CAJ | 학술논문

目的探讨低浓度一氧化氮(NO)吸入在实验猪肺栓塞中的作用机制及治疗意义.方法 15只健康幼猪分成两组,分别建立肺栓塞模型.对照组8只,不做任何处理;NO组7只,模型建立后,持续吸入10×10-6的NO.每组于栓塞前30 min,栓寨后0 min,30 min,60min,120 min 5个时间点分别测定生理死腔(VDphy)、肺泡死腔(VDalv)、肺内分流(Qs/Qt)、平均肺动脉压(PAP)、血压(SBP)、心率(HR)、心输出量(CO)、动脉血pH值(pH)、动脉血二氧化碳分压(PaCO2)、动脉血氧分压(PaO2).结果研究发现两组动物Vdphy[NO组栓寒前(64.1±18.0),栓塞后(109.1±30.0),(107.6±26.8),(97.1±24.1);对照组栓塞前(51.1±10.8),栓寨后(129.2±22.1),(116.9±32.5),(103.9±22.8)],VDalv[NO组栓塞前(8.8±4.3),栓寨后(64.3±26.9),(54.0±25.9),(45.7±22.4);对照组栓塞前(10.9±3.6),栓塞后(97.9±21.5),(80.7±25.3),(70.9±22.5)],Qs/Qt[NO组栓寨前(1.76±0.6),栓塞后(2.90±0.8),(3.1±0.6),(2.9±0.8);对照组栓塞前(1.05±1.5),栓塞后(3.4±0.7),(3.4±0.9),(3.5±0.8)],PAP[NO组栓塞前(16.6±3.4),栓塞后(31.7±3.1),(18.7±3.6),(18.0±3.4),(16.6±3.6);对照组栓塞前(15.8±2.6),栓塞后(35.4±3.3),(25.0±2.2),(25.0±3.5),(24.8±2.8)]栓塞后较栓塞前明显增大(P<0.01).PaO2栓塞后较栓塞前明显减小(P<0.05和P<0.01).HR、SBP、CO、pH、PaCO2栓塞前后差异无统计学意义(P>0.05).NO组PAP和VDalv较对照组明显减小(P<0.05和P<0.01),而PaCO2和PaO2较对照组明显增大(P<0.05).其余指标两组动物各时间点之间差异无统计学意义.结论肺栓塞发生后,低浓度NO吸入可以降低肺动脉压,使肺泡死腔减小,氧分压增大,但不会发生血液动力学恶化.
목적 탐토저농도일양화담(NO)흡입재실험저폐전새중적작용궤제급치료의의.방법 15지건강유저분성량조,분별건립폐전새모형.대조조8지,불주임하처리;NO조7지,모형건립후,지속흡입10×10-6적NO.매조우전새전30 min,전채후0 min,30 min,60min,120 min 5개시간점분별측정생리사강(VDphy)、폐포사강(VDalv)、폐내분류(Qs/Qt)、평균폐동맥압(PAP)、혈압(SBP)、심솔(HR)、심수출량(CO)、동맥혈pH치(pH)、동맥혈이양화탄분압(PaCO2)、동맥혈양분압(PaO2).결과 연구발현량조동물Vdphy[NO조전한전(64.1±18.0),전새후(109.1±30.0),(107.6±26.8),(97.1±24.1);대조조전새전(51.1±10.8),전채후(129.2±22.1),(116.9±32.5),(103.9±22.8)],VDalv[NO조전새전(8.8±4.3),전채후(64.3±26.9),(54.0±25.9),(45.7±22.4);대조조전새전(10.9±3.6),전새후(97.9±21.5),(80.7±25.3),(70.9±22.5)],Qs/Qt[NO조전채전(1.76±0.6),전새후(2.90±0.8),(3.1±0.6),(2.9±0.8);대조조전새전(1.05±1.5),전새후(3.4±0.7),(3.4±0.9),(3.5±0.8)],PAP[NO조전새전(16.6±3.4),전새후(31.7±3.1),(18.7±3.6),(18.0±3.4),(16.6±3.6);대조조전새전(15.8±2.6),전새후(35.4±3.3),(25.0±2.2),(25.0±3.5),(24.8±2.8)]전새후교전새전명현증대(P<0.01).PaO2전새후교전새전명현감소(P<0.05화P<0.01).HR、SBP、CO、pH、PaCO2전새전후차이무통계학의의(P>0.05).NO조PAP화VDalv교대조조명현감소(P<0.05화P<0.01),이PaCO2화PaO2교대조조명현증대(P<0.05).기여지표량조동물각시간점지간차이무통계학의의.결론 폐전새발생후,저농도NO흡입가이강저폐동맥압,사폐포사강감소,양분압증대,단불회발생혈액동역학악화.
Objective To investigate the mechanism and significance of low concentration nitric oxide (NO) inhalation in the treatment of pulmonary thromboembelism in swine. Method The pulmonary thromboem-bolism(PTE) model was made in 15 healthy infantile swines which were subsequently assigned to either control group (n = 8) or NO group (n = 7). Swines of the control group were not treated with any medicine, while 10 ppm of NO was administered by continuous inhalation for 2 hours to swines of NO group. Volume of physiological dead space (VDphy), volume of alveolar dead space (VDalv), intrapulmonary shunt (Qs/Qt), mean pulmonary arterial pressure (PAP), systolic blood pressure (SBP), heart rate (HR), cardiac output (CO), arterial blood pH (pH), arterial partial pressure of carbon dioxide (PaCO2) and arterial partial pressure of oxygen (PaO2) were measured 30 min before and 0 min, 30 min, 60 min, 120 min and 180 min after establishment of VIE. Results The post-FIE VDphy, VDalv, Qs/Qt and PAP in both groups increased markedly after PTE compared with the cor-responding pre-PTE measurements (P < 0.01). Post-FIE PaO2 of both groups decreased significandy (P <0.05 and P <0.01), while significance difference was found between pre- and post-PTE HR, SBP, CO, pH or PaCO2 in neither groups (P > 0.05). Both post-PTE PAP and VDalv in NO group were markedly lower(P <0.05 and P <0.01) and beth PaCO2 and PaO2 were much higher than those of the control group (P <0.05). No signi-fieant difference were found in other measurements between two groups. Conclusions Pulmonary arterial pressure may be lowered, alveoli dead space may be reduced and PaCO2 increased by low concentration NO inhalation for the treatment of PIE without decline in haemodynamic status.