견에서 저산소성 폐혈관 수축 및 스테로이드의 영향에 관한 실험적 연구

Abstract

The effects of unilateral hypoxic ventilation and steroids on pulmonary hemodynamics, alveolar-arterial oxygen tension differenee(A-aDO,) and intrapulmonary shunt in 10 dogs were studied under unilateral hypoxic ventilation with nitrogen. Heart rate, mean arterial pressure, central venous pressure, mean pulmonary arterial pressure. pulmonary capillary wedge pressure, cardiac output, blood gases and hemoglobin were measured during controlled ventilation with 100% oxygen and unilateral hypoxic ventilation, and after intravenous administration of 30mg/kg of methylprednisolone. Using above data, pulmonary hemodynamics. AaDO, and intrapulmonary shunt were calculated and the following results were obtained. 1. Mean pulmonary arterial pressure significantly increased(20%) from 20. G,_t2. GOmmHgto 21. S±2.1G mmHg(p<0.005) and pulmonary vascular resistance also significantly increased(13%) from 131±GS.1 dynes. sec/em' to G05±81. 0 dynes.sec/cm'(p<0.005), whereas cardiac output decreased(S%) from 1. 92± 0.23 l/min. to 1. 7G±0. 21 l/min(p<0.05) after unilateral hypoxic ventilation. After methylprednsiolone administration, there was further significant increase in mean pulmonary artery pressure from 24. 8±2. 4 mmHg to 26. 5±2. 5ImmHg(p<0. 05) and pulmonary vascular resistance from 605±8I. 0 dynes. sec/em' to 655±95.3 dynes.sec/cm'(p<0.05), whereas cardiac output did not change significantly. 2. Alveolar-arterial oxygen tension difference significantly increased from 180±23.2mmHg to 470± 31. 9mmHg(p<0. 005) after unilateral hypoxic ventilation but decreased significantly from 470±31. 9mmHg to 431±2S. 8mmHg after methylprednisolone administration. 3. Intrapulmonary shunt significantly increased from 9. 5±1. 40?~ to 24. 8j:2. 02% (p<0.005) after unilaterial hypoxic ventilatien, but it was much lower than the mathematically expected value (40% over) and there was significant decrease in intrapulmonary shunt from 21. 8±2. 02% to 22. 6±2. 51% (p<0.05) after methylprednisolone administration. The above findings suggest the operation of the protective mechanism which causes hypoxic pulmonary vasoconstriction in the unilateral hypoxic lung, and diverts blood flow from hypoxic to non-hypoxic lung and so minimizes the hypoxic effect on the arterial blood, and tbat tbe administration of methylprednisolone intensifies the hypoxic pulmonary vasoconstrictive phenomenon.