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KMID : 0364019920250060650
Korean Journal of Thoracic and Cardiovascular Surgery
1992 Volume.25 No. 6 p.650 ~ p.660
Endothelin-1 Levels in Patients with Heart Disease Associated with Pulmonary Hypertension: Potential role of Endothelin-1 in genesis of pulmonary artery vasospasm
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Abstract
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¡¾5.31pg/ml, ET-S, 3.10¡¾2.90pg/ml(p>0.05), Group B were ET-P, 1.63¡¾0.62pg/ml, ET-S, 1.99¡¾2.45pg/ml(p>0.05), Group C were ET-P, 1.97¡¾2.02pg/ml. ET-S, 1.72¡¾0.77pg/ml(p0.05). 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 resistance(Rp) (r=0.36, p<0.05), and negative correlation between ET-S and O2 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 gradualy 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 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.
KEYWORD
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