulation group. Results: 1) Vascular permeability of 1 min NANC stimulation group was increased trachea (208.2%, p<0.05), main bronchus (169.4%, p<0.05), and peripheral bronchus (123.6, p=0.18) compared with sham NANC group. 2) There was about l.5 times increase of vascular permeability in 2 min stimulation group compared with 1 min stimulation group (p<0,05), but not significantly increased permeability of lung parenchyme in both groups. 3) In L-NNA pretreated stimulation oup, there was increased vascular permeability of the trachea (133.3%, p<0.05), main bronchus (167.4%, p<0.05), and peripheral bronchus (197.1%, p<0.05) compared with 2 min stimulation group. 4) L-NNA and L-arginine pretreated stimulation group revealed suppressed vascular permeability com- pared with L-NNA pretreated stimulation group. Conclusion: These results revealed that neurogenic inflammation in the rat airway increases inflammatory responses according to duration of stimulation and blocking of NO synthetase increases neurogenic inflammation. These results provide that nitric oxide modulates inflammatory response of NANC stimulation of the vagal nerves in the rat airways.
원저 : 미주 신경의 전기적 자극으로 유발된 백서의 기도내 혈장 유출에 대한 FK224의 효과
심재정 ( Jae Jeong Shim ),이상엽 ( Sang Yeub Lee ),이상화 ( Sang Hwa Lee ),박상면 ( Sang Myun Park ),서정경 ( Jeong Kyung Seo ),조재연 ( Jae Yun Cho ),인광호 ( Kwang Ho In ),유세화 ( Se Hwa Yoo ),강경호 ( Kyung Ho Kang ) 대한결핵 및 호흡기학회 1995 Tuberculosis and Respiratory Diseases Vol.42 No.5
원저 : 기도 이중 양압(BiPAP)을 이용한 비강 간헐 양압환기의 임상적 적용
조재연 ( Jeo Youn Cho ),이상엽 ( Sang Youb Lee ),이상화 ( Sang Hwa Lee ),박상면 ( Sang Myun Park ),서정경 ( Jung Kyung Suh ),심재정 ( Jae Jeong Shim ),인광호 ( Kwang Ho In ),강경호 ( Kyung Ho Kang ),유세화 ( Se Hwa Yoo ) 대한결핵 및 호흡기학회 1995 Tuberculosis and Respiratory Diseases Vol.42 No.5
저산소성 폐질환에서 폐동맥압의 비관혈적 측정에 관한 연구
이진구(Jin Goo Lee),인광호(Kwang Ho In),박상면(Sang Myun Park),조재연(Jae Yeon Jho),심재정(Jae Jeong Shim),강경호(Kyung Ho Kang),심완주(Wan Joo Shim),유세화(Se Hwa Yoo) 대한내과학회 1995 대한내과학회지 Vol.49 No.4
N/A Objectives: The presence of pulmonary hypertension in patients with hypoxic lung disease is associated with poor prognosis. Right heart catheterization is the reference method for the diagnosis of pulmonary arterial hypertension but this invasive technique is not always well tolerated in all patients with hypoxic lung disease. There is a need for noninvasive method to allow the accurate estimation of pulmonary arterial pressure in these patients. To find reliable noninvasive methods of measuring pulmonary artery pressure, we evaluated the reliability of continuous wave Doppler echocardiography and gated cardiac blood pool scintigraphy in patents with hypoxic lung disease. Methods: Noninvasive measurements of systolic pulmonary artery pressure by continuous wave Doppler echocardiography and right ventricular ejection fraction by gated cardiac blood pool scintigraphy were compared with systolic pulmonary atery pressure measured by cardiac catheterization in 12 patients with hypoxic lung disease. Results: 1) The systolic pulmonary artery pressures estimated by continuous wave Doppler echocardiography correlated closely with those measured by cardiac catheterization (r=0.88, p<0.01) 2) The right ventricular ejection fraction estimated by gated cardiac blood pool scintigraphy was also correlated well with the systolic pulmonary artery pressure measured by cardiac catheterization (r=0.85, p<0.01). Conclusion: Continuous wave Doppler echocar-diographic estimation of systolic pulmonary artery pressure and gated car diac blood pool scintigraphic estimation of right ventricular ejection pressure are reliable and feasible noninvasive assessment of pulmonary hypertension in patients with hypoxic lung disease.