연구배경 : 만성폐쇄성폐질환에서 혈소판이 활성화되어 있는 근거가 있으며 이 질환의 예후 인자로 잘 알려진 폐동맥 고혈압이 활성화된 혈소판 및 손상된 내피세포가 관여하리라는 보고가 있다. 이에 만성폐쇄성폐질환에서 혈소판 활성화를 알아보고 혈소판 활성화가 폐동맥 고혈압에 미치는 영향을 알아보고자 연구를 시행하였다. 방법 : 대조군 및 만성폐쇄성폐질환의 폐동맥 정상혈압군과 고혈압군을 대상으로 혈소판 응집비 및 혈소판의 alpha-granule에 함유되어 있는 Platelet factor 4와 $eta$-thromboglobulin을 측정하여 다음과 같은 결과를 얻었다. 결과: 1) Platelet aggregation ratio (PAR)는 대조군 $0.99{pm}0.04$, 폐동맥 정상혈압군 $0.98{pm}0.05$, 폐동맥 고혈압군 $0.89{pm}0.08$으로 감소하는 추세를 보였으며, 폐동액 고혈압군에서 대조군보다 통계학적으로 의미 있게 감소 하였다(p<0.05) (Table 2, Fig. 1). 2) Platelet factor 4 (PF4, IU/ml)는 대조군 $4.7{pm}1.2$, 폐동맥 정상혈압군 $18.6{pm}4.9$, 폐동맥 고혈압군 $57.2{pm}12.7$으로 만성폐쇄성폐질환에서 대조군보다 통계학적으로 의미 있게 증가 하였으며(p<0.01), 폐동맥 고혈압군에서 폐동맥 정상혈압군보다 통계학적으로 의미 있게 증가 하였다(p<0.01) (Table 2, Fig. 2). 3) Beta-thromboglobulin (${eta}$-TG, IU/ml)은 대조군 $34.4{pm}5.8$, 폐동맥 정상혈압군 $80.4{pm}18.1$, 폐동맥 고혈압군 $93.0{pm}14.0$으로 만성폐쇄성폐질환에서 대조군보다 통계학적으로 의미 있게 증가 하였으며(p<0.01) 폐동맥 고혈압군에서 폐동맥 정상혈압군보다 통계학적인 의미는 없지만 증가하는 경향을 보였다(Table 2, Fig.3). 4) 임상 소견과 PAR, PF4 및 ${eta}$-TG 사이에는 상관 관계가 없었으나 PAR, PF4및 ${eta}$-TG 사이에는 통계학적으로 의미 있는 상관관계를 보였다 (Table 3). 결론 : 만성폐쇄성폐질환에서 혈소판이 뚜렷이 활성화되어 있었으며 폐동맥 고혈압군에서 좀더 활성화되는 경향을 보였다. 따라서 만성폐쇄성폐질환에서 혈소판 활성화가 폐동맥 고혈압의 유발 및 유지에 관여할 것으로 사료되며 치료에 대한 연구가 필요할 것으로 사료된다.
Background: There is evidence that platelet is activated in chronic obstructive pulmonary disease and activated platelet with injured endothelium contribute to the pathogenesis of pulmonary hypertension, prognostic factor of chronic obstructive pulmonary disease. So, we have investigated platelet function further in chronic obstructive pulmonary disease and effect of platelet activation on pulmonary hypertension. Method: We studied platelet aggregation ratio and alpha-granule products such as platelet factor 4(PF4) and beta-thromboglobulin (${eta}$-TG) in control subjects and COPD without and with pulmonary hypertension subjects. Result: 1) The platelet aggregation ratio (PAR) was $0.99{pm}0.04$ in control subjects, $0.98{pm}0.05$ in COPD without pulmonary hypertension subjects and $0.89{pm}0.08$ in COPD with pulmonary hypertension subjects. The platelet aggregation ratio of COPD subjects was tend to decrease than that of control subjects and the ratio of COPD with pulmonary hypertension subjects was significantly lower than that of control subjects. 2) The platelet factor 4 (PF4, IU/ml) was $4.7{pm}1.2$ in control subjects, $18.6{pm}4.9$ in COPD without pulmonary hypertension subjects and $57.2{pm}12.7$ in COPD with pulmonary hypertension subjects. The level of COPD subjects was significantly higher than that of control subjects and the level of COPD with pulmonary hypertension subjects was significantly higher than that of COPD without pulmonary hypertension subjects. 3) The beta-thromboglobulin (${eta}$-TG, IU/ml) was $34.4{pm}5.8$ in control subjects, $80.4{pm}18.1$ in COPD without pulmonary hypertension subjects and $93.0{pm}14.0$ in COPD with pulmonary hypertension subjects. The level of COPD subjects was significantly higher than that of conrtrol subjects and the level of COPD with pulmonary hypertension subjects was tend to increase than that of COPD without pulmonary hypertension subjects. 4) There was no correlation between the clinical parameters and PAR, PF4 and ${eta}$-TG but there was significant correlation among PAR, PF4 and ${eta}$-TG. Conclusion: The platelet is activated in chronic obstructive pulmonary disease and the platelet of COPD with pulmonary hypertension is tend to be activated more than that of COPD without pulmonary hypertension. So, activated platelet may involve in the pathogenesis and maintenance of pulmonary hypertension in COPD subjects and modulation of platelet activity that might reduce pulmonary hypertension needs to be determined.
