Sandberg K, Engelhardt B, Hellerqvist C, Sundell H
Department of Pediatrics and Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
J Appl Physiol (1985). 1987 Nov;63(5):2024-30. doi: 10.1152/jappl.1987.63.5.2024.
Marked respiratory distress is seen in severe early onset group B beta-hemolytic streptococcal (GBS) disease in newborn infants. To investigate the pathophysiological effects of a polysaccharide toxin from GBS type III cultures, obtained from an infant who died from this disease, young chronically instrumented, unanesthetized lambs were studied with measurements of lung mechanics, lung volumes, ventilation, hemodynamics, and lung vascular permeability. Intravenously administered GBS toxin resulted in a biphasic response with an early threefold increase in total lung resistance, 40% decrease in dynamic lung compliance, and 30% increase in minute ventilation coinciding with hypoxemia, pulmonary hypertension, and fever. A second phase of the response followed consisting of less prominent changes in these variables as well as increased lung lymph protein clearance compatible with increased vascular permeability. The temporal close relationship between marked leukopenia and increased lung lymph thromboxane B2 concentrations to the simultaneously occurring pulmonary hypertension and changes in lung mechanics suggests that leukocytes and thromboxane A2 may be mediators of these GBS toxin-induced effects.
在新生儿严重早发型B族β溶血性链球菌(GBS)疾病中可见明显的呼吸窘迫。为了研究从一名死于该疾病的婴儿身上获得的III型GBS培养物中一种多糖毒素的病理生理作用,对长期植入仪器、未麻醉的幼龄羔羊进行了研究,测量了肺力学、肺容量、通气、血流动力学和肺血管通透性。静脉注射GBS毒素导致双相反应,早期总肺阻力增加三倍,动态肺顺应性降低40%,分钟通气量增加30%,同时伴有低氧血症、肺动脉高压和发热。随后是反应的第二阶段,这些变量的变化不太明显,同时肺淋巴蛋白清除增加,这与血管通透性增加相一致。明显的白细胞减少和肺淋巴血栓素B2浓度增加与同时出现的肺动脉高压和肺力学变化之间的时间密切关系表明,白细胞和血栓素A2可能是这些GBS毒素诱导效应的介质。