Vaage J
Circ Shock. 1977;4(3):279-90.
Respiratory effects of long-lasting episodes of intravascular platelet aggregation have been studied in cats. Animals in 1 group had the chest opened and were given mechanical ventilation with a constant tidal volume. Animals of another group were breathing spontaneously. Platelet aggregation was induced by intravenous infusion (for 1 hr) of a suspension of collagen fibrils. Such infusions caused acute respiratory distress in both groups. Severe arterial hypoxemia and rapid breathing as well as constriction of airways and lung vessels occurred. Most of these changes were reversed within 2 hr after collagen infusion had ended. Deep lung inflations markedly improved lung function. It is concluded that an acute, but reversible pulmonary insufficiency might be caused by pulmonary microembolization due to intravascular platelet aggregation. The arterial hypoxemia is suggested to be caused by disturbances in the ventilation-perfusion ratio secondary to airway constriction and closure. The present findings also imply that besides platelet aggregation, some additional factors are necessary for irreversible or progressive respiratory insufficiency to develop.
已在猫身上研究了血管内血小板长期聚集发作的呼吸效应。一组动物打开胸腔并给予恒定潮气量的机械通气。另一组动物自主呼吸。通过静脉输注(持续1小时)胶原纤维悬液诱导血小板聚集。这种输注在两组中均引起急性呼吸窘迫。出现了严重的动脉低氧血症、呼吸急促以及气道和肺血管收缩。这些变化大多数在胶原输注结束后2小时内逆转。深度肺膨胀显著改善了肺功能。得出的结论是,血管内血小板聚集导致的肺微栓塞可能引起急性但可逆的肺功能不全。动脉低氧血症被认为是由气道收缩和闭合继发的通气-灌注比例失调所致。目前的研究结果还表明,除血小板聚集外,还需要一些其他因素才能导致不可逆或进行性呼吸功能不全的发生。