TY - JOUR
T1 - Studies on group B β-hemolytic streptococcus. II. Effects on pulmonary hemodynamics and vascular permeability in unanesthetized sheep
AU - Rojas, Jorge
AU - Green, Robert S.
AU - Hellerqvist, Carl G.
AU - Olegard, Ragnar
AU - Brigham, Kenneth L.
AU - Stahlman, Mildred T.
PY - 1981/6
Y1 - 1981/6
N2 - To study the effects of Group B β-hemolytic Streptococcus on the pulmonary circulation and lung fluid balance, live and heat- killed bacteria and their toxin were infused into an awake sheep lung-lymph preparation. In every case, the response was biphasic; there was an initial period of marked pulmonary hypertension and high flow of protein-poor lymph associated with tachypnea, chills, and fever. A second phase followed during which pulmonary vascular pressures returned to near baseline and remained stable, but lymph flow remained high. The changes seen in the initial phase resemble the previously reported response to mechanically increased pulmonary vascular pressure and suggest that the increase in fluid filtration is secondary to increased microvascular pressure. During the second phase after toxin infusion, the increase in lung lymph flow was paralleled by an increase in lymph protein clearance. This cannot be accounted for by the hemodynamic changes alone and suggests that the permeability of lung microvascular walls to protein was increased. It is concluded that group B β- hemolytic streptococcal toxin in the sheep model causes pulmonary hypertension and increased pulmonary vascular permeability. Speculation: The effects caused by group G β-hemolytic Streptococcus toxin on the pulmonary circulation may be relevant to the pathogenesis of the respiratory distress and shock seen in newborns with this infection. Further understanding of the effects of this toxin could provide means for therapeutic intervention.
AB - To study the effects of Group B β-hemolytic Streptococcus on the pulmonary circulation and lung fluid balance, live and heat- killed bacteria and their toxin were infused into an awake sheep lung-lymph preparation. In every case, the response was biphasic; there was an initial period of marked pulmonary hypertension and high flow of protein-poor lymph associated with tachypnea, chills, and fever. A second phase followed during which pulmonary vascular pressures returned to near baseline and remained stable, but lymph flow remained high. The changes seen in the initial phase resemble the previously reported response to mechanically increased pulmonary vascular pressure and suggest that the increase in fluid filtration is secondary to increased microvascular pressure. During the second phase after toxin infusion, the increase in lung lymph flow was paralleled by an increase in lymph protein clearance. This cannot be accounted for by the hemodynamic changes alone and suggests that the permeability of lung microvascular walls to protein was increased. It is concluded that group B β- hemolytic streptococcal toxin in the sheep model causes pulmonary hypertension and increased pulmonary vascular permeability. Speculation: The effects caused by group G β-hemolytic Streptococcus toxin on the pulmonary circulation may be relevant to the pathogenesis of the respiratory distress and shock seen in newborns with this infection. Further understanding of the effects of this toxin could provide means for therapeutic intervention.
UR - http://www.scopus.com/inward/record.url?scp=0019468759&partnerID=8YFLogxK
U2 - 10.1203/00006450-198106000-00003
DO - 10.1203/00006450-198106000-00003
M3 - Article
C2 - 7017566
AN - SCOPUS:0019468759
SN - 0031-3998
VL - 15
SP - 899
EP - 904
JO - Pediatric Research
JF - Pediatric Research
IS - 6
ER -