Tuberc Respir Dis > Volume 40(2); 1993 > Article
Tuberculosis and Respiratory Diseases 1993;40(2):135-146.
DOI: https://doi.org/10.4046/trd.1993.40.2.135    Published online April 1, 1993.
Effect of ketanserin and positive end expiratory pressure ventilation on hemodynamics and gas exchange in experimental acute pulmonary embolism.
Sang Do Lee1, Young Hyun Lee2, Sung Koo Han3, Young Soo Shim3, Keun Youl Kim3, Yong Chol Han3
1Department of lnternal Medicine, Chungbuk National Uníversity College of Medicine, Cheongju, Korea
2Department of lnternal Medicine, Dongguk Uníversity College of Medicine, Kyungju, Korea
3Department of lnternal Medicine, Seoul Nalional Uníversity College of Medícine, Seoul, Korea
Abstract
Background
In acute pulmonary embolism it has been postulated that the constriction of bronchi and pulmonary artery secondary to neurohumoral response plays an important role in cardiopulmonary dysfunction in addition to the mechanical obstruction of pulmonary artery. Serotonin is considered as the most important mediator. Positive end expiratory pressure (PEEP) stimulates PGI2 secretion from the vascular endothelium, but its role in acute pulmonary embolism is still in controversy
Methods
To study the cardiopulmonary effect and therapeutic role of Ketanserin, selective antagonist of 5-HT2 receptor, and PEEP in acute pulmonary embolism experimental acute pulmonary embolism was induced in dogs with autologous blood c1 0 t. The experimental animals were divided into 3 groups, that is control group, Ketanserin injection group and PEEP application group.
Results
Thirty minutes after embolization, mean pulmonary arterial pressure and pulmonary vascular resistance increased and cardiac output decreased. PaO2 PvO2and ox ygen transpo rt decreased and physiological shunt and PaCO2 increased. After injecti on of Ketanserin, comparing with control group , mean pulmonary arterial pressure, pulmonary vascular resistance and ph ysiologi-cal shunt decreased, while cardiac output, PaO, and oxygen transport increased. All these changes sustained till 4 hours after embolization. After PEEP application pulmonary vascular resistance, PaO2 and PaCO2increased, while physiological shunt, cardiac output and oxygen transport decreased After discontinuation of PEEP, mean pulmonary arterial pressure and pulmonary vascular resistance decreased and were lower than control group, while PaO2 and cardiac output increased and higher than control group. PaCO2 decreased but showed no significant difference comparing with control group.
Conclusion
It can be concluded that Ketanserin is effective for the treatment of acute pulmonary embolism. With PEEP hemodynamic status deteriorated, but improved better than control group after discontinuation of PEEP. Thus PEEP may be applied carefully for short period in acute pulmonary embolism if the hemodynamic status is tolerable.
Key Words: Pulmonary embolism, Ketanserin, PEEP


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