- 개심술 환자에서 술전및 술후의 폐동맥 고혈압및 혈역학적 변수들과 ET-1치와의 관계에 대한 연구
- ㆍ 저자명
- 박형주
- ㆍ 간행물명
- 大韓胸部外科學會誌
- ㆍ 권/호정보
- 1992년|25권 6호|pp.650-660 (11 pages)
- ㆍ 발행정보
- 대한흉부외과학회
- ㆍ 파일정보
- 정기간행물| PDF텍스트
- ㆍ 주제분야
- 기타
To elucidate a potential contribution of endotheline-1[ET-1] to the genesis of pulmonary hypertension and postoperative pulmonary hypertensive crisis in the patients with heart disease, we measured plasma levels of the ET-1 during perioperative period of open heart surgery. In addition, we examined changes of ET-1 during perioperative period and correlations between ET-1 levels and hemodynamic variables. 12 patients including 5 acquired heart disease and 7 congenital heart disease patients were selected randomly as a study group, Group A and B, respectively. 6 patients proved not having heart or hemodynamic problem were selected as a control, Group C. 110 blood samples from pulmonary artery[ET-P] and radial artery[ET-S] were taken and assayed by Sep-pak extraction and RIA. ET-1 levels of Group A were ET-P, 3.94$pm$5.31pg /ml, ET-S, 3.10$pm$2.90pg/ml[p>0.05], Group B were ET-P, 1.63$pm$0.62pg/ml, ET-S, 1.99$pm$2.45pg/ml[p>0.05], Group C were ET-P, 1.97$pm$2.02pg/ml, ET-S, 1.72$pm$0.77pg/ml[p>0.05]. There were no statistically significant differences of ET-1 levels among the Group A, B, C[p>0.05]. There was no correlation between pulmonary artery pressure[PAP] and ET-1 level[p>0.05], and ET-1 levels were not increased even in the cases of pulmonary hypertensive criwis or low cardiac output syndrome, whereas significant correlation between ET-S and pulmonary vascular res-istance[Rp] [r=0.36, p<0.05], and negative correlation between ET-S and OS saturation of pulmonary artery[OS-P][r= -0.49, p<0.01] were identified. Another significant finding was peak increase of ET-1 levels in the postoperative period 1 hour[p<0.05] and then gra-dualy decrease through the postoperative period. In conclusion, ET-1 has no correlation with PAP, whereas correlation with Rp, and inverse correlation with OS-P. It is suggested that ET-1 is neither the direct causative substance of pulmonary hypertension nor pulmonary vasospasm but there must be increased production of ET-1 in chronic pulmonary hypertensive state. Counter-regulatory mechanism to ET-1 is speculated during the pulmonary vasospasm.