Brun-Pascaud M, Pocidalo J J, Kernbaum S
Bull Eur Physiopathol Respir. 1985 Jan-Feb;21(1):37-41.
Pneumocystis carinii (P.c.) pneumonia was induced in 40 rats by a prolonged corticosteroid treatment (group 1); 40 healthy rats of equal weight constituted the control group (group 2); 9 rats received the same corticosteroid treatment as group 1, together with trimethoprim-sulfamethoxazole (TMP-SFZ) in order to prevent P.c. multiplication (group 3). We could distinguish the respiratory effects induced by corticosteroids from those caused by P.c. pneumonia (group 3 vs group 1). For six weeks the blood leukocyte count, the weight of the spleen and the thymus and the pulmonary status were monitored. Blood gases and acid-base status were measured in conscious rats. There was no pulmonary oedema. The infected P.c. rats had a low PaCO2 and a slight disturbance of blood oxygenation, exemplified by A-aDO2 of 30 mmHg, compared with 17.5 mmHg in control rats and 17 mmHg in TMP-SFZ treated rats. P.c. infected rats had a lymphocyte depletion induced by corticosteroids. They did not exhibit respiratory distress. P.c. pneumonia alone in rats did not cause frank hypoxemia.
通过长期给予皮质类固醇治疗使40只大鼠诱发卡氏肺孢子虫肺炎(第1组);40只体重相当的健康大鼠作为对照组(第2组);9只大鼠接受与第1组相同的皮质类固醇治疗,并同时给予甲氧苄啶-磺胺甲恶唑(TMP-SFZ)以预防卡氏肺孢子虫增殖(第3组)。我们能够区分皮质类固醇诱导的呼吸效应与卡氏肺孢子虫肺炎所致的呼吸效应(第3组与第1组对比)。持续六周监测血液白细胞计数、脾脏和胸腺重量以及肺部状况。对清醒大鼠测量血气和酸碱状态。未出现肺水肿。感染卡氏肺孢子虫的大鼠PaCO2降低,血液氧合有轻微紊乱,以肺泡-动脉血氧分压差(A-aDO2)为30 mmHg为例,而对照大鼠为17.5 mmHg,TMP-SFZ治疗的大鼠为17 mmHg。感染卡氏肺孢子虫的大鼠出现由皮质类固醇诱导的淋巴细胞减少。它们未表现出呼吸窘迫。大鼠单独感染卡氏肺孢子虫肺炎未导致明显低氧血症。